Orthopedics

L-ascorbic acid, more commonly know as vitamin C, is an essential micronutrient used in numerous metabolic pathways. It functions physiologically as a water-soluble antioxidant by virtue of its high reducing power, playing a key role in the function of leukocytes, protein metabolism, and production of neurotransmitters.^1-3 Vitamin C also contributes to musculoskeletal health through biosynthesis of carnitine and collagen⁴ and enhancement of intestinal absorption of dietary iron⁵ from plants and vegetables. Unlike most animals, humans are unable to synthesize this essential vitamin and therefore require intake from natural dietary sources or supplements.⁶ The ability of vitamin C to prevent or treat disease has been an area of research interest since the vitamin was identified and isolated by Szent-Györgyi in the 1930s.^7-16 Research in orthopedic surgery has focused on the effects of vitamin C on fracture healing, its potential use in preventing complex regional pain syndrome (CRPS), and its role in the pathophysiology of osteoarthritis. In this article, we review the basics of vitamin C metabolism and summarize the evidence surrounding the role of vitamin C supplementation in orthopedics.

Sources and Metabolism

Vitamin C is found naturally in many fruits and vegetables (Table 1) and is a common fortification in cereals, juices, and multivitamins. Daily recommended intake (Table 2) depends on age and smoking status. Absorption occurs in the distal small intestine, with blood plasma vitamin C concentrations reflecting dietary intake. Pharmacokinetic studies have shown that vitamin C concentrations are tightly regulated through absorption, tissue accumulation, and renal resorption, with plasma concentrations rarely exceeding 100 μmol/L without additional supplementation.¹⁷ Although the usual dietary doses of 100 mg/d (adult) are almost completely absorbed, producing a plasma concentration of 60 μmol/L, higher intake results in an increasingly smaller fraction absorbed.^1,18 Intake of more than 1000 mg/d results in less than 50% absorption¹⁹ (unmetabolized vitamin C is excreted in stool and urine¹). Even at higher doses, vitamin C has low toxicity³; the most common complaints are diarrhea, nausea, and abdominal cramps caused by the osmotic effect of unabsorbed vitamin C in the gastrointestinal tract.¹

Vitamin C Deficiency

The relationship between vitamin C deficiency and the development of scurvy has been documented for centuries. Symptoms are described in the ancient Egyptian, Greek, and Roman literature.²⁰ Ascorbic acid is essential for normal collagen function, as it is a required cofactor for enzymatic transfer of hydroxyl groups to select proline and lysine residues during procollagen formation. Hydroxylysine contributes to the intermolecular cross-links in collagen, and hydroxyproline stabilizes the triple-helix structure of collagen.²¹ Insufficient vitamin C during this process results in collagen that is non-cross-linked, nonhelical, structurally unstable, and weak.²¹ Clinical manifestations of scurvy stem from an underlying impairment of collagen production causing a systemic decrease in connective tissue integrity, capillary fragility, poor wound healing, fatigue, myalgias, arthritis, and even death.²² Vitamin C deficiency has also been implicated as a cause of diffuse bleeding in surgical patients with normal coagulation parameters secondary to capillary fragility.²³ In the United States, the 2003–2004 National Health and Nutrition Examination Survey (NHANES) measured serum vitamin C concentrations in 7277 noninstitutionalized patients 6 years old or older.²⁴ Age-adjusted incidence of subnormal serum vitamin C levels (<28 μmol/L) was 19.6%, and incidence of frank vitamin C deficiency (<11.4 μmol/L) was 7.1%. Reported rates of vitamin C deficiency in hospitalized patients are much higher, with 47% to 60% having subnormal values (<28 μmol/L) and 17% to 19% being vitamin C–deficient (<11.4 μmol/L).^22,25 Identified risk factors for hypovitaminosis C include advanced age, obesity, low socioeconomic status, unemployment, male sex, and concomitant alcohol and tobacco consumption.^22,24,25

Fracture Healing and Prevention

The effects of vitamin C deficiency on bone healing have been studied with animal models as early as the 1940s.^26,27 Early experiments using guinea pigs demonstrated failure of bone graft incorporation, delayed collagen maturation, and decreased collagen and callus formation in scorbutic animals compared with controls that received vitamin C supplementation.^26,27 Based on his work with guinea pigs, Bourne²⁶ reported in 1942 that vitamin C deficiency significantly inhibited the reparative process in damaged bone and that patients with fractures should receive vitamin C supplementation. Building on this early research, Yilmaz and colleagues²⁸ found faster histologic healing for tibia fractures in a rat model for animals that received a single injection of vitamin C 0.5 mg/kg compared with a nonscorbutic control group, and Sarisözen and colleagues²⁹ showed significantly accelerated histologic bone formation and mineralization at the fracture site for rats that received vitamin C supplementation. Moreover, Kipp and colleagues³⁰ found that scorbutic guinea pigs had lower bone mineral density (BMD), decreased bone mineral content, and impaired collagen synthesis of articular cartilage and tendons compared with nondeficient controls.

Besides promoting bone formation, vitamin C improves the mechanical strength of callus formation. Alcantara-Martos and colleagues³¹ used an osteogenic disorder Shionogi (ODS) rat model to examine the effects of vitamin C intake on femoral fracture healing. This particular animal model is unable to produce its own vitamin C. The groups with lower serum vitamin C levels demonstrated lower mechanical resistance of the fracture callus to torsional loads 5 weeks after fracture. Moreover, the group that received vitamin C supplementation showed higher histologic grade of callus formation and demonstrated faster healing rates. The authors suggested that subclinical vitamin C deficiency can delay fracture healing and that vitamin C supplementation in nondeficient patients would improve bone healing.

Other research has demonstrated a link between vitamin C and mesenchymal cell differentiation. Mohan and colleagues³² used an sfx mouse model to show that vitamin C deficiency results in decreased bone formation secondary to impaired osteoblast differentiation, diminished bone density, and development of spontaneous fractures. The authors indicated that not only is vitamin C essential for maintenance of differentiated functions of osteoblasts, but deficiency during early active growth may affect peak BMD levels in humans. Additional studies have demonstrated the role of vitamin C in endochondral bone formation through both induction of osteoblast differentiation and modulation of gene expression in hypertrophic chondrocytes.^33-36 Chronic vitamin C deficiency has been found to depress osteoblast function and differentiation of chondrocytes.³⁷ More recently, Kim and colleagues³⁸ examined the effect of vitamin C insufficiency in Gulo-deficient mice, which are unable to synthesize ascorbic acid. Ascorbic acid insufficiency over 4 weeks led to decreased plasma levels of osteocalcin and bone formation in vivo as well as significantly diminished metaphyseal trabecular bone. Despite all the evidence demonstrating the importance of vitamin C in bone formation and maintenance, many of the underlying processes in this relationship have yet to be determined.

Bone Mineral Density

Several observational studies have found a positive association between vitamin C intake and BMD in postmenopausal women. In a retrospective, cross-sectional study by Hall and Greendale,³⁹ a positive association was found between vitamin C intake and BMD of the femoral neck in 775 participants in the Postmenopausal Estrogen/Progestin Interventions trial. After calcium intake, physical activity level, smoking, estrogen use, age, and body mass index were adjusted for, each 100-mg increase in dietary vitamin C was associated with a 0.017 g/cm² increase in BMD. Wang and colleagues⁴⁰ found a positive association between dietary vitamin C intake and femoral neck BMD in a retrospective analysis of 125 postmenopausal Mexican American women. Other observational studies have reported that decreased intake of vitamin C is associated with osteoporosis⁴¹ and increased rates of BMD loss⁴² and that supplementation with vitamin C may suppress bone resorption in postmenopausal women.⁴³

The results of these studies contrast with the findings of Leveille and colleagues,⁴⁴ who examined the relationship between dietary vitamin C and hip BMD in 1892 postmenopausal women. Although the authors found that women (age, 55-64 years) using vitamin C supplements for more than 10 years had an average BMD 6.7% higher than that of nonusers, they did not find any association between dietary vitamin C intake and BMD. Moreover, NHANES III also found inconsistent associations between vitamin C and BMD among 13,080 adults surveyed in the United States.⁴⁵ Although for premenopausal women dietary ascorbic acid was associated with increased BMD, for postmenopausal women with a history of smoking and estrogen replacement, it was actually associated with lower BMD values. For other subgroups in the study, the relationship was also inconsistent or nonlinear.

The exact mechanism by which ascorbic acid contributes to BMD is not fully delineated. However, it likely is related to the known role of vitamin C in collagen formation, bone matrix development, osteoblast differentiation, and its antioxidant effects limiting bone resorption.^44,46

Hip Fractures

Besides demonstrating positive effects of vitamin C on bone healing and BMD, epidemiologic studies have found evidence of a protective effect of vitamin C on hip fracture risk. In a study of the Swedish Mammography cohort, 66,651 women (age, 40-76 years) were prospectively followed.⁴⁷ The authors found that the odds ratio (OR) for hip fractures among smokers with a low intake of vitamin E (median intake, ≤6.2 mg/d) was 3.0 (95% CI, 1.6-5.4) and for vitamin C (median intake, ≤67 mg/d) was 3.0 (95% CI, 1.6-5.6). Moreover, in smokers with a low intake of both vitamins E and C, OR increased to 4.9 (95% CI, 2.2-11.0). In addition, the Utah Study of Nutrition and Bone Health matched 1215 cases of hip fractures in patients who had ever smoked (age, >50 years) with 1349 controls and found that vitamin C intake above 159 mg/d had a significant protective effect on the incidence of hip fracture; however, a graded relationship was not observed.⁴⁸ Despite the inconsistencies in the NHANES III study regarding the relationship between vitamin C and BMD, Simon and Hudes⁴⁵ found that serum vitamin C was associated with lower risk for self-reported fracture in postmenopausal women who had ever smoked and had a history of estrogen therapy (OR, 0.51; 95% CI, 0.36-0.70). Finally, Sahni and colleagues⁴⁹ followed 958 Framingham cohort men and women (mean age, 75 years) over 17 years and found that those in the highest tertile of total vitamin C intake (median, 313 mg/d) had significantly fewer hip fractures and nonvertebral fractures compared with those in the lowest tertile of intake (median, 94 mg/d). Dietary vitamin C intake was not associated with fracture risk in this study.

Complex Regional Pain Syndrome

Type 1 CRPS is a debilitating condition characterized by severe pain, swelling, and vasomotor instability. It is commonly precipitated by an injury or surgery to an extremity and is a dreaded sequelae in orthopedics,⁵⁰ with incidence rates of 10% to 22% in wrist fractures^51-53 and 10% after foot and ankle surgery.⁵⁴ Although the pathophysiology of CRPS remains unknown, dysregulation and increased permeability of the vasculature caused by free radicals are thought to play an important role.⁵⁵ In dermal burns, high doses of vitamin C therapy slowed progression of vascular permeability and therefore reduced extravascular leakage of fluids and protein.^56,57 The ability of vitamin C to prevent CRPS has been studied in only a handful of trials.

In a double-blind trial, Zollinger and colleagues⁵¹ randomized 127 conservatively treated distal radius fractures to receive either vitamin C 500 mg or placebo daily for 50 days starting on day of injury. Incidence of CRPS (using the diagnostic criteria proposed by Veldman and colleagues⁵⁸) at 1-year follow-up was 22% in the placebo group and 7% in the vitamin C group (95% CI for difference, 2%-26%). Complaints while wearing the cast and fracture type increased the risk for developing CRPS. This initial study was followed up by a prospective, randomized, double-blind multicenter trial by the same authors,⁵² who had 416 patients with 427 wrist fractures receive either placebo or vitamin C 200 mg/d, 500 mg/d, or 1500 mg/d for 50 days. This follow-up study included both operative (11%) and nonoperative (89%) distal radius fractures. Incidence of CRPS was 10.1% in the placebo group and 2.4% in the vitamin C group (P < .002). Although there was an appreciable drop in the relative risk (RR) of developing CRPS between the vitamin C 200-mg/d and 500-mg/d groups (0.41-0.17), there was no additional benefit in the 1500-mg/d group. Pooling the data for these 2 randomized trials showed that the overall RR for developing CRPS was lower with vitamin C supplementation (RR, 0.28; 95% CI, 0.14-0.56; P = .0003).⁵⁹

Results of the 2 trials by Zollinger and colleagues^51,52 have been met with several concerns.^60-62 As a corollary to the unclear etiology of CRPS, several different sets of diagnostic criteria exist, and the criteria are somewhat subjective and imprecise. Although both trials used the Veldman criteria,⁵⁸ the incidence of CRPS in the placebo group dropped unexpectedly between trials, from 22% to 10.1%, and the results may have been different had other criteria been used. Moreover, the idea that toxic oxygen radicals have a role in CRPS and that vitamin C can scavenge these radicals is based on limited data.⁶¹ In the absence of a clear pathophysiologic explanation, some surgeons have been reluctant to treat patients with vitamin C supplementation.

Cazeneuve and colleagues⁵³ also studied the effect of vitamin C supplementation on CRPS in patients with distal radius fractures treated with reduction and intrafocal pinning. Group 1 consisted of 100 patients (treated from 1995 to 1998) who did not receive vitamin C supplementation, and group 2 consisted of 95 patients (treated from 1998 to 2002) who received vitamin C 1000 mg/d for 45 days starting on day of fracture. Patients were followed for up to 90 days after surgery. Incidence of CRPS type 1 was 10% in the untreated group and 2.1% in the group that received vitamin C supplementation.

Vitamin C prophylaxis for CRPS has also been studied in foot and ankle surgery. Besse and colleagues⁵⁴ prospectively compared 2 chronologically successive groups that received (235 feet) or did not receive (185 feet) vitamin C 1000-mg/d supplementation for 45 days. Incidence of CRPS type 1 as diagnosed with International Association for the Study of Pain (IASP) criteria dropped from 9.6% to 1.7% with vitamin C supplementation. In a case series, Zollinger and colleagues⁶³ examined CRPS type 1 rates after performing cementless total trapeziometacarpal semiconstrained joint prosthesis implantations for trapeziometacarpal arthritis. Forty implantations were performed in 34 patients. All patients received vitamin C 500 mg/d for CRPS prevention starting 2 days before surgery for 50 days. There were no cases of CRPS in the postoperative period, according to Veldman or IASP criteria. Although the results of the studies by Cazeneuve and colleagues⁵³ and Besse and colleagues⁵⁴ agree with those of the distal radius fracture trials by Zollinger and colleagues,^51,52 the quasi-experimental design and the lack of blinding and randomization temper the conclusions that can be drawn because of the risk for significant bias.

In a recent systematic review examining the effectiveness of vitamin C supplementation in preventing CRPS in trauma and surgery in the extremities, Shibuya and colleagues⁶⁴ concluded that taking at least 500 mg of vitamin C daily for 45 to 50 days after injury or surgery may help decrease the incidence of CRPS after a traumatic event.

Osteoarthritis

Damage caused by free radicals has long been thought to play an important role in osteoarthritis (OA).^65-67 A cross-sectional study in knee OA found that amounts of joint fluid antioxidants were lower in patients with severe arthritis than in those with intact cartilage, further implicating free radicals in the pathophysiology of OA.⁶⁸ Use of vitamin C for prophylaxis against development or progression of OA is therefore a hot research topic. Thus far, animal studies have had mixed results—several showing a chondroprotective effect of vitamin C^69,70 and others finding either no effect or even a positive association with the development of arthritis.⁷¹

The literature on human subjects, chiefly observational studies, is just as controversial. Wang and colleagues⁴⁰ found vitamin C intake associated with both a 50% risk reduction of bone marrow lesions on magnetic resonance imaging over a 10-year interval (OR, 0.5; 95% CI, 0.29-0.87) and inversely associated with the tibial plateau bone area. Similarly, the Clearwater Osteoarthritis Study, which followed 1023 patients (age, >40 years), showed that participants who took vitamin C supplements were 11% less likely to develop radiographic evidence of OA (RR, 0.89; 95% CI, 0.85-0.93).⁷² Nonetheless, other studies have failed to show such associations⁷³ or have demonstrated the opposite effect. Chaganti and colleagues⁷⁴ analyzed levels of vitamins C and E in the Multicenter Osteoarthritis Study (MOST) cohort of 3026 men and women (age, 50-79 years) and found higher vitamin levels were not protective against incidence of radiographic whole-knee OA and may even have been associated with increased risk.

Conclusion

Vitamin C is an essential micronutrient and a powerful water-soluble antioxidant in numerous biochemical pathways that influence bone health. It has been implicated in the biology of fracture healing, and vitamin C supplementation has been proposed as prophylaxis against hip fractures based on observational data. Results of 2 high-quality double-blind randomized trials support use of vitamin C as prophylaxis against CRPS in wrist fractures treated conservatively and operatively; the evidence for foot and ankle surgery is weaker. Use of vitamin C in OA prevention has tremendous potential, though animal and human study results are controversial. Heterogeneous results and lack of prospective trials preclude any recommendation at this time.

L-ascorbic acid, more commonly know as vitamin C, is an essential micronutrient used in numerous metabolic pathways. It functions physiologically as a water-soluble antioxidant by virtue of its high reducing power, playing a key role in the function of leukocytes, protein metabolism, and production of neurotransmitters.^1-3 Vitamin C also contributes to musculoskeletal health through biosynthesis of carnitine and collagen⁴ and enhancement of intestinal absorption of dietary iron⁵ from plants and vegetables. Unlike most animals, humans are unable to synthesize this essential vitamin and therefore require intake from natural dietary sources or supplements.⁶ The ability of vitamin C to prevent or treat disease has been an area of research interest since the vitamin was identified and isolated by Szent-Györgyi in the 1930s.^7-16 Research in orthopedic surgery has focused on the effects of vitamin C on fracture healing, its potential use in preventing complex regional pain syndrome (CRPS), and its role in the pathophysiology of osteoarthritis. In this article, we review the basics of vitamin C metabolism and summarize the evidence surrounding the role of vitamin C supplementation in orthopedics.

Sources and Metabolism

Vitamin C is found naturally in many fruits and vegetables (Table 1) and is a common fortification in cereals, juices, and multivitamins. Daily recommended intake (Table 2) depends on age and smoking status. Absorption occurs in the distal small intestine, with blood plasma vitamin C concentrations reflecting dietary intake. Pharmacokinetic studies have shown that vitamin C concentrations are tightly regulated through absorption, tissue accumulation, and renal resorption, with plasma concentrations rarely exceeding 100 μmol/L without additional supplementation.¹⁷ Although the usual dietary doses of 100 mg/d (adult) are almost completely absorbed, producing a plasma concentration of 60 μmol/L, higher intake results in an increasingly smaller fraction absorbed.^1,18 Intake of more than 1000 mg/d results in less than 50% absorption¹⁹ (unmetabolized vitamin C is excreted in stool and urine¹). Even at higher doses, vitamin C has low toxicity³; the most common complaints are diarrhea, nausea, and abdominal cramps caused by the osmotic effect of unabsorbed vitamin C in the gastrointestinal tract.¹

Vitamin C Deficiency

The relationship between vitamin C deficiency and the development of scurvy has been documented for centuries. Symptoms are described in the ancient Egyptian, Greek, and Roman literature.²⁰ Ascorbic acid is essential for normal collagen function, as it is a required cofactor for enzymatic transfer of hydroxyl groups to select proline and lysine residues during procollagen formation. Hydroxylysine contributes to the intermolecular cross-links in collagen, and hydroxyproline stabilizes the triple-helix structure of collagen.²¹ Insufficient vitamin C during this process results in collagen that is non-cross-linked, nonhelical, structurally unstable, and weak.²¹ Clinical manifestations of scurvy stem from an underlying impairment of collagen production causing a systemic decrease in connective tissue integrity, capillary fragility, poor wound healing, fatigue, myalgias, arthritis, and even death.²² Vitamin C deficiency has also been implicated as a cause of diffuse bleeding in surgical patients with normal coagulation parameters secondary to capillary fragility.²³ In the United States, the 2003–2004 National Health and Nutrition Examination Survey (NHANES) measured serum vitamin C concentrations in 7277 noninstitutionalized patients 6 years old or older.²⁴ Age-adjusted incidence of subnormal serum vitamin C levels (<28 μmol/L) was 19.6%, and incidence of frank vitamin C deficiency (<11.4 μmol/L) was 7.1%. Reported rates of vitamin C deficiency in hospitalized patients are much higher, with 47% to 60% having subnormal values (<28 μmol/L) and 17% to 19% being vitamin C–deficient (<11.4 μmol/L).^22,25 Identified risk factors for hypovitaminosis C include advanced age, obesity, low socioeconomic status, unemployment, male sex, and concomitant alcohol and tobacco consumption.^22,24,25

Fracture Healing and Prevention

The effects of vitamin C deficiency on bone healing have been studied with animal models as early as the 1940s.^26,27 Early experiments using guinea pigs demonstrated failure of bone graft incorporation, delayed collagen maturation, and decreased collagen and callus formation in scorbutic animals compared with controls that received vitamin C supplementation.^26,27 Based on his work with guinea pigs, Bourne²⁶ reported in 1942 that vitamin C deficiency significantly inhibited the reparative process in damaged bone and that patients with fractures should receive vitamin C supplementation. Building on this early research, Yilmaz and colleagues²⁸ found faster histologic healing for tibia fractures in a rat model for animals that received a single injection of vitamin C 0.5 mg/kg compared with a nonscorbutic control group, and Sarisözen and colleagues²⁹ showed significantly accelerated histologic bone formation and mineralization at the fracture site for rats that received vitamin C supplementation. Moreover, Kipp and colleagues³⁰ found that scorbutic guinea pigs had lower bone mineral density (BMD), decreased bone mineral content, and impaired collagen synthesis of articular cartilage and tendons compared with nondeficient controls.

Besides promoting bone formation, vitamin C improves the mechanical strength of callus formation. Alcantara-Martos and colleagues³¹ used an osteogenic disorder Shionogi (ODS) rat model to examine the effects of vitamin C intake on femoral fracture healing. This particular animal model is unable to produce its own vitamin C. The groups with lower serum vitamin C levels demonstrated lower mechanical resistance of the fracture callus to torsional loads 5 weeks after fracture. Moreover, the group that received vitamin C supplementation showed higher histologic grade of callus formation and demonstrated faster healing rates. The authors suggested that subclinical vitamin C deficiency can delay fracture healing and that vitamin C supplementation in nondeficient patients would improve bone healing.

Other research has demonstrated a link between vitamin C and mesenchymal cell differentiation. Mohan and colleagues³² used an sfx mouse model to show that vitamin C deficiency results in decreased bone formation secondary to impaired osteoblast differentiation, diminished bone density, and development of spontaneous fractures. The authors indicated that not only is vitamin C essential for maintenance of differentiated functions of osteoblasts, but deficiency during early active growth may affect peak BMD levels in humans. Additional studies have demonstrated the role of vitamin C in endochondral bone formation through both induction of osteoblast differentiation and modulation of gene expression in hypertrophic chondrocytes.^33-36 Chronic vitamin C deficiency has been found to depress osteoblast function and differentiation of chondrocytes.³⁷ More recently, Kim and colleagues³⁸ examined the effect of vitamin C insufficiency in Gulo-deficient mice, which are unable to synthesize ascorbic acid. Ascorbic acid insufficiency over 4 weeks led to decreased plasma levels of osteocalcin and bone formation in vivo as well as significantly diminished metaphyseal trabecular bone. Despite all the evidence demonstrating the importance of vitamin C in bone formation and maintenance, many of the underlying processes in this relationship have yet to be determined.

Bone Mineral Density

Several observational studies have found a positive association between vitamin C intake and BMD in postmenopausal women. In a retrospective, cross-sectional study by Hall and Greendale,³⁹ a positive association was found between vitamin C intake and BMD of the femoral neck in 775 participants in the Postmenopausal Estrogen/Progestin Interventions trial. After calcium intake, physical activity level, smoking, estrogen use, age, and body mass index were adjusted for, each 100-mg increase in dietary vitamin C was associated with a 0.017 g/cm² increase in BMD. Wang and colleagues⁴⁰ found a positive association between dietary vitamin C intake and femoral neck BMD in a retrospective analysis of 125 postmenopausal Mexican American women. Other observational studies have reported that decreased intake of vitamin C is associated with osteoporosis⁴¹ and increased rates of BMD loss⁴² and that supplementation with vitamin C may suppress bone resorption in postmenopausal women.⁴³

The results of these studies contrast with the findings of Leveille and colleagues,⁴⁴ who examined the relationship between dietary vitamin C and hip BMD in 1892 postmenopausal women. Although the authors found that women (age, 55-64 years) using vitamin C supplements for more than 10 years had an average BMD 6.7% higher than that of nonusers, they did not find any association between dietary vitamin C intake and BMD. Moreover, NHANES III also found inconsistent associations between vitamin C and BMD among 13,080 adults surveyed in the United States.⁴⁵ Although for premenopausal women dietary ascorbic acid was associated with increased BMD, for postmenopausal women with a history of smoking and estrogen replacement, it was actually associated with lower BMD values. For other subgroups in the study, the relationship was also inconsistent or nonlinear.

The exact mechanism by which ascorbic acid contributes to BMD is not fully delineated. However, it likely is related to the known role of vitamin C in collagen formation, bone matrix development, osteoblast differentiation, and its antioxidant effects limiting bone resorption.^44,46

Hip Fractures

Besides demonstrating positive effects of vitamin C on bone healing and BMD, epidemiologic studies have found evidence of a protective effect of vitamin C on hip fracture risk. In a study of the Swedish Mammography cohort, 66,651 women (age, 40-76 years) were prospectively followed.⁴⁷ The authors found that the odds ratio (OR) for hip fractures among smokers with a low intake of vitamin E (median intake, ≤6.2 mg/d) was 3.0 (95% CI, 1.6-5.4) and for vitamin C (median intake, ≤67 mg/d) was 3.0 (95% CI, 1.6-5.6). Moreover, in smokers with a low intake of both vitamins E and C, OR increased to 4.9 (95% CI, 2.2-11.0). In addition, the Utah Study of Nutrition and Bone Health matched 1215 cases of hip fractures in patients who had ever smoked (age, >50 years) with 1349 controls and found that vitamin C intake above 159 mg/d had a significant protective effect on the incidence of hip fracture; however, a graded relationship was not observed.⁴⁸ Despite the inconsistencies in the NHANES III study regarding the relationship between vitamin C and BMD, Simon and Hudes⁴⁵ found that serum vitamin C was associated with lower risk for self-reported fracture in postmenopausal women who had ever smoked and had a history of estrogen therapy (OR, 0.51; 95% CI, 0.36-0.70). Finally, Sahni and colleagues⁴⁹ followed 958 Framingham cohort men and women (mean age, 75 years) over 17 years and found that those in the highest tertile of total vitamin C intake (median, 313 mg/d) had significantly fewer hip fractures and nonvertebral fractures compared with those in the lowest tertile of intake (median, 94 mg/d). Dietary vitamin C intake was not associated with fracture risk in this study.

Complex Regional Pain Syndrome

Type 1 CRPS is a debilitating condition characterized by severe pain, swelling, and vasomotor instability. It is commonly precipitated by an injury or surgery to an extremity and is a dreaded sequelae in orthopedics,⁵⁰ with incidence rates of 10% to 22% in wrist fractures^51-53 and 10% after foot and ankle surgery.⁵⁴ Although the pathophysiology of CRPS remains unknown, dysregulation and increased permeability of the vasculature caused by free radicals are thought to play an important role.⁵⁵ In dermal burns, high doses of vitamin C therapy slowed progression of vascular permeability and therefore reduced extravascular leakage of fluids and protein.^56,57 The ability of vitamin C to prevent CRPS has been studied in only a handful of trials.

In a double-blind trial, Zollinger and colleagues⁵¹ randomized 127 conservatively treated distal radius fractures to receive either vitamin C 500 mg or placebo daily for 50 days starting on day of injury. Incidence of CRPS (using the diagnostic criteria proposed by Veldman and colleagues⁵⁸) at 1-year follow-up was 22% in the placebo group and 7% in the vitamin C group (95% CI for difference, 2%-26%). Complaints while wearing the cast and fracture type increased the risk for developing CRPS. This initial study was followed up by a prospective, randomized, double-blind multicenter trial by the same authors,⁵² who had 416 patients with 427 wrist fractures receive either placebo or vitamin C 200 mg/d, 500 mg/d, or 1500 mg/d for 50 days. This follow-up study included both operative (11%) and nonoperative (89%) distal radius fractures. Incidence of CRPS was 10.1% in the placebo group and 2.4% in the vitamin C group (P < .002). Although there was an appreciable drop in the relative risk (RR) of developing CRPS between the vitamin C 200-mg/d and 500-mg/d groups (0.41-0.17), there was no additional benefit in the 1500-mg/d group. Pooling the data for these 2 randomized trials showed that the overall RR for developing CRPS was lower with vitamin C supplementation (RR, 0.28; 95% CI, 0.14-0.56; P = .0003).⁵⁹

Results of the 2 trials by Zollinger and colleagues^51,52 have been met with several concerns.^60-62 As a corollary to the unclear etiology of CRPS, several different sets of diagnostic criteria exist, and the criteria are somewhat subjective and imprecise. Although both trials used the Veldman criteria,⁵⁸ the incidence of CRPS in the placebo group dropped unexpectedly between trials, from 22% to 10.1%, and the results may have been different had other criteria been used. Moreover, the idea that toxic oxygen radicals have a role in CRPS and that vitamin C can scavenge these radicals is based on limited data.⁶¹ In the absence of a clear pathophysiologic explanation, some surgeons have been reluctant to treat patients with vitamin C supplementation.

Cazeneuve and colleagues⁵³ also studied the effect of vitamin C supplementation on CRPS in patients with distal radius fractures treated with reduction and intrafocal pinning. Group 1 consisted of 100 patients (treated from 1995 to 1998) who did not receive vitamin C supplementation, and group 2 consisted of 95 patients (treated from 1998 to 2002) who received vitamin C 1000 mg/d for 45 days starting on day of fracture. Patients were followed for up to 90 days after surgery. Incidence of CRPS type 1 was 10% in the untreated group and 2.1% in the group that received vitamin C supplementation.

Vitamin C prophylaxis for CRPS has also been studied in foot and ankle surgery. Besse and colleagues⁵⁴ prospectively compared 2 chronologically successive groups that received (235 feet) or did not receive (185 feet) vitamin C 1000-mg/d supplementation for 45 days. Incidence of CRPS type 1 as diagnosed with International Association for the Study of Pain (IASP) criteria dropped from 9.6% to 1.7% with vitamin C supplementation. In a case series, Zollinger and colleagues⁶³ examined CRPS type 1 rates after performing cementless total trapeziometacarpal semiconstrained joint prosthesis implantations for trapeziometacarpal arthritis. Forty implantations were performed in 34 patients. All patients received vitamin C 500 mg/d for CRPS prevention starting 2 days before surgery for 50 days. There were no cases of CRPS in the postoperative period, according to Veldman or IASP criteria. Although the results of the studies by Cazeneuve and colleagues⁵³ and Besse and colleagues⁵⁴ agree with those of the distal radius fracture trials by Zollinger and colleagues,^51,52 the quasi-experimental design and the lack of blinding and randomization temper the conclusions that can be drawn because of the risk for significant bias.

In a recent systematic review examining the effectiveness of vitamin C supplementation in preventing CRPS in trauma and surgery in the extremities, Shibuya and colleagues⁶⁴ concluded that taking at least 500 mg of vitamin C daily for 45 to 50 days after injury or surgery may help decrease the incidence of CRPS after a traumatic event.

Osteoarthritis

Damage caused by free radicals has long been thought to play an important role in osteoarthritis (OA).^65-67 A cross-sectional study in knee OA found that amounts of joint fluid antioxidants were lower in patients with severe arthritis than in those with intact cartilage, further implicating free radicals in the pathophysiology of OA.⁶⁸ Use of vitamin C for prophylaxis against development or progression of OA is therefore a hot research topic. Thus far, animal studies have had mixed results—several showing a chondroprotective effect of vitamin C^69,70 and others finding either no effect or even a positive association with the development of arthritis.⁷¹

The literature on human subjects, chiefly observational studies, is just as controversial. Wang and colleagues⁴⁰ found vitamin C intake associated with both a 50% risk reduction of bone marrow lesions on magnetic resonance imaging over a 10-year interval (OR, 0.5; 95% CI, 0.29-0.87) and inversely associated with the tibial plateau bone area. Similarly, the Clearwater Osteoarthritis Study, which followed 1023 patients (age, >40 years), showed that participants who took vitamin C supplements were 11% less likely to develop radiographic evidence of OA (RR, 0.89; 95% CI, 0.85-0.93).⁷² Nonetheless, other studies have failed to show such associations⁷³ or have demonstrated the opposite effect. Chaganti and colleagues⁷⁴ analyzed levels of vitamins C and E in the Multicenter Osteoarthritis Study (MOST) cohort of 3026 men and women (age, 50-79 years) and found higher vitamin levels were not protective against incidence of radiographic whole-knee OA and may even have been associated with increased risk.

Conclusion

Vitamin C is an essential micronutrient and a powerful water-soluble antioxidant in numerous biochemical pathways that influence bone health. It has been implicated in the biology of fracture healing, and vitamin C supplementation has been proposed as prophylaxis against hip fractures based on observational data. Results of 2 high-quality double-blind randomized trials support use of vitamin C as prophylaxis against CRPS in wrist fractures treated conservatively and operatively; the evidence for foot and ankle surgery is weaker. Use of vitamin C in OA prevention has tremendous potential, though animal and human study results are controversial. Heterogeneous results and lack of prospective trials preclude any recommendation at this time.

L-ascorbic acid, more commonly know as vitamin C, is an essential micronutrient used in numerous metabolic pathways. It functions physiologically as a water-soluble antioxidant by virtue of its high reducing power, playing a key role in the function of leukocytes, protein metabolism, and production of neurotransmitters.^1-3 Vitamin C also contributes to musculoskeletal health through biosynthesis of carnitine and collagen⁴ and enhancement of intestinal absorption of dietary iron⁵ from plants and vegetables. Unlike most animals, humans are unable to synthesize this essential vitamin and therefore require intake from natural dietary sources or supplements.⁶ The ability of vitamin C to prevent or treat disease has been an area of research interest since the vitamin was identified and isolated by Szent-Györgyi in the 1930s.^7-16 Research in orthopedic surgery has focused on the effects of vitamin C on fracture healing, its potential use in preventing complex regional pain syndrome (CRPS), and its role in the pathophysiology of osteoarthritis. In this article, we review the basics of vitamin C metabolism and summarize the evidence surrounding the role of vitamin C supplementation in orthopedics.

Sources and Metabolism

Vitamin C is found naturally in many fruits and vegetables (Table 1) and is a common fortification in cereals, juices, and multivitamins. Daily recommended intake (Table 2) depends on age and smoking status. Absorption occurs in the distal small intestine, with blood plasma vitamin C concentrations reflecting dietary intake. Pharmacokinetic studies have shown that vitamin C concentrations are tightly regulated through absorption, tissue accumulation, and renal resorption, with plasma concentrations rarely exceeding 100 μmol/L without additional supplementation.¹⁷ Although the usual dietary doses of 100 mg/d (adult) are almost completely absorbed, producing a plasma concentration of 60 μmol/L, higher intake results in an increasingly smaller fraction absorbed.^1,18 Intake of more than 1000 mg/d results in less than 50% absorption¹⁹ (unmetabolized vitamin C is excreted in stool and urine¹). Even at higher doses, vitamin C has low toxicity³; the most common complaints are diarrhea, nausea, and abdominal cramps caused by the osmotic effect of unabsorbed vitamin C in the gastrointestinal tract.¹

Vitamin C Deficiency

The relationship between vitamin C deficiency and the development of scurvy has been documented for centuries. Symptoms are described in the ancient Egyptian, Greek, and Roman literature.²⁰ Ascorbic acid is essential for normal collagen function, as it is a required cofactor for enzymatic transfer of hydroxyl groups to select proline and lysine residues during procollagen formation. Hydroxylysine contributes to the intermolecular cross-links in collagen, and hydroxyproline stabilizes the triple-helix structure of collagen.²¹ Insufficient vitamin C during this process results in collagen that is non-cross-linked, nonhelical, structurally unstable, and weak.²¹ Clinical manifestations of scurvy stem from an underlying impairment of collagen production causing a systemic decrease in connective tissue integrity, capillary fragility, poor wound healing, fatigue, myalgias, arthritis, and even death.²² Vitamin C deficiency has also been implicated as a cause of diffuse bleeding in surgical patients with normal coagulation parameters secondary to capillary fragility.²³ In the United States, the 2003–2004 National Health and Nutrition Examination Survey (NHANES) measured serum vitamin C concentrations in 7277 noninstitutionalized patients 6 years old or older.²⁴ Age-adjusted incidence of subnormal serum vitamin C levels (<28 μmol/L) was 19.6%, and incidence of frank vitamin C deficiency (<11.4 μmol/L) was 7.1%. Reported rates of vitamin C deficiency in hospitalized patients are much higher, with 47% to 60% having subnormal values (<28 μmol/L) and 17% to 19% being vitamin C–deficient (<11.4 μmol/L).^22,25 Identified risk factors for hypovitaminosis C include advanced age, obesity, low socioeconomic status, unemployment, male sex, and concomitant alcohol and tobacco consumption.^22,24,25

Fracture Healing and Prevention

The effects of vitamin C deficiency on bone healing have been studied with animal models as early as the 1940s.^26,27 Early experiments using guinea pigs demonstrated failure of bone graft incorporation, delayed collagen maturation, and decreased collagen and callus formation in scorbutic animals compared with controls that received vitamin C supplementation.^26,27 Based on his work with guinea pigs, Bourne²⁶ reported in 1942 that vitamin C deficiency significantly inhibited the reparative process in damaged bone and that patients with fractures should receive vitamin C supplementation. Building on this early research, Yilmaz and colleagues²⁸ found faster histologic healing for tibia fractures in a rat model for animals that received a single injection of vitamin C 0.5 mg/kg compared with a nonscorbutic control group, and Sarisözen and colleagues²⁹ showed significantly accelerated histologic bone formation and mineralization at the fracture site for rats that received vitamin C supplementation. Moreover, Kipp and colleagues³⁰ found that scorbutic guinea pigs had lower bone mineral density (BMD), decreased bone mineral content, and impaired collagen synthesis of articular cartilage and tendons compared with nondeficient controls.

Besides promoting bone formation, vitamin C improves the mechanical strength of callus formation. Alcantara-Martos and colleagues³¹ used an osteogenic disorder Shionogi (ODS) rat model to examine the effects of vitamin C intake on femoral fracture healing. This particular animal model is unable to produce its own vitamin C. The groups with lower serum vitamin C levels demonstrated lower mechanical resistance of the fracture callus to torsional loads 5 weeks after fracture. Moreover, the group that received vitamin C supplementation showed higher histologic grade of callus formation and demonstrated faster healing rates. The authors suggested that subclinical vitamin C deficiency can delay fracture healing and that vitamin C supplementation in nondeficient patients would improve bone healing.

Other research has demonstrated a link between vitamin C and mesenchymal cell differentiation. Mohan and colleagues³² used an sfx mouse model to show that vitamin C deficiency results in decreased bone formation secondary to impaired osteoblast differentiation, diminished bone density, and development of spontaneous fractures. The authors indicated that not only is vitamin C essential for maintenance of differentiated functions of osteoblasts, but deficiency during early active growth may affect peak BMD levels in humans. Additional studies have demonstrated the role of vitamin C in endochondral bone formation through both induction of osteoblast differentiation and modulation of gene expression in hypertrophic chondrocytes.^33-36 Chronic vitamin C deficiency has been found to depress osteoblast function and differentiation of chondrocytes.³⁷ More recently, Kim and colleagues³⁸ examined the effect of vitamin C insufficiency in Gulo-deficient mice, which are unable to synthesize ascorbic acid. Ascorbic acid insufficiency over 4 weeks led to decreased plasma levels of osteocalcin and bone formation in vivo as well as significantly diminished metaphyseal trabecular bone. Despite all the evidence demonstrating the importance of vitamin C in bone formation and maintenance, many of the underlying processes in this relationship have yet to be determined.

Bone Mineral Density

Several observational studies have found a positive association between vitamin C intake and BMD in postmenopausal women. In a retrospective, cross-sectional study by Hall and Greendale,³⁹ a positive association was found between vitamin C intake and BMD of the femoral neck in 775 participants in the Postmenopausal Estrogen/Progestin Interventions trial. After calcium intake, physical activity level, smoking, estrogen use, age, and body mass index were adjusted for, each 100-mg increase in dietary vitamin C was associated with a 0.017 g/cm² increase in BMD. Wang and colleagues⁴⁰ found a positive association between dietary vitamin C intake and femoral neck BMD in a retrospective analysis of 125 postmenopausal Mexican American women. Other observational studies have reported that decreased intake of vitamin C is associated with osteoporosis⁴¹ and increased rates of BMD loss⁴² and that supplementation with vitamin C may suppress bone resorption in postmenopausal women.⁴³

The results of these studies contrast with the findings of Leveille and colleagues,⁴⁴ who examined the relationship between dietary vitamin C and hip BMD in 1892 postmenopausal women. Although the authors found that women (age, 55-64 years) using vitamin C supplements for more than 10 years had an average BMD 6.7% higher than that of nonusers, they did not find any association between dietary vitamin C intake and BMD. Moreover, NHANES III also found inconsistent associations between vitamin C and BMD among 13,080 adults surveyed in the United States.⁴⁵ Although for premenopausal women dietary ascorbic acid was associated with increased BMD, for postmenopausal women with a history of smoking and estrogen replacement, it was actually associated with lower BMD values. For other subgroups in the study, the relationship was also inconsistent or nonlinear.

The exact mechanism by which ascorbic acid contributes to BMD is not fully delineated. However, it likely is related to the known role of vitamin C in collagen formation, bone matrix development, osteoblast differentiation, and its antioxidant effects limiting bone resorption.^44,46

Hip Fractures

Besides demonstrating positive effects of vitamin C on bone healing and BMD, epidemiologic studies have found evidence of a protective effect of vitamin C on hip fracture risk. In a study of the Swedish Mammography cohort, 66,651 women (age, 40-76 years) were prospectively followed.⁴⁷ The authors found that the odds ratio (OR) for hip fractures among smokers with a low intake of vitamin E (median intake, ≤6.2 mg/d) was 3.0 (95% CI, 1.6-5.4) and for vitamin C (median intake, ≤67 mg/d) was 3.0 (95% CI, 1.6-5.6). Moreover, in smokers with a low intake of both vitamins E and C, OR increased to 4.9 (95% CI, 2.2-11.0). In addition, the Utah Study of Nutrition and Bone Health matched 1215 cases of hip fractures in patients who had ever smoked (age, >50 years) with 1349 controls and found that vitamin C intake above 159 mg/d had a significant protective effect on the incidence of hip fracture; however, a graded relationship was not observed.⁴⁸ Despite the inconsistencies in the NHANES III study regarding the relationship between vitamin C and BMD, Simon and Hudes⁴⁵ found that serum vitamin C was associated with lower risk for self-reported fracture in postmenopausal women who had ever smoked and had a history of estrogen therapy (OR, 0.51; 95% CI, 0.36-0.70). Finally, Sahni and colleagues⁴⁹ followed 958 Framingham cohort men and women (mean age, 75 years) over 17 years and found that those in the highest tertile of total vitamin C intake (median, 313 mg/d) had significantly fewer hip fractures and nonvertebral fractures compared with those in the lowest tertile of intake (median, 94 mg/d). Dietary vitamin C intake was not associated with fracture risk in this study.

Complex Regional Pain Syndrome

Type 1 CRPS is a debilitating condition characterized by severe pain, swelling, and vasomotor instability. It is commonly precipitated by an injury or surgery to an extremity and is a dreaded sequelae in orthopedics,⁵⁰ with incidence rates of 10% to 22% in wrist fractures^51-53 and 10% after foot and ankle surgery.⁵⁴ Although the pathophysiology of CRPS remains unknown, dysregulation and increased permeability of the vasculature caused by free radicals are thought to play an important role.⁵⁵ In dermal burns, high doses of vitamin C therapy slowed progression of vascular permeability and therefore reduced extravascular leakage of fluids and protein.^56,57 The ability of vitamin C to prevent CRPS has been studied in only a handful of trials.

In a double-blind trial, Zollinger and colleagues⁵¹ randomized 127 conservatively treated distal radius fractures to receive either vitamin C 500 mg or placebo daily for 50 days starting on day of injury. Incidence of CRPS (using the diagnostic criteria proposed by Veldman and colleagues⁵⁸) at 1-year follow-up was 22% in the placebo group and 7% in the vitamin C group (95% CI for difference, 2%-26%). Complaints while wearing the cast and fracture type increased the risk for developing CRPS. This initial study was followed up by a prospective, randomized, double-blind multicenter trial by the same authors,⁵² who had 416 patients with 427 wrist fractures receive either placebo or vitamin C 200 mg/d, 500 mg/d, or 1500 mg/d for 50 days. This follow-up study included both operative (11%) and nonoperative (89%) distal radius fractures. Incidence of CRPS was 10.1% in the placebo group and 2.4% in the vitamin C group (P < .002). Although there was an appreciable drop in the relative risk (RR) of developing CRPS between the vitamin C 200-mg/d and 500-mg/d groups (0.41-0.17), there was no additional benefit in the 1500-mg/d group. Pooling the data for these 2 randomized trials showed that the overall RR for developing CRPS was lower with vitamin C supplementation (RR, 0.28; 95% CI, 0.14-0.56; P = .0003).⁵⁹

Results of the 2 trials by Zollinger and colleagues^51,52 have been met with several concerns.^60-62 As a corollary to the unclear etiology of CRPS, several different sets of diagnostic criteria exist, and the criteria are somewhat subjective and imprecise. Although both trials used the Veldman criteria,⁵⁸ the incidence of CRPS in the placebo group dropped unexpectedly between trials, from 22% to 10.1%, and the results may have been different had other criteria been used. Moreover, the idea that toxic oxygen radicals have a role in CRPS and that vitamin C can scavenge these radicals is based on limited data.⁶¹ In the absence of a clear pathophysiologic explanation, some surgeons have been reluctant to treat patients with vitamin C supplementation.

Cazeneuve and colleagues⁵³ also studied the effect of vitamin C supplementation on CRPS in patients with distal radius fractures treated with reduction and intrafocal pinning. Group 1 consisted of 100 patients (treated from 1995 to 1998) who did not receive vitamin C supplementation, and group 2 consisted of 95 patients (treated from 1998 to 2002) who received vitamin C 1000 mg/d for 45 days starting on day of fracture. Patients were followed for up to 90 days after surgery. Incidence of CRPS type 1 was 10% in the untreated group and 2.1% in the group that received vitamin C supplementation.

Vitamin C prophylaxis for CRPS has also been studied in foot and ankle surgery. Besse and colleagues⁵⁴ prospectively compared 2 chronologically successive groups that received (235 feet) or did not receive (185 feet) vitamin C 1000-mg/d supplementation for 45 days. Incidence of CRPS type 1 as diagnosed with International Association for the Study of Pain (IASP) criteria dropped from 9.6% to 1.7% with vitamin C supplementation. In a case series, Zollinger and colleagues⁶³ examined CRPS type 1 rates after performing cementless total trapeziometacarpal semiconstrained joint prosthesis implantations for trapeziometacarpal arthritis. Forty implantations were performed in 34 patients. All patients received vitamin C 500 mg/d for CRPS prevention starting 2 days before surgery for 50 days. There were no cases of CRPS in the postoperative period, according to Veldman or IASP criteria. Although the results of the studies by Cazeneuve and colleagues⁵³ and Besse and colleagues⁵⁴ agree with those of the distal radius fracture trials by Zollinger and colleagues,^51,52 the quasi-experimental design and the lack of blinding and randomization temper the conclusions that can be drawn because of the risk for significant bias.

In a recent systematic review examining the effectiveness of vitamin C supplementation in preventing CRPS in trauma and surgery in the extremities, Shibuya and colleagues⁶⁴ concluded that taking at least 500 mg of vitamin C daily for 45 to 50 days after injury or surgery may help decrease the incidence of CRPS after a traumatic event.

Osteoarthritis

Damage caused by free radicals has long been thought to play an important role in osteoarthritis (OA).^65-67 A cross-sectional study in knee OA found that amounts of joint fluid antioxidants were lower in patients with severe arthritis than in those with intact cartilage, further implicating free radicals in the pathophysiology of OA.⁶⁸ Use of vitamin C for prophylaxis against development or progression of OA is therefore a hot research topic. Thus far, animal studies have had mixed results—several showing a chondroprotective effect of vitamin C^69,70 and others finding either no effect or even a positive association with the development of arthritis.⁷¹

The literature on human subjects, chiefly observational studies, is just as controversial. Wang and colleagues⁴⁰ found vitamin C intake associated with both a 50% risk reduction of bone marrow lesions on magnetic resonance imaging over a 10-year interval (OR, 0.5; 95% CI, 0.29-0.87) and inversely associated with the tibial plateau bone area. Similarly, the Clearwater Osteoarthritis Study, which followed 1023 patients (age, >40 years), showed that participants who took vitamin C supplements were 11% less likely to develop radiographic evidence of OA (RR, 0.89; 95% CI, 0.85-0.93).⁷² Nonetheless, other studies have failed to show such associations⁷³ or have demonstrated the opposite effect. Chaganti and colleagues⁷⁴ analyzed levels of vitamins C and E in the Multicenter Osteoarthritis Study (MOST) cohort of 3026 men and women (age, 50-79 years) and found higher vitamin levels were not protective against incidence of radiographic whole-knee OA and may even have been associated with increased risk.

Conclusion

Vitamin C is an essential micronutrient and a powerful water-soluble antioxidant in numerous biochemical pathways that influence bone health. It has been implicated in the biology of fracture healing, and vitamin C supplementation has been proposed as prophylaxis against hip fractures based on observational data. Results of 2 high-quality double-blind randomized trials support use of vitamin C as prophylaxis against CRPS in wrist fractures treated conservatively and operatively; the evidence for foot and ankle surgery is weaker. Use of vitamin C in OA prevention has tremendous potential, though animal and human study results are controversial. Heterogeneous results and lack of prospective trials preclude any recommendation at this time.

The extensor mechanism of the knee comprises the quadriceps tendon, the patella, and the patellar tendon. The extensor mechanism may be damaged by injury to these structures, with consequences such as the inability to actively extend the knee and hemarthrosis.^1,2 Disruption of this mechanism is rare, and the most common injury pattern is an eccentric contraction of the quadriceps tendon on a flexed knee causing a tendon (quadriceps or patellar) rupture or a patella fracture.^1,2

Patellar tendon ruptures are more common in persons younger than 40 years.¹ Treatment is surgical, regardless of age and physical activity. In the acute setting, repair can be end-to-end suture or transosseous tunnel insertion. End-to-end suturing is difficult in chronic patellar tendon ruptures because of patella alta secondary to quadriceps contraction.³ Treatment options for chronic ruptures may involve transpatellar traction⁴ or tendon reinforcement with fascia lata, a semitendinosus band, or synthetic materials.^3-5 Alternatively, tendon autograft and allografts have also been recommended, especially in extreme situations.^1,6 Furthermore, animal experiments have shown that a compact platelet-rich fibrin scaffold (CPFS) has the potential to accelerate healing of patellar tendon defects and to act as a bioscaffold for graft augmentation.⁷

We describe the case of a 30-year-old man who underwent extensor mechanism reconstruction with cadaveric tendon–patellar tendon–bone allograft for failure of an infected primary end-to-end repair. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 30-year-old healthy man landed on an empty glass fish tank, resulting in a traumatic right-knee arthrotomy. On initial evaluation, the patient had a negative straight-leg-raise test and impaired knee extension. The patient was taken urgently to the operating room for irrigation and débridement and concurrent repair of the patellar tendon laceration. Antibiotic prophylaxis with 2 g of intravenous (IV) cefazolin was given in the emergency room.

Intraoperatively, after visualizing the patellar tendon laceration and excluding any associated chondral lesions, we proceeded with extensive débridement and irrigation using 9 L of normal saline pulse lavage. After we achieved a clean site, we proceeded to repair the patellar tendon using No. 2 FiberWire sutures (Arthrex, Naples, Florida) with a classic Krackow repair⁸ consisting of 2 sutures run in a 4-row fashion through the patella and the patellar tendon. The suture was securely tightened and then tested for stability to at least 90° of knee flexion. The retinaculum was repaired using No. 0 Vicryl sutures (Ethicon, Somerville, New Jersey). After wound closure and dressing, the patient was placed in a hinged knee brace locked in extension at all times after surgery. Antibiotic treatment with IV cefazolin was administered for 48 hours.

Postoperative management consisted of weight-bearing as tolerated on the operative limb and appropriate deep venous thrombosis prophylaxis. The patient followed up in clinic 2 weeks and 4 weeks after surgery. At 4 weeks, the patient was noted to have a secondary wound infection with superficial dehiscence and serosanguineous drainage. No wound opening was noticed, and local wound care was performed with a 1-week course of oral cephalexin. The patient was scheduled to follow up a few weeks later but did not follow up for a year.

At 1-year follow-up, the patient reported that he had had a steady progression of his knee range of motion (ROM) with decreased pain. However, over time, the patient noted subjective instability of the knee, with frequent falls occurring close to his 1-year follow-up. Examination of his knee showed that his active ROM ranged from 20° in extension to 120° in flexion, with a weak extensor mechanism. Passively, his knee could be brought to full extension. His incision was well healed, but it had an area of bogginess in the middle. Radiographs showed patella alta on the affected knee, with a lengthening of the patellar tendon of 7.70 cm on the right compared with 5.18 cm on the left. Magnetic resonance imaging (MRI) showed moderate-to-severe patellar tendinosis with small fluid pockets around the surgical material and evidence of acute patellar enthesopathy. The laboratory values showed a white blood cell count of 7580/μL (normal, 4500-11,000/μL), an erythrocyte sedimentation rate of 2 mm/h (normal, 1-15 mm/h), and a C-reactive protein level of 1.93 mg/dL (normal, 0.00-0.29 mg/dL). Based on the clinical examination and imaging findings, there was a concern for a possible chronic deep-tissue infection, in addition to failure of the primary patellar tendon repair. Operative versus nonoperative management options were discussed with the patient, and he elected to undergo surgery.

During surgery, the patellar laxity was confirmed, and the patellar tendon was noticed to be chronically thickened and surrounded by unhealthy tissue. Initially, an extensive soft-tissue débridement was performed, and all patellar tendon loculations visualized on the preoperative MRI were drained; a solid purulent-like fluid was expressed. Unfortunately, the extensive and required débridement did not allow the preservation of the patellar tendon. Appropriate cultures were taken and sent for immediate Gram-stain analysis, which returned negative. Tissue samples from the patellar tendon were also sent to the pathology department for analysis. Intraoperatively, the infrapatellar defect was filled temporarily with a tobramycin cement spacer mixed with 2 g of vancomycin in a manner similar to that of the Masquelet technique used for infected long-bone nonunions with bone loss.^9,10 This technique is a 2-stage procedure that promotes the formation of a biologic membrane that allows bone healing in the reconstruction of long-bone defects. The first stage consists of a radical débridement with soft-tissue repair by flaps when needed, with the insertion of a polymethylmethacrylate cement spacer into the bone defect. The second stage is usually performed 6 to 8 weeks later, with removal of the spacer and preservation of the induced membrane, which is filled with iliac crest bone autograft augmented (if necessary) with demineralized allograft.

The incision was closed primarily, and after surgery, the patient was allowed to bear weight as tolerated in a hinged knee brace locked in extension. Final laboratory analysis from cultures and tissue samples revealed acute and chronic inflammation with more than 20 neutrophils per high-powered field. No organisms grew from aerobic, anaerobic, fungal, or mycobacterial cultures. The infectious disease service was consulted and recommended oral cephalexin.

Because all cultures were negative, all laboratory examinations did not indicate any residual infections, and no bony involvement was noticed intraoperatively or in the preoperative knee MRI, we decided to proceed with the second stage of the Masquelet technique after 2 weeks. The patient returned to the operating room for final reconstruction of his patellar tendon using a custom-ordered cadaveric tendon–patellar tendon–bone allograft, the length of which was determined by measuring the contralateral patellar tendon, ie, 5.18 cm (Figure 1A). The previous anterior knee incision was reopened and extended distally past the tibial tuberosity and proximally toward the quadriceps tendon. The antibiotic spacer was removed. We proceeded with a repeat irrigation and débridement and the allograft transfer. The selected allograft was customized by reducing the tibial bone component to an approximately 1×2-cm bone block and by reducing the allograft patellar thickness with an oscillating saw, leaving an approximately 2-mm thick patellar bone graft attached to the patellar tendon. In a similar technique using an oscillating saw, we shaved off the anterior cortex of the patient’s patella to accommodate, in a sandwich fashion, the patellar allograft. Proximally, the quadriceps tendon insertion was split longitudinally and partially separated from the superior pole of the patellar tendon to allow seating and fixation of the modified quadriceps allograft tendon component.

We proceeded with the fixation of the allograft first distally on the patella. The anterior cortex of the tibial tuberosity was resected to allow the perfect seating of the bone block allograft. The graft was secured with a 4.0-mm fully threaded cancellous lag screw and reinforced with a 2.4-mm, 3-hole T-volar buttress plate (Synthes, Paoli, Pennsylvania). The plate was contoured to better fit the patient’s tibia. We sutured the patellar allograft tendon to the patella using two No. 2-0 FiberWire sutures in Krackow suture technique⁸ (Figures 1B, 1C). We obtained good fixation of the patellar tendon, and the distance between the patellar insertion and the inferior patellar pole was the same as before surgery: 5.57 cm and comparable to the contralateral side (Figures 2A-2C). The patellar allograft and autograft sandwich were secured with additional No. 2-0 FiberWire sutures, and the quadriceps allograft and autograft were secured with the cross-stitch technique with the same material. Fine suturing of the quadriceps tendon was done with No. 0 Vicryl sutures. After the fixation was completed, we tested the stability of the reconstruction and found good flexion up to 120°.

The postoperative protocol consisted of weight-bearing as tolerated in full extension and passive knee ROM, using a continuous passive ROM machine from 0° to 45° for the first 4 weeks, followed by active ROM, increased as tolerated, during the next 8 weeks.

The patient was seen in clinic 3 and 9 months after surgery. At the 3-month follow-up appointment, the patient’s examination showed knee ROM from 0° extension to 130° of flexion, no secondary infection signs, and radiographic evidence of a well-healing patellar allograft with symmetric patellar tendon length to the contralateral side. At 9-month follow-up, the patient’s active ROM was from 0° extension to 140° flexion (Figures 3A, 3B), and he had returned to his preinjury level of functioning.

Discussion

This case report describes the successful reconstruction of a patellar tendon defect with cadaveric tendon–patellar tendon–bone allograft. Extensor mechanism injuries are uncommon in general, and the incidence of patellar tendon injury is higher in men than in women.² Patellar tendon tears occur frequently in active patients younger than 40 years, usually as a result of sudden quadriceps contraction with the knee slightly flexed.¹ Treatment of patellar tendon injury is surgical, and functional outcomes for patients with this injury are equivalent to those of patients with quadriceps tendon injuries or patellar fractures.² Acute patellar tendon tears can be repaired by end-to-end suturing or transosseous tunnel insertion in the tibia or patella.¹ Reinforcement is often added between the patella and tibial tuberosity, using a semitendinosus band or wire.¹ End-to-end suture is performed using a thick resorbable suture. It is important to avoid patella alta during suturing, comparing the position of the patella with the contralateral patella with the knee in 45° of flexion. In proximal avulsion, the tendon is anchored to the bone by 2 thick nonresorbable sutures through 2 parallel bone tunnels to the proximal pole of the patella. Distal avulsion is rare in adults, but it can be managed by using staples or suture anchors.¹

End-to-end suturing of chronic patellar tendon defects is difficult more than 45 days after injury primarily because of difficulties in correcting patella alta secondary to the upward force exerted by the quadriceps tendon.^1,3 Extreme situations similar to the case we present warrant Achilles or patellar tendon allograft for reconstruction of the extensor mechanism.^1,3,6,9

Extensor mechanism allograft also provides an effective remedy for severe quadriceps deficiency caused by loss of the patella, patellar tendon, and quadriceps tendon in total knee arthroplasty.¹⁰ However, in such cases, late failure is common, and major quadriceps deficiency occurs after removal of the allograft material.¹⁰ To improve outcome, a novel technique using the medial gastrocnemius muscle transferred to the muscular portion of the vastus medialis and lateralis flaps provides a secure and strong closure of the anterior knee, thereby restoring the extensor mechanism of the knee.¹⁰

Patellar tendon reconstruction with allograft tissue has been successfully used, especially in cases related to chronic patellar tendon ruptures¹¹ and total knee arthroplasty.^6,12-14 Crossett and colleagues¹² showed that, at 2-year follow-up, the average knee score for pain, ROM, and stability had improved from 26 points (range, 6-39 points) before surgery to 81 points (range, 40-92 points). The average knee score for function had also improved: 14 points (range, 0-35 points) before surgery to 53 points (range, 30-90 points).¹² Primary repair may succeed in early intervention, but in an established rupture, allograft reconstruction is often necessary. Achilles tendon is the preferred allograft, with the calcaneus fragment embedded into the proximal tibia as a new tubercle and the tendon sutured into the remaining extensor mechanism.^1,11 The repair is further protected using a cable loop from the superior pole of the patella to a drill hole in the upper tibia.⁹ Techniques have also been described involving passage of the proximal aspect of the allograft tendon through patellar bone tunnels and suture fixation to the native quadriceps tendon.^11,15 However, in our technique, we shaved off the anterior cortex of the patient’s patella to allow a sandwich-type over-position of the allograft to secure fixation to the patella.

Another alternative to allograft reconstruction involves biocompatible scaffolds. Such scaffolds incorporate the use of platelets in a fibrin framework. A CPFS, produced from blood and calcium gluconate to improve healing of patellar tendon defects, has been described in animal studies.⁷ In the rabbit model, CPFS acts as a provisional bioscaffold that can accelerate healing of an injured patellar tendon repair, potentially secondary to several growth factors derived from platelets.⁷ Platelets are biocompatible sources of growth factors, and CPFS can act as a scaffold to restore the mechanical integrity of injured soft tissue.^7,16 In addition, CPFS can act to lower donor-site morbidity associated with harvesting tissue autograft.⁷ However, to our knowledge, such scaffolds have not been used in human trials. The LARS biocompatible ligament (Corin Group PLC, Cirencester, United Kingdom), currently not approved by the US Food and Drug Administration, is used for reconstructions of isolated or multiple knee ligament injuries.¹⁷ This graft requires the presence of healthy tissue with good blood supply from which new tendon or ligament can grow in. Sometimes it is also used for extensor mechanism reconstruction after radical tumor resection around the knee; however, good results are achieved in only 59% of cases,¹⁸ and to our knowledge, only 1 case of primary repair of a patellar tendon rupture has been published.¹⁹

Techniques involving the use of tendon–patellar tendon–bone graft with fixation via the sandwich-type over-position of the allograft for chronic patellar tendon rupture have not been described in the literature. In our patient, given the extensive patellar tendon lesion and inflammation with chronic tissue degeneration, there was no option but to use allograft. To improve the patient’s outcome, we chose the strongest possible allograft, tendon–patellar tendon–bone graft.

Conclusion

Revision patellar tendon reconstruction is a challenging, but necessary, procedure to restore the extensor mechanism of the knee, especially in young, active individuals. Various options to reconstruct the tissue defects are available. Our patient was successfully treated with a tendon–patellar tendon–bone allograft reconstruction.

The extensor mechanism of the knee comprises the quadriceps tendon, the patella, and the patellar tendon. The extensor mechanism may be damaged by injury to these structures, with consequences such as the inability to actively extend the knee and hemarthrosis.^1,2 Disruption of this mechanism is rare, and the most common injury pattern is an eccentric contraction of the quadriceps tendon on a flexed knee causing a tendon (quadriceps or patellar) rupture or a patella fracture.^1,2

Patellar tendon ruptures are more common in persons younger than 40 years.¹ Treatment is surgical, regardless of age and physical activity. In the acute setting, repair can be end-to-end suture or transosseous tunnel insertion. End-to-end suturing is difficult in chronic patellar tendon ruptures because of patella alta secondary to quadriceps contraction.³ Treatment options for chronic ruptures may involve transpatellar traction⁴ or tendon reinforcement with fascia lata, a semitendinosus band, or synthetic materials.^3-5 Alternatively, tendon autograft and allografts have also been recommended, especially in extreme situations.^1,6 Furthermore, animal experiments have shown that a compact platelet-rich fibrin scaffold (CPFS) has the potential to accelerate healing of patellar tendon defects and to act as a bioscaffold for graft augmentation.⁷

We describe the case of a 30-year-old man who underwent extensor mechanism reconstruction with cadaveric tendon–patellar tendon–bone allograft for failure of an infected primary end-to-end repair. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 30-year-old healthy man landed on an empty glass fish tank, resulting in a traumatic right-knee arthrotomy. On initial evaluation, the patient had a negative straight-leg-raise test and impaired knee extension. The patient was taken urgently to the operating room for irrigation and débridement and concurrent repair of the patellar tendon laceration. Antibiotic prophylaxis with 2 g of intravenous (IV) cefazolin was given in the emergency room.

Intraoperatively, after visualizing the patellar tendon laceration and excluding any associated chondral lesions, we proceeded with extensive débridement and irrigation using 9 L of normal saline pulse lavage. After we achieved a clean site, we proceeded to repair the patellar tendon using No. 2 FiberWire sutures (Arthrex, Naples, Florida) with a classic Krackow repair⁸ consisting of 2 sutures run in a 4-row fashion through the patella and the patellar tendon. The suture was securely tightened and then tested for stability to at least 90° of knee flexion. The retinaculum was repaired using No. 0 Vicryl sutures (Ethicon, Somerville, New Jersey). After wound closure and dressing, the patient was placed in a hinged knee brace locked in extension at all times after surgery. Antibiotic treatment with IV cefazolin was administered for 48 hours.

Postoperative management consisted of weight-bearing as tolerated on the operative limb and appropriate deep venous thrombosis prophylaxis. The patient followed up in clinic 2 weeks and 4 weeks after surgery. At 4 weeks, the patient was noted to have a secondary wound infection with superficial dehiscence and serosanguineous drainage. No wound opening was noticed, and local wound care was performed with a 1-week course of oral cephalexin. The patient was scheduled to follow up a few weeks later but did not follow up for a year.

At 1-year follow-up, the patient reported that he had had a steady progression of his knee range of motion (ROM) with decreased pain. However, over time, the patient noted subjective instability of the knee, with frequent falls occurring close to his 1-year follow-up. Examination of his knee showed that his active ROM ranged from 20° in extension to 120° in flexion, with a weak extensor mechanism. Passively, his knee could be brought to full extension. His incision was well healed, but it had an area of bogginess in the middle. Radiographs showed patella alta on the affected knee, with a lengthening of the patellar tendon of 7.70 cm on the right compared with 5.18 cm on the left. Magnetic resonance imaging (MRI) showed moderate-to-severe patellar tendinosis with small fluid pockets around the surgical material and evidence of acute patellar enthesopathy. The laboratory values showed a white blood cell count of 7580/μL (normal, 4500-11,000/μL), an erythrocyte sedimentation rate of 2 mm/h (normal, 1-15 mm/h), and a C-reactive protein level of 1.93 mg/dL (normal, 0.00-0.29 mg/dL). Based on the clinical examination and imaging findings, there was a concern for a possible chronic deep-tissue infection, in addition to failure of the primary patellar tendon repair. Operative versus nonoperative management options were discussed with the patient, and he elected to undergo surgery.

During surgery, the patellar laxity was confirmed, and the patellar tendon was noticed to be chronically thickened and surrounded by unhealthy tissue. Initially, an extensive soft-tissue débridement was performed, and all patellar tendon loculations visualized on the preoperative MRI were drained; a solid purulent-like fluid was expressed. Unfortunately, the extensive and required débridement did not allow the preservation of the patellar tendon. Appropriate cultures were taken and sent for immediate Gram-stain analysis, which returned negative. Tissue samples from the patellar tendon were also sent to the pathology department for analysis. Intraoperatively, the infrapatellar defect was filled temporarily with a tobramycin cement spacer mixed with 2 g of vancomycin in a manner similar to that of the Masquelet technique used for infected long-bone nonunions with bone loss.^9,10 This technique is a 2-stage procedure that promotes the formation of a biologic membrane that allows bone healing in the reconstruction of long-bone defects. The first stage consists of a radical débridement with soft-tissue repair by flaps when needed, with the insertion of a polymethylmethacrylate cement spacer into the bone defect. The second stage is usually performed 6 to 8 weeks later, with removal of the spacer and preservation of the induced membrane, which is filled with iliac crest bone autograft augmented (if necessary) with demineralized allograft.

The incision was closed primarily, and after surgery, the patient was allowed to bear weight as tolerated in a hinged knee brace locked in extension. Final laboratory analysis from cultures and tissue samples revealed acute and chronic inflammation with more than 20 neutrophils per high-powered field. No organisms grew from aerobic, anaerobic, fungal, or mycobacterial cultures. The infectious disease service was consulted and recommended oral cephalexin.

Because all cultures were negative, all laboratory examinations did not indicate any residual infections, and no bony involvement was noticed intraoperatively or in the preoperative knee MRI, we decided to proceed with the second stage of the Masquelet technique after 2 weeks. The patient returned to the operating room for final reconstruction of his patellar tendon using a custom-ordered cadaveric tendon–patellar tendon–bone allograft, the length of which was determined by measuring the contralateral patellar tendon, ie, 5.18 cm (Figure 1A). The previous anterior knee incision was reopened and extended distally past the tibial tuberosity and proximally toward the quadriceps tendon. The antibiotic spacer was removed. We proceeded with a repeat irrigation and débridement and the allograft transfer. The selected allograft was customized by reducing the tibial bone component to an approximately 1×2-cm bone block and by reducing the allograft patellar thickness with an oscillating saw, leaving an approximately 2-mm thick patellar bone graft attached to the patellar tendon. In a similar technique using an oscillating saw, we shaved off the anterior cortex of the patient’s patella to accommodate, in a sandwich fashion, the patellar allograft. Proximally, the quadriceps tendon insertion was split longitudinally and partially separated from the superior pole of the patellar tendon to allow seating and fixation of the modified quadriceps allograft tendon component.

We proceeded with the fixation of the allograft first distally on the patella. The anterior cortex of the tibial tuberosity was resected to allow the perfect seating of the bone block allograft. The graft was secured with a 4.0-mm fully threaded cancellous lag screw and reinforced with a 2.4-mm, 3-hole T-volar buttress plate (Synthes, Paoli, Pennsylvania). The plate was contoured to better fit the patient’s tibia. We sutured the patellar allograft tendon to the patella using two No. 2-0 FiberWire sutures in Krackow suture technique⁸ (Figures 1B, 1C). We obtained good fixation of the patellar tendon, and the distance between the patellar insertion and the inferior patellar pole was the same as before surgery: 5.57 cm and comparable to the contralateral side (Figures 2A-2C). The patellar allograft and autograft sandwich were secured with additional No. 2-0 FiberWire sutures, and the quadriceps allograft and autograft were secured with the cross-stitch technique with the same material. Fine suturing of the quadriceps tendon was done with No. 0 Vicryl sutures. After the fixation was completed, we tested the stability of the reconstruction and found good flexion up to 120°.

The postoperative protocol consisted of weight-bearing as tolerated in full extension and passive knee ROM, using a continuous passive ROM machine from 0° to 45° for the first 4 weeks, followed by active ROM, increased as tolerated, during the next 8 weeks.

The patient was seen in clinic 3 and 9 months after surgery. At the 3-month follow-up appointment, the patient’s examination showed knee ROM from 0° extension to 130° of flexion, no secondary infection signs, and radiographic evidence of a well-healing patellar allograft with symmetric patellar tendon length to the contralateral side. At 9-month follow-up, the patient’s active ROM was from 0° extension to 140° flexion (Figures 3A, 3B), and he had returned to his preinjury level of functioning.

Discussion

This case report describes the successful reconstruction of a patellar tendon defect with cadaveric tendon–patellar tendon–bone allograft. Extensor mechanism injuries are uncommon in general, and the incidence of patellar tendon injury is higher in men than in women.² Patellar tendon tears occur frequently in active patients younger than 40 years, usually as a result of sudden quadriceps contraction with the knee slightly flexed.¹ Treatment of patellar tendon injury is surgical, and functional outcomes for patients with this injury are equivalent to those of patients with quadriceps tendon injuries or patellar fractures.² Acute patellar tendon tears can be repaired by end-to-end suturing or transosseous tunnel insertion in the tibia or patella.¹ Reinforcement is often added between the patella and tibial tuberosity, using a semitendinosus band or wire.¹ End-to-end suture is performed using a thick resorbable suture. It is important to avoid patella alta during suturing, comparing the position of the patella with the contralateral patella with the knee in 45° of flexion. In proximal avulsion, the tendon is anchored to the bone by 2 thick nonresorbable sutures through 2 parallel bone tunnels to the proximal pole of the patella. Distal avulsion is rare in adults, but it can be managed by using staples or suture anchors.¹

End-to-end suturing of chronic patellar tendon defects is difficult more than 45 days after injury primarily because of difficulties in correcting patella alta secondary to the upward force exerted by the quadriceps tendon.^1,3 Extreme situations similar to the case we present warrant Achilles or patellar tendon allograft for reconstruction of the extensor mechanism.^1,3,6,9

Extensor mechanism allograft also provides an effective remedy for severe quadriceps deficiency caused by loss of the patella, patellar tendon, and quadriceps tendon in total knee arthroplasty.¹⁰ However, in such cases, late failure is common, and major quadriceps deficiency occurs after removal of the allograft material.¹⁰ To improve outcome, a novel technique using the medial gastrocnemius muscle transferred to the muscular portion of the vastus medialis and lateralis flaps provides a secure and strong closure of the anterior knee, thereby restoring the extensor mechanism of the knee.¹⁰

Patellar tendon reconstruction with allograft tissue has been successfully used, especially in cases related to chronic patellar tendon ruptures¹¹ and total knee arthroplasty.^6,12-14 Crossett and colleagues¹² showed that, at 2-year follow-up, the average knee score for pain, ROM, and stability had improved from 26 points (range, 6-39 points) before surgery to 81 points (range, 40-92 points). The average knee score for function had also improved: 14 points (range, 0-35 points) before surgery to 53 points (range, 30-90 points).¹² Primary repair may succeed in early intervention, but in an established rupture, allograft reconstruction is often necessary. Achilles tendon is the preferred allograft, with the calcaneus fragment embedded into the proximal tibia as a new tubercle and the tendon sutured into the remaining extensor mechanism.^1,11 The repair is further protected using a cable loop from the superior pole of the patella to a drill hole in the upper tibia.⁹ Techniques have also been described involving passage of the proximal aspect of the allograft tendon through patellar bone tunnels and suture fixation to the native quadriceps tendon.^11,15 However, in our technique, we shaved off the anterior cortex of the patient’s patella to allow a sandwich-type over-position of the allograft to secure fixation to the patella.

Another alternative to allograft reconstruction involves biocompatible scaffolds. Such scaffolds incorporate the use of platelets in a fibrin framework. A CPFS, produced from blood and calcium gluconate to improve healing of patellar tendon defects, has been described in animal studies.⁷ In the rabbit model, CPFS acts as a provisional bioscaffold that can accelerate healing of an injured patellar tendon repair, potentially secondary to several growth factors derived from platelets.⁷ Platelets are biocompatible sources of growth factors, and CPFS can act as a scaffold to restore the mechanical integrity of injured soft tissue.^7,16 In addition, CPFS can act to lower donor-site morbidity associated with harvesting tissue autograft.⁷ However, to our knowledge, such scaffolds have not been used in human trials. The LARS biocompatible ligament (Corin Group PLC, Cirencester, United Kingdom), currently not approved by the US Food and Drug Administration, is used for reconstructions of isolated or multiple knee ligament injuries.¹⁷ This graft requires the presence of healthy tissue with good blood supply from which new tendon or ligament can grow in. Sometimes it is also used for extensor mechanism reconstruction after radical tumor resection around the knee; however, good results are achieved in only 59% of cases,¹⁸ and to our knowledge, only 1 case of primary repair of a patellar tendon rupture has been published.¹⁹

Techniques involving the use of tendon–patellar tendon–bone graft with fixation via the sandwich-type over-position of the allograft for chronic patellar tendon rupture have not been described in the literature. In our patient, given the extensive patellar tendon lesion and inflammation with chronic tissue degeneration, there was no option but to use allograft. To improve the patient’s outcome, we chose the strongest possible allograft, tendon–patellar tendon–bone graft.

Conclusion

Revision patellar tendon reconstruction is a challenging, but necessary, procedure to restore the extensor mechanism of the knee, especially in young, active individuals. Various options to reconstruct the tissue defects are available. Our patient was successfully treated with a tendon–patellar tendon–bone allograft reconstruction.

The extensor mechanism of the knee comprises the quadriceps tendon, the patella, and the patellar tendon. The extensor mechanism may be damaged by injury to these structures, with consequences such as the inability to actively extend the knee and hemarthrosis.^1,2 Disruption of this mechanism is rare, and the most common injury pattern is an eccentric contraction of the quadriceps tendon on a flexed knee causing a tendon (quadriceps or patellar) rupture or a patella fracture.^1,2

Patellar tendon ruptures are more common in persons younger than 40 years.¹ Treatment is surgical, regardless of age and physical activity. In the acute setting, repair can be end-to-end suture or transosseous tunnel insertion. End-to-end suturing is difficult in chronic patellar tendon ruptures because of patella alta secondary to quadriceps contraction.³ Treatment options for chronic ruptures may involve transpatellar traction⁴ or tendon reinforcement with fascia lata, a semitendinosus band, or synthetic materials.^3-5 Alternatively, tendon autograft and allografts have also been recommended, especially in extreme situations.^1,6 Furthermore, animal experiments have shown that a compact platelet-rich fibrin scaffold (CPFS) has the potential to accelerate healing of patellar tendon defects and to act as a bioscaffold for graft augmentation.⁷

We describe the case of a 30-year-old man who underwent extensor mechanism reconstruction with cadaveric tendon–patellar tendon–bone allograft for failure of an infected primary end-to-end repair. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 30-year-old healthy man landed on an empty glass fish tank, resulting in a traumatic right-knee arthrotomy. On initial evaluation, the patient had a negative straight-leg-raise test and impaired knee extension. The patient was taken urgently to the operating room for irrigation and débridement and concurrent repair of the patellar tendon laceration. Antibiotic prophylaxis with 2 g of intravenous (IV) cefazolin was given in the emergency room.

Intraoperatively, after visualizing the patellar tendon laceration and excluding any associated chondral lesions, we proceeded with extensive débridement and irrigation using 9 L of normal saline pulse lavage. After we achieved a clean site, we proceeded to repair the patellar tendon using No. 2 FiberWire sutures (Arthrex, Naples, Florida) with a classic Krackow repair⁸ consisting of 2 sutures run in a 4-row fashion through the patella and the patellar tendon. The suture was securely tightened and then tested for stability to at least 90° of knee flexion. The retinaculum was repaired using No. 0 Vicryl sutures (Ethicon, Somerville, New Jersey). After wound closure and dressing, the patient was placed in a hinged knee brace locked in extension at all times after surgery. Antibiotic treatment with IV cefazolin was administered for 48 hours.

Postoperative management consisted of weight-bearing as tolerated on the operative limb and appropriate deep venous thrombosis prophylaxis. The patient followed up in clinic 2 weeks and 4 weeks after surgery. At 4 weeks, the patient was noted to have a secondary wound infection with superficial dehiscence and serosanguineous drainage. No wound opening was noticed, and local wound care was performed with a 1-week course of oral cephalexin. The patient was scheduled to follow up a few weeks later but did not follow up for a year.

At 1-year follow-up, the patient reported that he had had a steady progression of his knee range of motion (ROM) with decreased pain. However, over time, the patient noted subjective instability of the knee, with frequent falls occurring close to his 1-year follow-up. Examination of his knee showed that his active ROM ranged from 20° in extension to 120° in flexion, with a weak extensor mechanism. Passively, his knee could be brought to full extension. His incision was well healed, but it had an area of bogginess in the middle. Radiographs showed patella alta on the affected knee, with a lengthening of the patellar tendon of 7.70 cm on the right compared with 5.18 cm on the left. Magnetic resonance imaging (MRI) showed moderate-to-severe patellar tendinosis with small fluid pockets around the surgical material and evidence of acute patellar enthesopathy. The laboratory values showed a white blood cell count of 7580/μL (normal, 4500-11,000/μL), an erythrocyte sedimentation rate of 2 mm/h (normal, 1-15 mm/h), and a C-reactive protein level of 1.93 mg/dL (normal, 0.00-0.29 mg/dL). Based on the clinical examination and imaging findings, there was a concern for a possible chronic deep-tissue infection, in addition to failure of the primary patellar tendon repair. Operative versus nonoperative management options were discussed with the patient, and he elected to undergo surgery.

During surgery, the patellar laxity was confirmed, and the patellar tendon was noticed to be chronically thickened and surrounded by unhealthy tissue. Initially, an extensive soft-tissue débridement was performed, and all patellar tendon loculations visualized on the preoperative MRI were drained; a solid purulent-like fluid was expressed. Unfortunately, the extensive and required débridement did not allow the preservation of the patellar tendon. Appropriate cultures were taken and sent for immediate Gram-stain analysis, which returned negative. Tissue samples from the patellar tendon were also sent to the pathology department for analysis. Intraoperatively, the infrapatellar defect was filled temporarily with a tobramycin cement spacer mixed with 2 g of vancomycin in a manner similar to that of the Masquelet technique used for infected long-bone nonunions with bone loss.^9,10 This technique is a 2-stage procedure that promotes the formation of a biologic membrane that allows bone healing in the reconstruction of long-bone defects. The first stage consists of a radical débridement with soft-tissue repair by flaps when needed, with the insertion of a polymethylmethacrylate cement spacer into the bone defect. The second stage is usually performed 6 to 8 weeks later, with removal of the spacer and preservation of the induced membrane, which is filled with iliac crest bone autograft augmented (if necessary) with demineralized allograft.

The incision was closed primarily, and after surgery, the patient was allowed to bear weight as tolerated in a hinged knee brace locked in extension. Final laboratory analysis from cultures and tissue samples revealed acute and chronic inflammation with more than 20 neutrophils per high-powered field. No organisms grew from aerobic, anaerobic, fungal, or mycobacterial cultures. The infectious disease service was consulted and recommended oral cephalexin.

Because all cultures were negative, all laboratory examinations did not indicate any residual infections, and no bony involvement was noticed intraoperatively or in the preoperative knee MRI, we decided to proceed with the second stage of the Masquelet technique after 2 weeks. The patient returned to the operating room for final reconstruction of his patellar tendon using a custom-ordered cadaveric tendon–patellar tendon–bone allograft, the length of which was determined by measuring the contralateral patellar tendon, ie, 5.18 cm (Figure 1A). The previous anterior knee incision was reopened and extended distally past the tibial tuberosity and proximally toward the quadriceps tendon. The antibiotic spacer was removed. We proceeded with a repeat irrigation and débridement and the allograft transfer. The selected allograft was customized by reducing the tibial bone component to an approximately 1×2-cm bone block and by reducing the allograft patellar thickness with an oscillating saw, leaving an approximately 2-mm thick patellar bone graft attached to the patellar tendon. In a similar technique using an oscillating saw, we shaved off the anterior cortex of the patient’s patella to accommodate, in a sandwich fashion, the patellar allograft. Proximally, the quadriceps tendon insertion was split longitudinally and partially separated from the superior pole of the patellar tendon to allow seating and fixation of the modified quadriceps allograft tendon component.

We proceeded with the fixation of the allograft first distally on the patella. The anterior cortex of the tibial tuberosity was resected to allow the perfect seating of the bone block allograft. The graft was secured with a 4.0-mm fully threaded cancellous lag screw and reinforced with a 2.4-mm, 3-hole T-volar buttress plate (Synthes, Paoli, Pennsylvania). The plate was contoured to better fit the patient’s tibia. We sutured the patellar allograft tendon to the patella using two No. 2-0 FiberWire sutures in Krackow suture technique⁸ (Figures 1B, 1C). We obtained good fixation of the patellar tendon, and the distance between the patellar insertion and the inferior patellar pole was the same as before surgery: 5.57 cm and comparable to the contralateral side (Figures 2A-2C). The patellar allograft and autograft sandwich were secured with additional No. 2-0 FiberWire sutures, and the quadriceps allograft and autograft were secured with the cross-stitch technique with the same material. Fine suturing of the quadriceps tendon was done with No. 0 Vicryl sutures. After the fixation was completed, we tested the stability of the reconstruction and found good flexion up to 120°.

The postoperative protocol consisted of weight-bearing as tolerated in full extension and passive knee ROM, using a continuous passive ROM machine from 0° to 45° for the first 4 weeks, followed by active ROM, increased as tolerated, during the next 8 weeks.

The patient was seen in clinic 3 and 9 months after surgery. At the 3-month follow-up appointment, the patient’s examination showed knee ROM from 0° extension to 130° of flexion, no secondary infection signs, and radiographic evidence of a well-healing patellar allograft with symmetric patellar tendon length to the contralateral side. At 9-month follow-up, the patient’s active ROM was from 0° extension to 140° flexion (Figures 3A, 3B), and he had returned to his preinjury level of functioning.

Discussion

This case report describes the successful reconstruction of a patellar tendon defect with cadaveric tendon–patellar tendon–bone allograft. Extensor mechanism injuries are uncommon in general, and the incidence of patellar tendon injury is higher in men than in women.² Patellar tendon tears occur frequently in active patients younger than 40 years, usually as a result of sudden quadriceps contraction with the knee slightly flexed.¹ Treatment of patellar tendon injury is surgical, and functional outcomes for patients with this injury are equivalent to those of patients with quadriceps tendon injuries or patellar fractures.² Acute patellar tendon tears can be repaired by end-to-end suturing or transosseous tunnel insertion in the tibia or patella.¹ Reinforcement is often added between the patella and tibial tuberosity, using a semitendinosus band or wire.¹ End-to-end suture is performed using a thick resorbable suture. It is important to avoid patella alta during suturing, comparing the position of the patella with the contralateral patella with the knee in 45° of flexion. In proximal avulsion, the tendon is anchored to the bone by 2 thick nonresorbable sutures through 2 parallel bone tunnels to the proximal pole of the patella. Distal avulsion is rare in adults, but it can be managed by using staples or suture anchors.¹

End-to-end suturing of chronic patellar tendon defects is difficult more than 45 days after injury primarily because of difficulties in correcting patella alta secondary to the upward force exerted by the quadriceps tendon.^1,3 Extreme situations similar to the case we present warrant Achilles or patellar tendon allograft for reconstruction of the extensor mechanism.^1,3,6,9

Extensor mechanism allograft also provides an effective remedy for severe quadriceps deficiency caused by loss of the patella, patellar tendon, and quadriceps tendon in total knee arthroplasty.¹⁰ However, in such cases, late failure is common, and major quadriceps deficiency occurs after removal of the allograft material.¹⁰ To improve outcome, a novel technique using the medial gastrocnemius muscle transferred to the muscular portion of the vastus medialis and lateralis flaps provides a secure and strong closure of the anterior knee, thereby restoring the extensor mechanism of the knee.¹⁰

Patellar tendon reconstruction with allograft tissue has been successfully used, especially in cases related to chronic patellar tendon ruptures¹¹ and total knee arthroplasty.^6,12-14 Crossett and colleagues¹² showed that, at 2-year follow-up, the average knee score for pain, ROM, and stability had improved from 26 points (range, 6-39 points) before surgery to 81 points (range, 40-92 points). The average knee score for function had also improved: 14 points (range, 0-35 points) before surgery to 53 points (range, 30-90 points).¹² Primary repair may succeed in early intervention, but in an established rupture, allograft reconstruction is often necessary. Achilles tendon is the preferred allograft, with the calcaneus fragment embedded into the proximal tibia as a new tubercle and the tendon sutured into the remaining extensor mechanism.^1,11 The repair is further protected using a cable loop from the superior pole of the patella to a drill hole in the upper tibia.⁹ Techniques have also been described involving passage of the proximal aspect of the allograft tendon through patellar bone tunnels and suture fixation to the native quadriceps tendon.^11,15 However, in our technique, we shaved off the anterior cortex of the patient’s patella to allow a sandwich-type over-position of the allograft to secure fixation to the patella.

Another alternative to allograft reconstruction involves biocompatible scaffolds. Such scaffolds incorporate the use of platelets in a fibrin framework. A CPFS, produced from blood and calcium gluconate to improve healing of patellar tendon defects, has been described in animal studies.⁷ In the rabbit model, CPFS acts as a provisional bioscaffold that can accelerate healing of an injured patellar tendon repair, potentially secondary to several growth factors derived from platelets.⁷ Platelets are biocompatible sources of growth factors, and CPFS can act as a scaffold to restore the mechanical integrity of injured soft tissue.^7,16 In addition, CPFS can act to lower donor-site morbidity associated with harvesting tissue autograft.⁷ However, to our knowledge, such scaffolds have not been used in human trials. The LARS biocompatible ligament (Corin Group PLC, Cirencester, United Kingdom), currently not approved by the US Food and Drug Administration, is used for reconstructions of isolated or multiple knee ligament injuries.¹⁷ This graft requires the presence of healthy tissue with good blood supply from which new tendon or ligament can grow in. Sometimes it is also used for extensor mechanism reconstruction after radical tumor resection around the knee; however, good results are achieved in only 59% of cases,¹⁸ and to our knowledge, only 1 case of primary repair of a patellar tendon rupture has been published.¹⁹

Techniques involving the use of tendon–patellar tendon–bone graft with fixation via the sandwich-type over-position of the allograft for chronic patellar tendon rupture have not been described in the literature. In our patient, given the extensive patellar tendon lesion and inflammation with chronic tissue degeneration, there was no option but to use allograft. To improve the patient’s outcome, we chose the strongest possible allograft, tendon–patellar tendon–bone graft.

Conclusion

Revision patellar tendon reconstruction is a challenging, but necessary, procedure to restore the extensor mechanism of the knee, especially in young, active individuals. Various options to reconstruct the tissue defects are available. Our patient was successfully treated with a tendon–patellar tendon–bone allograft reconstruction.

In 1887, Midelfart¹ first reported on an intra-articular dislocation of the patella, and since then approximately 50 cases have been reported in the worldwide literature.² Also known as an inferior patellar dislocation, these rare traumatic events occur when the patella dislocates intra-articularly. Because the patella commonly rotates about its horizontal axis, the articular surface is facing proximally or distally. The patella becomes lodged within the trochlea and locks the knee joint. Most cases described in the literature involved adolescent boys, with the patella difficult to reduce. Most patients required open reduction, while those who underwent successful closed reduction often needed general anesthesia.³

Similarly, coronal shear fractures of the femoral condyle (ie, Hoffa fractures) are an uncommon fracture pattern typically seen in adults. These fractures are even more infrequent in skeletally immature patients, with fewer than 5 cases documented in the literature.^4-7 In our case report, we present a 14-year-old boy with a coronal shear fracture of the femoral condyle associated with an intra-articular patellar dislocation. To our knowledge, this constellation of injuries has not been reported. Additionally, closed reduction of the patella was successful after intra-articular lidocaine injection, without the need for sedation or general anesthesia. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Case Report

A 14-year-old boy presented to our institution after sustaining a direct blow to his left knee. The injury occurred as he jumped and landed on a flexed knee while playing with friends. The patient was unable to ambulate after the injury, and his left knee was locked in a slightly flexed position. Examination in the emergency department showed the knee to be held in approximately 60º of flexion, with an obvious bony prominence noted anteriorly over the femoral condyles. The patient was unable to perform a straight leg raise or any active range of motion (ROM) at the knee. Radiographs performed with the knee maintained in flexion confirmed that the patella was displaced into the knee joint and was rotated with the articular surface facing distally. Also noted was a coronal shear fracture of the lateral femoral condyle (Figures 1A, 1B).

The patient received pain medication and an intra-articular lidocaine injection prior to a reduction attempt by the orthopedic resident. With the patient supine, the hip was gently flexed to relax the quadriceps muscle. As the knee was flexed up to 110º, the prominent patella was gripped between the thumb and fingers to gently free and elevate the patella out of the intercondylar notch.

After reduction, an immediate return of normal patellar contour and patellofemoral tracking was observed as the knee was gently extended. There was no obvious defect to the patellar or quadriceps tendons, and the patient was able to perform a straight-leg raise, confirming the integrity of the extensor mechanism. Radiographs performed after the reduction confirmed relocation of the patella in correct anatomic position, as well as a lateral femoral condyle fracture (Figures 2A, 2B). Magnetic resonance imaging (MRI) of the knee confirmed no full-thickness quadriceps or patellar tendon tear. A computed tomography (CT) scan of the knee showed a comminuted fracture of the lateral femoral condyle in the coronal plane, as well as multiple bone fragments within the joint (Figures 3A, 3B). The patient was placed in a bulky soft dressing and underwent open reduction and internal fixation of the fracture.

A 10-cm incision was made over the anterior aspect of the knee, and after dissection to the level of the retinaculum, a lateral parapatellar arthrotomy was performed. The patella was retracted medially to identify and free the fracture fragments. The fracture fragments were provisionally reduced and stabilized with three 0.065-in Kirschner wires. An area of osteochondral impaction proximal to the fracture was elevated and allograft bone was incorporated below the articular surface (Figures 4A, 4B). Rigid fixation of the fracture was achieved using 3 screws (2 Bio-Compression Screws [Arthrex Inc., Naples, Florida] and 1 Synthes cannulated screw [Synthes, West Chester, Pennsylvania]). The screws were placed in posteroanterior (PA) direction and inserted into the weight-bearing articular surface of the femoral condyle (Figures 4C, 4D). The screws were countersunk, and stable fixation with compression of the fracture was achieved. Reduction and screw position were verified with fluoroscopic views. The wound was closed in layers, and the patient was discharged home the next day.

Postoperatively, the patient was non-weight-bearing on the affected limb with a hinged-knee brace to allow for knee ROM exercises immediately. He was also given a continuous passive motion device to maintain knee motion. At the 6-week mark, the patient’s fracture alignment appeared to be well-maintained and showed interval healing. Clinically, the patient was noted to have limited knee ROM. The decision was made to take the patient to the operating room primarily for a manipulation under anesthesia and resection of scar tissue from postoperative arthrofibrosis. Arthroscopic screw removal was also planned as a secondary procedure at the same time in order to prevent the possibility of chondral injury from screw migration. During the procedure, the patient was noted to have improved ROM from 5º to 85º premanipulation to 5º to 110º postoperatively. At 3 months after the initial injury, the patient was allowed to begin progressive weight-bearing on the left knee. At most recent follow-up, after 12 months, the patient was able to ambulate and bear weight on the left leg without pain. Plain radiographs show a well-healed fracture with no evidence of collapse of the femoral condyle (Figures 5A, 5B). His active ROM of the left knee was 5º to 110º without pain (Figures 5C, 5D).

Discussion

In the vast majority of patellar dislocations, the patella dislocates laterally over the trochlear groove. Inferior, or intra-articular, dislocations of the patella are rare. The mechanism of injury is usually a blow onto the patella with a flexed knee. The 2 groups commonly involved are adolescent boys and the elderly.^8,9 In young men, it is thought that lax patellar attachments place adolescents at higher risk for this type of injury.^10-12 While patella fractures and frank extensor mechanism ruptures are uncommon in this age group, the same mechanism of injury can lead to stripping of the deep fibers of the patellar tendon from the superior pole of the patella.^3,13 The intact superficial fibers of the tendon allow the patella to hinge and displace into the joint.¹⁴

Inferior dislocations of the patella are classified into 2 types based on the orientation of the articular surface and the presence of osteophytes.¹⁵ Type I inferior dislocations occur after a direct blow to a flexed knee forces the superior pole of the patella into the intercondylar notch. Type II dislocations are caused by osteophytes on the superior pole of the patella that become wedged in the intercondylar notch and dislocate the patella inferiorly. In type I dislocations, the patella is rotated in the horizontal plane and the articular surface often faces inferiorly, but type II dislocations do not involve rotation of the articular surface. Type II injuries are seen more commonly in the elderly.

Our patient was able to tolerate a closed reduction of the patella after an intra-articular lidocaine injection, and a successful reduction was achieved without great difficulty. However, the majority of reports describe the need for an open reduction of inferior patellar dislocations.^3,8 When closed reductions were a success, they were performed under general anesthesia or conscious sedation.³ It is thought that the difficulty of reduction results from the tension of the quadriceps muscle pulling the patella superiorly into intercondylar notch.^11,16 However, successful closed reduction may be more likely in patients with less patellar rotation and entrapment within the intercondylar notch, as well as in patients whose knee is near full extension at presentation.^17-19 Successful closed reduction is also seen in elderly patients, where dislocation is generally caused by less forceful impact and held by osteophytes. In these patients, the knee is commonly held in extension.^12,15,20-22

The fracture pattern seen in this case also shows a rare fracture in skeletally immature patients, with only a few case reports in the literature. Isolated coronal plane femur fractures account for 0.65% of all femur fractures and are usually seen in adults after high-energy trauma.²³ In the skeletally immature, the fracture can occur with lower-energy mechanisms. The typical mechanism is thought to be a shearing force to the femur caused by an axial load to the knee in 90° or more of flexion.^4,24 A CT scan is recommended for better identification of the fracture and to plan treatment.^25,26 Because of their intra-articular nature and tenuous blood supply, Hoffa fractures tend to do poorly with nonoperative treatment and are prone to displacement and nonunion.^27,28 The goal of operative treatment is to obtain anatomic reduction and rigid fixation. While operative fixation techniques are varied, screw fixation with multiple smaller diameter screws has equal pullout strength compared to larger screws and may minimize damage to the articular cartilage.^29-31 By preserving blood supply to the fracture, and allowing for early active mobilization, operative treatment generally provides good long-term functional outcomes in these fracture patterns.²⁴

Conclusion

We describe a case in which the patella of an adolescent boy dislocated inferiorly into the knee joint, with an associated coronal shear fracture of the lateral femoral condyle. To our knowledge, this constellation of injuries has not been reported. For this uncommon injury pattern, we recommend a sequential treatment algorithm to minimize morbidity. We recommend first attempting a closed reduction of the patella with adequate pain control to avoid the morbidity associated with general anesthesia. After a successful reduction, an advanced imaging study (eg, MRI) is advisable to assess for concomitant soft-tissue injuries and preoperative planning, if necessary. The mechanism of injury and force required to cause a patellar dislocation of this nature leaves a high likelihood of other injuries. When a fracture is noted on plain radiographs after reduction, a CT scan can provide important information for planning surgical fixation of the fracture. Even in a skeletally immature patient, the principle of direct reduction and stable interfragmentary fixation of an articular fracture is critical for long-term function, even after a significant trauma to the knee.

In 1887, Midelfart¹ first reported on an intra-articular dislocation of the patella, and since then approximately 50 cases have been reported in the worldwide literature.² Also known as an inferior patellar dislocation, these rare traumatic events occur when the patella dislocates intra-articularly. Because the patella commonly rotates about its horizontal axis, the articular surface is facing proximally or distally. The patella becomes lodged within the trochlea and locks the knee joint. Most cases described in the literature involved adolescent boys, with the patella difficult to reduce. Most patients required open reduction, while those who underwent successful closed reduction often needed general anesthesia.³

Similarly, coronal shear fractures of the femoral condyle (ie, Hoffa fractures) are an uncommon fracture pattern typically seen in adults. These fractures are even more infrequent in skeletally immature patients, with fewer than 5 cases documented in the literature.^4-7 In our case report, we present a 14-year-old boy with a coronal shear fracture of the femoral condyle associated with an intra-articular patellar dislocation. To our knowledge, this constellation of injuries has not been reported. Additionally, closed reduction of the patella was successful after intra-articular lidocaine injection, without the need for sedation or general anesthesia. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Case Report

A 14-year-old boy presented to our institution after sustaining a direct blow to his left knee. The injury occurred as he jumped and landed on a flexed knee while playing with friends. The patient was unable to ambulate after the injury, and his left knee was locked in a slightly flexed position. Examination in the emergency department showed the knee to be held in approximately 60º of flexion, with an obvious bony prominence noted anteriorly over the femoral condyles. The patient was unable to perform a straight leg raise or any active range of motion (ROM) at the knee. Radiographs performed with the knee maintained in flexion confirmed that the patella was displaced into the knee joint and was rotated with the articular surface facing distally. Also noted was a coronal shear fracture of the lateral femoral condyle (Figures 1A, 1B).

The patient received pain medication and an intra-articular lidocaine injection prior to a reduction attempt by the orthopedic resident. With the patient supine, the hip was gently flexed to relax the quadriceps muscle. As the knee was flexed up to 110º, the prominent patella was gripped between the thumb and fingers to gently free and elevate the patella out of the intercondylar notch.

After reduction, an immediate return of normal patellar contour and patellofemoral tracking was observed as the knee was gently extended. There was no obvious defect to the patellar or quadriceps tendons, and the patient was able to perform a straight-leg raise, confirming the integrity of the extensor mechanism. Radiographs performed after the reduction confirmed relocation of the patella in correct anatomic position, as well as a lateral femoral condyle fracture (Figures 2A, 2B). Magnetic resonance imaging (MRI) of the knee confirmed no full-thickness quadriceps or patellar tendon tear. A computed tomography (CT) scan of the knee showed a comminuted fracture of the lateral femoral condyle in the coronal plane, as well as multiple bone fragments within the joint (Figures 3A, 3B). The patient was placed in a bulky soft dressing and underwent open reduction and internal fixation of the fracture.

A 10-cm incision was made over the anterior aspect of the knee, and after dissection to the level of the retinaculum, a lateral parapatellar arthrotomy was performed. The patella was retracted medially to identify and free the fracture fragments. The fracture fragments were provisionally reduced and stabilized with three 0.065-in Kirschner wires. An area of osteochondral impaction proximal to the fracture was elevated and allograft bone was incorporated below the articular surface (Figures 4A, 4B). Rigid fixation of the fracture was achieved using 3 screws (2 Bio-Compression Screws [Arthrex Inc., Naples, Florida] and 1 Synthes cannulated screw [Synthes, West Chester, Pennsylvania]). The screws were placed in posteroanterior (PA) direction and inserted into the weight-bearing articular surface of the femoral condyle (Figures 4C, 4D). The screws were countersunk, and stable fixation with compression of the fracture was achieved. Reduction and screw position were verified with fluoroscopic views. The wound was closed in layers, and the patient was discharged home the next day.

Postoperatively, the patient was non-weight-bearing on the affected limb with a hinged-knee brace to allow for knee ROM exercises immediately. He was also given a continuous passive motion device to maintain knee motion. At the 6-week mark, the patient’s fracture alignment appeared to be well-maintained and showed interval healing. Clinically, the patient was noted to have limited knee ROM. The decision was made to take the patient to the operating room primarily for a manipulation under anesthesia and resection of scar tissue from postoperative arthrofibrosis. Arthroscopic screw removal was also planned as a secondary procedure at the same time in order to prevent the possibility of chondral injury from screw migration. During the procedure, the patient was noted to have improved ROM from 5º to 85º premanipulation to 5º to 110º postoperatively. At 3 months after the initial injury, the patient was allowed to begin progressive weight-bearing on the left knee. At most recent follow-up, after 12 months, the patient was able to ambulate and bear weight on the left leg without pain. Plain radiographs show a well-healed fracture with no evidence of collapse of the femoral condyle (Figures 5A, 5B). His active ROM of the left knee was 5º to 110º without pain (Figures 5C, 5D).

Discussion

In the vast majority of patellar dislocations, the patella dislocates laterally over the trochlear groove. Inferior, or intra-articular, dislocations of the patella are rare. The mechanism of injury is usually a blow onto the patella with a flexed knee. The 2 groups commonly involved are adolescent boys and the elderly.^8,9 In young men, it is thought that lax patellar attachments place adolescents at higher risk for this type of injury.^10-12 While patella fractures and frank extensor mechanism ruptures are uncommon in this age group, the same mechanism of injury can lead to stripping of the deep fibers of the patellar tendon from the superior pole of the patella.^3,13 The intact superficial fibers of the tendon allow the patella to hinge and displace into the joint.¹⁴

Inferior dislocations of the patella are classified into 2 types based on the orientation of the articular surface and the presence of osteophytes.¹⁵ Type I inferior dislocations occur after a direct blow to a flexed knee forces the superior pole of the patella into the intercondylar notch. Type II dislocations are caused by osteophytes on the superior pole of the patella that become wedged in the intercondylar notch and dislocate the patella inferiorly. In type I dislocations, the patella is rotated in the horizontal plane and the articular surface often faces inferiorly, but type II dislocations do not involve rotation of the articular surface. Type II injuries are seen more commonly in the elderly.

Our patient was able to tolerate a closed reduction of the patella after an intra-articular lidocaine injection, and a successful reduction was achieved without great difficulty. However, the majority of reports describe the need for an open reduction of inferior patellar dislocations.^3,8 When closed reductions were a success, they were performed under general anesthesia or conscious sedation.³ It is thought that the difficulty of reduction results from the tension of the quadriceps muscle pulling the patella superiorly into intercondylar notch.^11,16 However, successful closed reduction may be more likely in patients with less patellar rotation and entrapment within the intercondylar notch, as well as in patients whose knee is near full extension at presentation.^17-19 Successful closed reduction is also seen in elderly patients, where dislocation is generally caused by less forceful impact and held by osteophytes. In these patients, the knee is commonly held in extension.^12,15,20-22

The fracture pattern seen in this case also shows a rare fracture in skeletally immature patients, with only a few case reports in the literature. Isolated coronal plane femur fractures account for 0.65% of all femur fractures and are usually seen in adults after high-energy trauma.²³ In the skeletally immature, the fracture can occur with lower-energy mechanisms. The typical mechanism is thought to be a shearing force to the femur caused by an axial load to the knee in 90° or more of flexion.^4,24 A CT scan is recommended for better identification of the fracture and to plan treatment.^25,26 Because of their intra-articular nature and tenuous blood supply, Hoffa fractures tend to do poorly with nonoperative treatment and are prone to displacement and nonunion.^27,28 The goal of operative treatment is to obtain anatomic reduction and rigid fixation. While operative fixation techniques are varied, screw fixation with multiple smaller diameter screws has equal pullout strength compared to larger screws and may minimize damage to the articular cartilage.^29-31 By preserving blood supply to the fracture, and allowing for early active mobilization, operative treatment generally provides good long-term functional outcomes in these fracture patterns.²⁴

Conclusion

We describe a case in which the patella of an adolescent boy dislocated inferiorly into the knee joint, with an associated coronal shear fracture of the lateral femoral condyle. To our knowledge, this constellation of injuries has not been reported. For this uncommon injury pattern, we recommend a sequential treatment algorithm to minimize morbidity. We recommend first attempting a closed reduction of the patella with adequate pain control to avoid the morbidity associated with general anesthesia. After a successful reduction, an advanced imaging study (eg, MRI) is advisable to assess for concomitant soft-tissue injuries and preoperative planning, if necessary. The mechanism of injury and force required to cause a patellar dislocation of this nature leaves a high likelihood of other injuries. When a fracture is noted on plain radiographs after reduction, a CT scan can provide important information for planning surgical fixation of the fracture. Even in a skeletally immature patient, the principle of direct reduction and stable interfragmentary fixation of an articular fracture is critical for long-term function, even after a significant trauma to the knee.

In 1887, Midelfart¹ first reported on an intra-articular dislocation of the patella, and since then approximately 50 cases have been reported in the worldwide literature.² Also known as an inferior patellar dislocation, these rare traumatic events occur when the patella dislocates intra-articularly. Because the patella commonly rotates about its horizontal axis, the articular surface is facing proximally or distally. The patella becomes lodged within the trochlea and locks the knee joint. Most cases described in the literature involved adolescent boys, with the patella difficult to reduce. Most patients required open reduction, while those who underwent successful closed reduction often needed general anesthesia.³

Similarly, coronal shear fractures of the femoral condyle (ie, Hoffa fractures) are an uncommon fracture pattern typically seen in adults. These fractures are even more infrequent in skeletally immature patients, with fewer than 5 cases documented in the literature.^4-7 In our case report, we present a 14-year-old boy with a coronal shear fracture of the femoral condyle associated with an intra-articular patellar dislocation. To our knowledge, this constellation of injuries has not been reported. Additionally, closed reduction of the patella was successful after intra-articular lidocaine injection, without the need for sedation or general anesthesia. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Case Report

A 14-year-old boy presented to our institution after sustaining a direct blow to his left knee. The injury occurred as he jumped and landed on a flexed knee while playing with friends. The patient was unable to ambulate after the injury, and his left knee was locked in a slightly flexed position. Examination in the emergency department showed the knee to be held in approximately 60º of flexion, with an obvious bony prominence noted anteriorly over the femoral condyles. The patient was unable to perform a straight leg raise or any active range of motion (ROM) at the knee. Radiographs performed with the knee maintained in flexion confirmed that the patella was displaced into the knee joint and was rotated with the articular surface facing distally. Also noted was a coronal shear fracture of the lateral femoral condyle (Figures 1A, 1B).

The patient received pain medication and an intra-articular lidocaine injection prior to a reduction attempt by the orthopedic resident. With the patient supine, the hip was gently flexed to relax the quadriceps muscle. As the knee was flexed up to 110º, the prominent patella was gripped between the thumb and fingers to gently free and elevate the patella out of the intercondylar notch.

After reduction, an immediate return of normal patellar contour and patellofemoral tracking was observed as the knee was gently extended. There was no obvious defect to the patellar or quadriceps tendons, and the patient was able to perform a straight-leg raise, confirming the integrity of the extensor mechanism. Radiographs performed after the reduction confirmed relocation of the patella in correct anatomic position, as well as a lateral femoral condyle fracture (Figures 2A, 2B). Magnetic resonance imaging (MRI) of the knee confirmed no full-thickness quadriceps or patellar tendon tear. A computed tomography (CT) scan of the knee showed a comminuted fracture of the lateral femoral condyle in the coronal plane, as well as multiple bone fragments within the joint (Figures 3A, 3B). The patient was placed in a bulky soft dressing and underwent open reduction and internal fixation of the fracture.

A 10-cm incision was made over the anterior aspect of the knee, and after dissection to the level of the retinaculum, a lateral parapatellar arthrotomy was performed. The patella was retracted medially to identify and free the fracture fragments. The fracture fragments were provisionally reduced and stabilized with three 0.065-in Kirschner wires. An area of osteochondral impaction proximal to the fracture was elevated and allograft bone was incorporated below the articular surface (Figures 4A, 4B). Rigid fixation of the fracture was achieved using 3 screws (2 Bio-Compression Screws [Arthrex Inc., Naples, Florida] and 1 Synthes cannulated screw [Synthes, West Chester, Pennsylvania]). The screws were placed in posteroanterior (PA) direction and inserted into the weight-bearing articular surface of the femoral condyle (Figures 4C, 4D). The screws were countersunk, and stable fixation with compression of the fracture was achieved. Reduction and screw position were verified with fluoroscopic views. The wound was closed in layers, and the patient was discharged home the next day.

Postoperatively, the patient was non-weight-bearing on the affected limb with a hinged-knee brace to allow for knee ROM exercises immediately. He was also given a continuous passive motion device to maintain knee motion. At the 6-week mark, the patient’s fracture alignment appeared to be well-maintained and showed interval healing. Clinically, the patient was noted to have limited knee ROM. The decision was made to take the patient to the operating room primarily for a manipulation under anesthesia and resection of scar tissue from postoperative arthrofibrosis. Arthroscopic screw removal was also planned as a secondary procedure at the same time in order to prevent the possibility of chondral injury from screw migration. During the procedure, the patient was noted to have improved ROM from 5º to 85º premanipulation to 5º to 110º postoperatively. At 3 months after the initial injury, the patient was allowed to begin progressive weight-bearing on the left knee. At most recent follow-up, after 12 months, the patient was able to ambulate and bear weight on the left leg without pain. Plain radiographs show a well-healed fracture with no evidence of collapse of the femoral condyle (Figures 5A, 5B). His active ROM of the left knee was 5º to 110º without pain (Figures 5C, 5D).

Discussion

In the vast majority of patellar dislocations, the patella dislocates laterally over the trochlear groove. Inferior, or intra-articular, dislocations of the patella are rare. The mechanism of injury is usually a blow onto the patella with a flexed knee. The 2 groups commonly involved are adolescent boys and the elderly.^8,9 In young men, it is thought that lax patellar attachments place adolescents at higher risk for this type of injury.^10-12 While patella fractures and frank extensor mechanism ruptures are uncommon in this age group, the same mechanism of injury can lead to stripping of the deep fibers of the patellar tendon from the superior pole of the patella.^3,13 The intact superficial fibers of the tendon allow the patella to hinge and displace into the joint.¹⁴

Inferior dislocations of the patella are classified into 2 types based on the orientation of the articular surface and the presence of osteophytes.¹⁵ Type I inferior dislocations occur after a direct blow to a flexed knee forces the superior pole of the patella into the intercondylar notch. Type II dislocations are caused by osteophytes on the superior pole of the patella that become wedged in the intercondylar notch and dislocate the patella inferiorly. In type I dislocations, the patella is rotated in the horizontal plane and the articular surface often faces inferiorly, but type II dislocations do not involve rotation of the articular surface. Type II injuries are seen more commonly in the elderly.

Our patient was able to tolerate a closed reduction of the patella after an intra-articular lidocaine injection, and a successful reduction was achieved without great difficulty. However, the majority of reports describe the need for an open reduction of inferior patellar dislocations.^3,8 When closed reductions were a success, they were performed under general anesthesia or conscious sedation.³ It is thought that the difficulty of reduction results from the tension of the quadriceps muscle pulling the patella superiorly into intercondylar notch.^11,16 However, successful closed reduction may be more likely in patients with less patellar rotation and entrapment within the intercondylar notch, as well as in patients whose knee is near full extension at presentation.^17-19 Successful closed reduction is also seen in elderly patients, where dislocation is generally caused by less forceful impact and held by osteophytes. In these patients, the knee is commonly held in extension.^12,15,20-22

The fracture pattern seen in this case also shows a rare fracture in skeletally immature patients, with only a few case reports in the literature. Isolated coronal plane femur fractures account for 0.65% of all femur fractures and are usually seen in adults after high-energy trauma.²³ In the skeletally immature, the fracture can occur with lower-energy mechanisms. The typical mechanism is thought to be a shearing force to the femur caused by an axial load to the knee in 90° or more of flexion.^4,24 A CT scan is recommended for better identification of the fracture and to plan treatment.^25,26 Because of their intra-articular nature and tenuous blood supply, Hoffa fractures tend to do poorly with nonoperative treatment and are prone to displacement and nonunion.^27,28 The goal of operative treatment is to obtain anatomic reduction and rigid fixation. While operative fixation techniques are varied, screw fixation with multiple smaller diameter screws has equal pullout strength compared to larger screws and may minimize damage to the articular cartilage.^29-31 By preserving blood supply to the fracture, and allowing for early active mobilization, operative treatment generally provides good long-term functional outcomes in these fracture patterns.²⁴

Conclusion

We describe a case in which the patella of an adolescent boy dislocated inferiorly into the knee joint, with an associated coronal shear fracture of the lateral femoral condyle. To our knowledge, this constellation of injuries has not been reported. For this uncommon injury pattern, we recommend a sequential treatment algorithm to minimize morbidity. We recommend first attempting a closed reduction of the patella with adequate pain control to avoid the morbidity associated with general anesthesia. After a successful reduction, an advanced imaging study (eg, MRI) is advisable to assess for concomitant soft-tissue injuries and preoperative planning, if necessary. The mechanism of injury and force required to cause a patellar dislocation of this nature leaves a high likelihood of other injuries. When a fracture is noted on plain radiographs after reduction, a CT scan can provide important information for planning surgical fixation of the fracture. Even in a skeletally immature patient, the principle of direct reduction and stable interfragmentary fixation of an articular fracture is critical for long-term function, even after a significant trauma to the knee.

Since Neer described the rotator interval in 1970, its closure, often used in conjunction with capsulorrhaphy, has become an important surgical technique in managing shoulder instability.^1-11 Numerous studies have sought to define the function of the rotator interval.^1-3,6-20 The etiology of lesions of the rotator interval has been debated, and there is evidence that such lesions may be in part congenital.²¹ Increased rotator interval depth and width, along with increased size of the distended inferior and posteroinferior joint capsule on magnetic resonance arthrography, have been reported in cases of multidirectional shoulder instability.²² However, confusion remains about the role of the rotator interval in shoulder instability and about the effect its closure has on shoulder function. No one knows the degree of volume reduction that results from closure of the rotator interval and whether medial and lateral sutures differ in the volume reduction achieved.

Cadaveric studies have shown that the rotator interval has an important role in shoulder motion.^{6,13-16,19,20,23} Harryman and colleagues¹³ found that sectioning the coracohumeral ligament (CHL) increased shoulder range of motion (ROM), and medial-to-lateral closure of the rotator interval restricted motion in all planes. Most notably, interval closure limited inferior translation in the adducted shoulder, posterior translation in the flexed adducted shoulder, and external rotation in the neutral position. Subsequent studies,^17,18 using rotator interval closure combined with thermal capsulorrhaphy, confirmed the results reported by Harryman and colleagues.¹³

More recent cadaveric studies using superior-to-inferior rotator interval closures have shown a decrease in anterior translation but not posterior translation.^14-16,19-21 A superior-to-inferior interval closure technique limited external rotation less than a medial-to-lateral closure did.^13-16,19-21 The majority of arthroscopically described rotator interval closures involve a superior-to-inferior technique and use 2 or 3 sutures.^1,3,9-11

Plausinis and colleagues¹⁵ examined the effects of an isolated medial, an isolated lateral, and a medial combined with a lateral closure of the rotator interval. They noted that all 3 methods limited anterior translation and motion by means of 6° flexion and 10° external rotation; however, there was no statistical difference between methods. They also found that occasionally the medial interval closure resulted in massive loss of external rotation. Earlier, Jost and colleagues¹⁴ noted that a medial rotator interval could cause this massive loss by tethering the CHL, resulting in a medial-to-lateral imbrication of the CHL.

Arthroscopic rotator interval closure has clinically demonstrated an additive effect on shoulder stability. The recurrence rate was lower for arthroscopic Bankart repair combined with arthroscopic rotator interval closure (8%) than for arthroscopic Bankart repair alone (13%).²⁴ In addition, time to recurrent dislocation was longer (42 vs 13 months) for the group that underwent the combination of Bankart repair and rotator interval closure. Regarding the concern about loss of motion after arthroscopic rotator interval closure, Chiang and colleagues²⁵ recently noted no significant loss of motion 5 years after arthroscopic Bankart repair with rotator interval closure.

What effect rotator interval closure has on intra-articular glenohumeral volume (GHV) remains unknown. Using a cadaveric model, Yamamoto and colleagues²⁰ showed that decreasing GHV can increase the responsiveness of the glenohumeral joint to the intra-articular pressure. Thus, reducing the volume can improve stability in vitro by increasing the magnitude of negative pressure stabilizing the glenohumeral joint.

We conducted a study to quantify the effects of arthroscopic rotator interval closure on capsular volume and to determine whether medial and lateral interval closures resulted in different degrees of volume reduction. Our hypothesis was that shoulder volume would be significantly reduced by closing the rotator interval.

Materials and Methods

Previous studies have not specifically evaluated GHV after rotator interval closure. Our power analysis was performed with data from a study by Karas and colleagues,²⁶ who evaluated GHV after capsular plication. To detect a capsular volume reduction of 20% per stitch, with a 2-sided 5% significance level and a power of 80%, we needed a sample size of 5 specimens per group.

After receiving institutional review board approval for this study, we obtained 10 cadaveric shoulders (5 matched pairs). Exclusion criteria included arthroscopic evaluation revealing a full-thickness rotator cuff tear or significant osteoarthritis. Two shoulders had full-thickness cuff tears, leaving 8 shoulders to be tested; 6 of these were matched pairs. The shoulders were from 1 man (matched pair) and 4 women (2 matched pairs). Age ranged from 38 to 70 years (mean, 59.6 years). Differences in material properties between the specimens were accounted for by using primarily matched pairs.

The 2 study groups consisted of 4 shoulders each. After specimens were thawed, the skin, subcutaneous tissues, and periscapular muscles were removed from the shoulder. Only the capsule, biceps, and rotator cuff remained. For measurement purposes, the shoulders were mounted in a vice clamp in a beach-chair orientation. We placed a total of 2 portals with fully threaded 8.25-mm cannulas (Arthrex, Naples, Florida). A standard posterior portal was placed in the soft spot. A low anterior portal was then placed just superior to the subscapularis tendon. For arthroscopic examination and instrumentation in a saline environment, the shoulders were rotated into the lateral decubitus position, with suspension in 30° abduction and 20° forward flexion, by a rope attached to a pin in the distal shaft of the humerus.

In both groups, medial and lateral stitches with No. 2 FiberWire (Arthrex) were used to close the interval. The medial interval closure stitch was placed more than 10 mm away from the glenoid to prevent unpredictable CHL tethering; the lateral closure stitch was placed 10 mm lateral to the medial stitch (Figure 1).¹⁴ All sutures were placed intra-articularly under direct arthroscopic visualization, similar to the methods described in the literature.^1,3,9-11 Sutures were passed through the superior glenohumeral ligament (SGHL) and through the upper subscapularis using a suture shuttle (SutureLasso; Arthrex) and Penetrator II Suture Retriever (Arthrex). The upper subscapularis was incorporated because of the unpredictable nature of the middle glenohumeral ligament (MGHL). Both rotator interval sutures were placed before tying either. In the medial group, the medial stitch was tied first, using alternating half-hitches, followed by the lateral stitch. In the lateral group, the lateral stitch was tied first, followed by the medial stitch. GHV was measured at baseline and after tying each stitch. Dr. Ponce instrumented all shoulders.

Modifying a beach-chair technique described by Miller and colleagues,²⁷ we used a viscous fatty-acid sulfate solution, liquid soap, to measure GHV.^27-29 A small slit in line with the fibers was made in the supraspinatus tendon just lateral to the musculotendinous junction. A 3-way stop-cock was placed into the joint though this defect. A 20-mL syringe with a 16-gauge needle was used to inject the soap. The needle was inserted into the rotator cuff interval, and the viscous solution was injected in 5-mL increments until there was active extravasation through the supraspinatus cannula (Figure 2). This technique, the “volcano method,” marked the maximum capacity of the joint. The joint was then copiously irrigated with normal saline and suctioned until all normal saline was evacuated. Dr. Rosenzweig took 2 measurements on each shoulder, and their mean was used for analysis.

The baseline measurement was taken with the 2 working cannulas in the shoulder joint. Measurements were obtained with cannulas to simulate normal clinical conditions. Subsequent measurements were done with the cannulas in place and inserted up to the same thread each time so as not to change the volume. The capsule and the rotator cuff were then dissected from the humerus so the size of the capsulolabral plication could be directly evaluated. Methylene blue was used to mark the capsular suture holes before removing the sutures. With use of a caliper, the size of the plication bite was measured (in millimeters).

Statistical Analysis

The primary outcome was percent reduction in GHV as a function of number of plications and size of plication. When only the first plication was tightened, the effect of position (medial or lateral) was also of interest. Percent volume reduction was calculated as (original – new) / original × 100. SAS 8.02 (SAS Institute, Cary, North Carolina) was used to fit a repeated random-intercept regression model for each outcome. This technique properly accounts for the paired nature of the specimens and the repeated measures (baseline plus 2 plications). Model fit was assessed by the method of difference in log likelihood.

Results

In the medial group, GHV was reduced by a mean of 24.2% with a single medial stitch; in the lateral group, GHV was reduced by a mean of 35.1% (Figure 3). The difference was significant (P < .02). In the medial group, when a second lateral stitch was used, GHV was reduced by another 18.7%; in the lateral group, when a medial stitch was added, GHV was reduced by another 11.4%. Final GHV for the medial and lateral groups was 42.9% and 46.5%, respectively. There was no statistical difference in final GHV, regardless of which stitch was placed first. When the 2 groups were combined, GHV was reduced by 44.9% with use of medial and lateral rotator interval closure stitches.

Mean amount of tissue purchased, or “bite size,” was 18 mm with a lateral suture and 15 mm with a medial suture (P < .05). In addition, an increase in bite size to GHV reduction was essentially linear, where an increase in bite size of 1 mm reduced GHV by about 1% (Figure 4).

Discussion

Although there have been numerous clinical series and biomechanical studies focused on isolated rotator interval closure (or its use as an adjunct) in shoulder stabilization, the precise function of the rotator interval remains poorly understood.^1-3,6-11,19 Consequently, the in vivo effects of interval closure are unknown.

Initial studies proposed that rotator interval closure limited inferior and posterior translation.³⁰ More recent studies have demonstrated that rotator interval closure confers little effect on posterior instability but increases anterior stability in cadaveric models.^15,16 Clinical series have provided evidence that rotator interval closure can increase anterior stability.^1,3,7,9,12 In a series of isolated rotator interval closures for multidirectional instability, Field and colleagues¹² found that preoperative anterior and inferior symptoms predominated over posterior symptoms. Isolated closure of the rotator interval resulted in 100% excellent results with no cases of recurrent instability. Moon and colleagues³¹ reported that arthroscopic rotator interval closure with or without inferior capsular plication in multidirectional instability and predominant symptomatic inferior instability has shown benefit by improving function and stability. Other clinical reports of rotator interval closure in conjunction with arthroscopic Bankart repair have suggested it has an additive effect on anterior shoulder stability without limiting motion.^24,25

In our study, arthroscopic closure of the rotator interval with 2 superior-to-inferior stitches reduced intracapsular volume by 45%. Even though open capsular shifts use different surgical techniques, similar technique volume reduction studies have reported reductions between 34% and 54% with open shifts.^27,30 It is unknown if the stability resulting from decreased GHV is primarily from increasing intra-articular pressures or from restricting ROM, or from a combination of both. In shoulders with multidirectional instability, the joint volume may be increased, the joint capsule may be enlarged, or the glenohumeral ligaments may be lax and thin.^4,6,32,33 Yamamoto and colleagues¹⁹ stated that intra-articular pressure is determined by 3 factors: load, joint volume, and material properties of the capsule. Load is a constant; joint volume and material properties can be changed.¹⁹ In our study, material properties were controlled by using a majority of matched specimens. Regardless of the stabilizing mechanism, our study results demonstrated that arthroscopic rotator interval closure may be a powerful tool in reducing shoulder volume, a consistent principle of surgical techniques used in reestablishing shoulder stability.^19,20

When a single rotator interval closure stitch was used, volume reduction with a lateral stitch was superior to that with a medial stitch. This finding is logical, as anatomically the dimensions of the rotator interval are larger laterally as the CHL fans out to insert on the greater and lesser tuberosities.¹⁴ This finding has also been reported in open capsular shifts for multidirectional instability, with a lateral humeral shift having a larger volume reduction than a medial glenoid shift.²⁷ Miller and colleagues²⁷ used the image of a cone, with its larger opening facing the humerus and narrower side facing the glenoid, to illustrate this difference in open capsular shifts.

Our study also showed a larger volume reduction with 2 rotator interval closure stitches than with a single interval stitch. As ROM testing has not shown a difference between results with 1 and 2 sutures, we recommend a minimum of 2 sutures for arthroscopic rotator interval closure.¹⁵ If a single plication stitch is preferred, a lateral stitch (vs a medial stitch) can be used for a significantly larger reduction in shoulder volume. We think this is because of a larger amount of capsule being purchased with lateral closure (Figure 5). However, if a medial stitch is used, it is important to not place it too near the glenoid to avoid CHL tethering and subsequent excessive loss of external rotation.¹⁵

This study had several weaknesses. First, it was a cadaveric study, and use of specimens not known to have instability or specific rotator interval injury may make generalization to a clinical situation difficult. Second, although our power analysis called for 5 shoulders in each group, full-thickness rotator cuff tears rendered 2 shoulders unusable. This reduced our sample sizes and potentially decreased the power of the study, though the data demonstrated statistically significant differences. Third, we did not compare the effects of an open medial-to-lateral imbrication of the rotator interval on intracapsular volume with the effects of our arthroscopic method. We also did not assess our specimens’ ROM, effects of interval closure stitches on shoulder stability, or glenohumeral contact surface pressures, as these factors have already been studied.^13-19 Instead, we focused on the effects of rotator interval closure on intracapsular volume, which had not been quantified until now. The clinical significance of such a volume reduction is unknown, especially with respect to influence on ROM, but the degree of volume reduction was larger than with previously reported arthroscopic instability repairs and smaller than with open capsular shifts, demonstrating that it may be a powerful tool in restoring stability in an unstable shoulder.^26-30,34 Fourth, the role of isolated rotator interval closure is poorly defined, as only 1 clinical series of isolated rotator interval closure has been reported thus far.¹² It has been far more common for rotator interval closure to be used with Bankart repair or capsulorrhaphy.^1-3,7-9

In a cadaveric study by Provencher and colleagues,¹⁶ open rotator interval closure with medial-to-lateral imbrication of the interval altered shoulder kinematics differently from what occurred with arthroscopic closure of the MGHL to the SGHL, resulting in superior-to-inferior shift. Comparing the 2 methods may therefore be inappropriate. Currently we reserve rotator interval closure for infrequent cases of revision instability and cases in which glenoid bone loss is marginal (5%-15%) and there is a willingness to potentially sacrifice ROM to restore stability and avoid an open stabilization procedure. Continued investigation into the clinical role of rotator interval closure in shoulder stability is needed. We should identify the pathology in a patient with instability and use this technique as an adjuvant to other stabilization procedures. 

Conclusion

Arthroscopic rotator interval closure with 2 plication stitches is a powerful tool in reducing the intracapsular volume of the shoulder. If a single plication stitch is preferred, a lateral rotator interval closure stitch (vs a medial stitch) can be used for a larger reduction in shoulder volume.

Since Neer described the rotator interval in 1970, its closure, often used in conjunction with capsulorrhaphy, has become an important surgical technique in managing shoulder instability.^1-11 Numerous studies have sought to define the function of the rotator interval.^1-3,6-20 The etiology of lesions of the rotator interval has been debated, and there is evidence that such lesions may be in part congenital.²¹ Increased rotator interval depth and width, along with increased size of the distended inferior and posteroinferior joint capsule on magnetic resonance arthrography, have been reported in cases of multidirectional shoulder instability.²² However, confusion remains about the role of the rotator interval in shoulder instability and about the effect its closure has on shoulder function. No one knows the degree of volume reduction that results from closure of the rotator interval and whether medial and lateral sutures differ in the volume reduction achieved.

Cadaveric studies have shown that the rotator interval has an important role in shoulder motion.^{6,13-16,19,20,23} Harryman and colleagues¹³ found that sectioning the coracohumeral ligament (CHL) increased shoulder range of motion (ROM), and medial-to-lateral closure of the rotator interval restricted motion in all planes. Most notably, interval closure limited inferior translation in the adducted shoulder, posterior translation in the flexed adducted shoulder, and external rotation in the neutral position. Subsequent studies,^17,18 using rotator interval closure combined with thermal capsulorrhaphy, confirmed the results reported by Harryman and colleagues.¹³

More recent cadaveric studies using superior-to-inferior rotator interval closures have shown a decrease in anterior translation but not posterior translation.^14-16,19-21 A superior-to-inferior interval closure technique limited external rotation less than a medial-to-lateral closure did.^13-16,19-21 The majority of arthroscopically described rotator interval closures involve a superior-to-inferior technique and use 2 or 3 sutures.^1,3,9-11

Plausinis and colleagues¹⁵ examined the effects of an isolated medial, an isolated lateral, and a medial combined with a lateral closure of the rotator interval. They noted that all 3 methods limited anterior translation and motion by means of 6° flexion and 10° external rotation; however, there was no statistical difference between methods. They also found that occasionally the medial interval closure resulted in massive loss of external rotation. Earlier, Jost and colleagues¹⁴ noted that a medial rotator interval could cause this massive loss by tethering the CHL, resulting in a medial-to-lateral imbrication of the CHL.

Arthroscopic rotator interval closure has clinically demonstrated an additive effect on shoulder stability. The recurrence rate was lower for arthroscopic Bankart repair combined with arthroscopic rotator interval closure (8%) than for arthroscopic Bankart repair alone (13%).²⁴ In addition, time to recurrent dislocation was longer (42 vs 13 months) for the group that underwent the combination of Bankart repair and rotator interval closure. Regarding the concern about loss of motion after arthroscopic rotator interval closure, Chiang and colleagues²⁵ recently noted no significant loss of motion 5 years after arthroscopic Bankart repair with rotator interval closure.

What effect rotator interval closure has on intra-articular glenohumeral volume (GHV) remains unknown. Using a cadaveric model, Yamamoto and colleagues²⁰ showed that decreasing GHV can increase the responsiveness of the glenohumeral joint to the intra-articular pressure. Thus, reducing the volume can improve stability in vitro by increasing the magnitude of negative pressure stabilizing the glenohumeral joint.

We conducted a study to quantify the effects of arthroscopic rotator interval closure on capsular volume and to determine whether medial and lateral interval closures resulted in different degrees of volume reduction. Our hypothesis was that shoulder volume would be significantly reduced by closing the rotator interval.

Materials and Methods

Previous studies have not specifically evaluated GHV after rotator interval closure. Our power analysis was performed with data from a study by Karas and colleagues,²⁶ who evaluated GHV after capsular plication. To detect a capsular volume reduction of 20% per stitch, with a 2-sided 5% significance level and a power of 80%, we needed a sample size of 5 specimens per group.

After receiving institutional review board approval for this study, we obtained 10 cadaveric shoulders (5 matched pairs). Exclusion criteria included arthroscopic evaluation revealing a full-thickness rotator cuff tear or significant osteoarthritis. Two shoulders had full-thickness cuff tears, leaving 8 shoulders to be tested; 6 of these were matched pairs. The shoulders were from 1 man (matched pair) and 4 women (2 matched pairs). Age ranged from 38 to 70 years (mean, 59.6 years). Differences in material properties between the specimens were accounted for by using primarily matched pairs.

The 2 study groups consisted of 4 shoulders each. After specimens were thawed, the skin, subcutaneous tissues, and periscapular muscles were removed from the shoulder. Only the capsule, biceps, and rotator cuff remained. For measurement purposes, the shoulders were mounted in a vice clamp in a beach-chair orientation. We placed a total of 2 portals with fully threaded 8.25-mm cannulas (Arthrex, Naples, Florida). A standard posterior portal was placed in the soft spot. A low anterior portal was then placed just superior to the subscapularis tendon. For arthroscopic examination and instrumentation in a saline environment, the shoulders were rotated into the lateral decubitus position, with suspension in 30° abduction and 20° forward flexion, by a rope attached to a pin in the distal shaft of the humerus.

In both groups, medial and lateral stitches with No. 2 FiberWire (Arthrex) were used to close the interval. The medial interval closure stitch was placed more than 10 mm away from the glenoid to prevent unpredictable CHL tethering; the lateral closure stitch was placed 10 mm lateral to the medial stitch (Figure 1).¹⁴ All sutures were placed intra-articularly under direct arthroscopic visualization, similar to the methods described in the literature.^1,3,9-11 Sutures were passed through the superior glenohumeral ligament (SGHL) and through the upper subscapularis using a suture shuttle (SutureLasso; Arthrex) and Penetrator II Suture Retriever (Arthrex). The upper subscapularis was incorporated because of the unpredictable nature of the middle glenohumeral ligament (MGHL). Both rotator interval sutures were placed before tying either. In the medial group, the medial stitch was tied first, using alternating half-hitches, followed by the lateral stitch. In the lateral group, the lateral stitch was tied first, followed by the medial stitch. GHV was measured at baseline and after tying each stitch. Dr. Ponce instrumented all shoulders.

Modifying a beach-chair technique described by Miller and colleagues,²⁷ we used a viscous fatty-acid sulfate solution, liquid soap, to measure GHV.^27-29 A small slit in line with the fibers was made in the supraspinatus tendon just lateral to the musculotendinous junction. A 3-way stop-cock was placed into the joint though this defect. A 20-mL syringe with a 16-gauge needle was used to inject the soap. The needle was inserted into the rotator cuff interval, and the viscous solution was injected in 5-mL increments until there was active extravasation through the supraspinatus cannula (Figure 2). This technique, the “volcano method,” marked the maximum capacity of the joint. The joint was then copiously irrigated with normal saline and suctioned until all normal saline was evacuated. Dr. Rosenzweig took 2 measurements on each shoulder, and their mean was used for analysis.

The baseline measurement was taken with the 2 working cannulas in the shoulder joint. Measurements were obtained with cannulas to simulate normal clinical conditions. Subsequent measurements were done with the cannulas in place and inserted up to the same thread each time so as not to change the volume. The capsule and the rotator cuff were then dissected from the humerus so the size of the capsulolabral plication could be directly evaluated. Methylene blue was used to mark the capsular suture holes before removing the sutures. With use of a caliper, the size of the plication bite was measured (in millimeters).

Statistical Analysis

The primary outcome was percent reduction in GHV as a function of number of plications and size of plication. When only the first plication was tightened, the effect of position (medial or lateral) was also of interest. Percent volume reduction was calculated as (original – new) / original × 100. SAS 8.02 (SAS Institute, Cary, North Carolina) was used to fit a repeated random-intercept regression model for each outcome. This technique properly accounts for the paired nature of the specimens and the repeated measures (baseline plus 2 plications). Model fit was assessed by the method of difference in log likelihood.

Results

In the medial group, GHV was reduced by a mean of 24.2% with a single medial stitch; in the lateral group, GHV was reduced by a mean of 35.1% (Figure 3). The difference was significant (P < .02). In the medial group, when a second lateral stitch was used, GHV was reduced by another 18.7%; in the lateral group, when a medial stitch was added, GHV was reduced by another 11.4%. Final GHV for the medial and lateral groups was 42.9% and 46.5%, respectively. There was no statistical difference in final GHV, regardless of which stitch was placed first. When the 2 groups were combined, GHV was reduced by 44.9% with use of medial and lateral rotator interval closure stitches.

Mean amount of tissue purchased, or “bite size,” was 18 mm with a lateral suture and 15 mm with a medial suture (P < .05). In addition, an increase in bite size to GHV reduction was essentially linear, where an increase in bite size of 1 mm reduced GHV by about 1% (Figure 4).

Discussion

Although there have been numerous clinical series and biomechanical studies focused on isolated rotator interval closure (or its use as an adjunct) in shoulder stabilization, the precise function of the rotator interval remains poorly understood.^1-3,6-11,19 Consequently, the in vivo effects of interval closure are unknown.

Initial studies proposed that rotator interval closure limited inferior and posterior translation.³⁰ More recent studies have demonstrated that rotator interval closure confers little effect on posterior instability but increases anterior stability in cadaveric models.^15,16 Clinical series have provided evidence that rotator interval closure can increase anterior stability.^1,3,7,9,12 In a series of isolated rotator interval closures for multidirectional instability, Field and colleagues¹² found that preoperative anterior and inferior symptoms predominated over posterior symptoms. Isolated closure of the rotator interval resulted in 100% excellent results with no cases of recurrent instability. Moon and colleagues³¹ reported that arthroscopic rotator interval closure with or without inferior capsular plication in multidirectional instability and predominant symptomatic inferior instability has shown benefit by improving function and stability. Other clinical reports of rotator interval closure in conjunction with arthroscopic Bankart repair have suggested it has an additive effect on anterior shoulder stability without limiting motion.^24,25

In our study, arthroscopic closure of the rotator interval with 2 superior-to-inferior stitches reduced intracapsular volume by 45%. Even though open capsular shifts use different surgical techniques, similar technique volume reduction studies have reported reductions between 34% and 54% with open shifts.^27,30 It is unknown if the stability resulting from decreased GHV is primarily from increasing intra-articular pressures or from restricting ROM, or from a combination of both. In shoulders with multidirectional instability, the joint volume may be increased, the joint capsule may be enlarged, or the glenohumeral ligaments may be lax and thin.^4,6,32,33 Yamamoto and colleagues¹⁹ stated that intra-articular pressure is determined by 3 factors: load, joint volume, and material properties of the capsule. Load is a constant; joint volume and material properties can be changed.¹⁹ In our study, material properties were controlled by using a majority of matched specimens. Regardless of the stabilizing mechanism, our study results demonstrated that arthroscopic rotator interval closure may be a powerful tool in reducing shoulder volume, a consistent principle of surgical techniques used in reestablishing shoulder stability.^19,20

When a single rotator interval closure stitch was used, volume reduction with a lateral stitch was superior to that with a medial stitch. This finding is logical, as anatomically the dimensions of the rotator interval are larger laterally as the CHL fans out to insert on the greater and lesser tuberosities.¹⁴ This finding has also been reported in open capsular shifts for multidirectional instability, with a lateral humeral shift having a larger volume reduction than a medial glenoid shift.²⁷ Miller and colleagues²⁷ used the image of a cone, with its larger opening facing the humerus and narrower side facing the glenoid, to illustrate this difference in open capsular shifts.

Our study also showed a larger volume reduction with 2 rotator interval closure stitches than with a single interval stitch. As ROM testing has not shown a difference between results with 1 and 2 sutures, we recommend a minimum of 2 sutures for arthroscopic rotator interval closure.¹⁵ If a single plication stitch is preferred, a lateral stitch (vs a medial stitch) can be used for a significantly larger reduction in shoulder volume. We think this is because of a larger amount of capsule being purchased with lateral closure (Figure 5). However, if a medial stitch is used, it is important to not place it too near the glenoid to avoid CHL tethering and subsequent excessive loss of external rotation.¹⁵

This study had several weaknesses. First, it was a cadaveric study, and use of specimens not known to have instability or specific rotator interval injury may make generalization to a clinical situation difficult. Second, although our power analysis called for 5 shoulders in each group, full-thickness rotator cuff tears rendered 2 shoulders unusable. This reduced our sample sizes and potentially decreased the power of the study, though the data demonstrated statistically significant differences. Third, we did not compare the effects of an open medial-to-lateral imbrication of the rotator interval on intracapsular volume with the effects of our arthroscopic method. We also did not assess our specimens’ ROM, effects of interval closure stitches on shoulder stability, or glenohumeral contact surface pressures, as these factors have already been studied.^13-19 Instead, we focused on the effects of rotator interval closure on intracapsular volume, which had not been quantified until now. The clinical significance of such a volume reduction is unknown, especially with respect to influence on ROM, but the degree of volume reduction was larger than with previously reported arthroscopic instability repairs and smaller than with open capsular shifts, demonstrating that it may be a powerful tool in restoring stability in an unstable shoulder.^26-30,34 Fourth, the role of isolated rotator interval closure is poorly defined, as only 1 clinical series of isolated rotator interval closure has been reported thus far.¹² It has been far more common for rotator interval closure to be used with Bankart repair or capsulorrhaphy.^1-3,7-9

In a cadaveric study by Provencher and colleagues,¹⁶ open rotator interval closure with medial-to-lateral imbrication of the interval altered shoulder kinematics differently from what occurred with arthroscopic closure of the MGHL to the SGHL, resulting in superior-to-inferior shift. Comparing the 2 methods may therefore be inappropriate. Currently we reserve rotator interval closure for infrequent cases of revision instability and cases in which glenoid bone loss is marginal (5%-15%) and there is a willingness to potentially sacrifice ROM to restore stability and avoid an open stabilization procedure. Continued investigation into the clinical role of rotator interval closure in shoulder stability is needed. We should identify the pathology in a patient with instability and use this technique as an adjuvant to other stabilization procedures. 

Conclusion

Arthroscopic rotator interval closure with 2 plication stitches is a powerful tool in reducing the intracapsular volume of the shoulder. If a single plication stitch is preferred, a lateral rotator interval closure stitch (vs a medial stitch) can be used for a larger reduction in shoulder volume.

Since Neer described the rotator interval in 1970, its closure, often used in conjunction with capsulorrhaphy, has become an important surgical technique in managing shoulder instability.^1-11 Numerous studies have sought to define the function of the rotator interval.^1-3,6-20 The etiology of lesions of the rotator interval has been debated, and there is evidence that such lesions may be in part congenital.²¹ Increased rotator interval depth and width, along with increased size of the distended inferior and posteroinferior joint capsule on magnetic resonance arthrography, have been reported in cases of multidirectional shoulder instability.²² However, confusion remains about the role of the rotator interval in shoulder instability and about the effect its closure has on shoulder function. No one knows the degree of volume reduction that results from closure of the rotator interval and whether medial and lateral sutures differ in the volume reduction achieved.

Cadaveric studies have shown that the rotator interval has an important role in shoulder motion.^{6,13-16,19,20,23} Harryman and colleagues¹³ found that sectioning the coracohumeral ligament (CHL) increased shoulder range of motion (ROM), and medial-to-lateral closure of the rotator interval restricted motion in all planes. Most notably, interval closure limited inferior translation in the adducted shoulder, posterior translation in the flexed adducted shoulder, and external rotation in the neutral position. Subsequent studies,^17,18 using rotator interval closure combined with thermal capsulorrhaphy, confirmed the results reported by Harryman and colleagues.¹³

More recent cadaveric studies using superior-to-inferior rotator interval closures have shown a decrease in anterior translation but not posterior translation.^14-16,19-21 A superior-to-inferior interval closure technique limited external rotation less than a medial-to-lateral closure did.^13-16,19-21 The majority of arthroscopically described rotator interval closures involve a superior-to-inferior technique and use 2 or 3 sutures.^1,3,9-11

Plausinis and colleagues¹⁵ examined the effects of an isolated medial, an isolated lateral, and a medial combined with a lateral closure of the rotator interval. They noted that all 3 methods limited anterior translation and motion by means of 6° flexion and 10° external rotation; however, there was no statistical difference between methods. They also found that occasionally the medial interval closure resulted in massive loss of external rotation. Earlier, Jost and colleagues¹⁴ noted that a medial rotator interval could cause this massive loss by tethering the CHL, resulting in a medial-to-lateral imbrication of the CHL.

Arthroscopic rotator interval closure has clinically demonstrated an additive effect on shoulder stability. The recurrence rate was lower for arthroscopic Bankart repair combined with arthroscopic rotator interval closure (8%) than for arthroscopic Bankart repair alone (13%).²⁴ In addition, time to recurrent dislocation was longer (42 vs 13 months) for the group that underwent the combination of Bankart repair and rotator interval closure. Regarding the concern about loss of motion after arthroscopic rotator interval closure, Chiang and colleagues²⁵ recently noted no significant loss of motion 5 years after arthroscopic Bankart repair with rotator interval closure.

What effect rotator interval closure has on intra-articular glenohumeral volume (GHV) remains unknown. Using a cadaveric model, Yamamoto and colleagues²⁰ showed that decreasing GHV can increase the responsiveness of the glenohumeral joint to the intra-articular pressure. Thus, reducing the volume can improve stability in vitro by increasing the magnitude of negative pressure stabilizing the glenohumeral joint.

We conducted a study to quantify the effects of arthroscopic rotator interval closure on capsular volume and to determine whether medial and lateral interval closures resulted in different degrees of volume reduction. Our hypothesis was that shoulder volume would be significantly reduced by closing the rotator interval.

Materials and Methods

Previous studies have not specifically evaluated GHV after rotator interval closure. Our power analysis was performed with data from a study by Karas and colleagues,²⁶ who evaluated GHV after capsular plication. To detect a capsular volume reduction of 20% per stitch, with a 2-sided 5% significance level and a power of 80%, we needed a sample size of 5 specimens per group.

After receiving institutional review board approval for this study, we obtained 10 cadaveric shoulders (5 matched pairs). Exclusion criteria included arthroscopic evaluation revealing a full-thickness rotator cuff tear or significant osteoarthritis. Two shoulders had full-thickness cuff tears, leaving 8 shoulders to be tested; 6 of these were matched pairs. The shoulders were from 1 man (matched pair) and 4 women (2 matched pairs). Age ranged from 38 to 70 years (mean, 59.6 years). Differences in material properties between the specimens were accounted for by using primarily matched pairs.

The 2 study groups consisted of 4 shoulders each. After specimens were thawed, the skin, subcutaneous tissues, and periscapular muscles were removed from the shoulder. Only the capsule, biceps, and rotator cuff remained. For measurement purposes, the shoulders were mounted in a vice clamp in a beach-chair orientation. We placed a total of 2 portals with fully threaded 8.25-mm cannulas (Arthrex, Naples, Florida). A standard posterior portal was placed in the soft spot. A low anterior portal was then placed just superior to the subscapularis tendon. For arthroscopic examination and instrumentation in a saline environment, the shoulders were rotated into the lateral decubitus position, with suspension in 30° abduction and 20° forward flexion, by a rope attached to a pin in the distal shaft of the humerus.

In both groups, medial and lateral stitches with No. 2 FiberWire (Arthrex) were used to close the interval. The medial interval closure stitch was placed more than 10 mm away from the glenoid to prevent unpredictable CHL tethering; the lateral closure stitch was placed 10 mm lateral to the medial stitch (Figure 1).¹⁴ All sutures were placed intra-articularly under direct arthroscopic visualization, similar to the methods described in the literature.^1,3,9-11 Sutures were passed through the superior glenohumeral ligament (SGHL) and through the upper subscapularis using a suture shuttle (SutureLasso; Arthrex) and Penetrator II Suture Retriever (Arthrex). The upper subscapularis was incorporated because of the unpredictable nature of the middle glenohumeral ligament (MGHL). Both rotator interval sutures were placed before tying either. In the medial group, the medial stitch was tied first, using alternating half-hitches, followed by the lateral stitch. In the lateral group, the lateral stitch was tied first, followed by the medial stitch. GHV was measured at baseline and after tying each stitch. Dr. Ponce instrumented all shoulders.

Modifying a beach-chair technique described by Miller and colleagues,²⁷ we used a viscous fatty-acid sulfate solution, liquid soap, to measure GHV.^27-29 A small slit in line with the fibers was made in the supraspinatus tendon just lateral to the musculotendinous junction. A 3-way stop-cock was placed into the joint though this defect. A 20-mL syringe with a 16-gauge needle was used to inject the soap. The needle was inserted into the rotator cuff interval, and the viscous solution was injected in 5-mL increments until there was active extravasation through the supraspinatus cannula (Figure 2). This technique, the “volcano method,” marked the maximum capacity of the joint. The joint was then copiously irrigated with normal saline and suctioned until all normal saline was evacuated. Dr. Rosenzweig took 2 measurements on each shoulder, and their mean was used for analysis.

The baseline measurement was taken with the 2 working cannulas in the shoulder joint. Measurements were obtained with cannulas to simulate normal clinical conditions. Subsequent measurements were done with the cannulas in place and inserted up to the same thread each time so as not to change the volume. The capsule and the rotator cuff were then dissected from the humerus so the size of the capsulolabral plication could be directly evaluated. Methylene blue was used to mark the capsular suture holes before removing the sutures. With use of a caliper, the size of the plication bite was measured (in millimeters).

Statistical Analysis

The primary outcome was percent reduction in GHV as a function of number of plications and size of plication. When only the first plication was tightened, the effect of position (medial or lateral) was also of interest. Percent volume reduction was calculated as (original – new) / original × 100. SAS 8.02 (SAS Institute, Cary, North Carolina) was used to fit a repeated random-intercept regression model for each outcome. This technique properly accounts for the paired nature of the specimens and the repeated measures (baseline plus 2 plications). Model fit was assessed by the method of difference in log likelihood.

Results

In the medial group, GHV was reduced by a mean of 24.2% with a single medial stitch; in the lateral group, GHV was reduced by a mean of 35.1% (Figure 3). The difference was significant (P < .02). In the medial group, when a second lateral stitch was used, GHV was reduced by another 18.7%; in the lateral group, when a medial stitch was added, GHV was reduced by another 11.4%. Final GHV for the medial and lateral groups was 42.9% and 46.5%, respectively. There was no statistical difference in final GHV, regardless of which stitch was placed first. When the 2 groups were combined, GHV was reduced by 44.9% with use of medial and lateral rotator interval closure stitches.

Mean amount of tissue purchased, or “bite size,” was 18 mm with a lateral suture and 15 mm with a medial suture (P < .05). In addition, an increase in bite size to GHV reduction was essentially linear, where an increase in bite size of 1 mm reduced GHV by about 1% (Figure 4).

Discussion

Although there have been numerous clinical series and biomechanical studies focused on isolated rotator interval closure (or its use as an adjunct) in shoulder stabilization, the precise function of the rotator interval remains poorly understood.^1-3,6-11,19 Consequently, the in vivo effects of interval closure are unknown.

Initial studies proposed that rotator interval closure limited inferior and posterior translation.³⁰ More recent studies have demonstrated that rotator interval closure confers little effect on posterior instability but increases anterior stability in cadaveric models.^15,16 Clinical series have provided evidence that rotator interval closure can increase anterior stability.^1,3,7,9,12 In a series of isolated rotator interval closures for multidirectional instability, Field and colleagues¹² found that preoperative anterior and inferior symptoms predominated over posterior symptoms. Isolated closure of the rotator interval resulted in 100% excellent results with no cases of recurrent instability. Moon and colleagues³¹ reported that arthroscopic rotator interval closure with or without inferior capsular plication in multidirectional instability and predominant symptomatic inferior instability has shown benefit by improving function and stability. Other clinical reports of rotator interval closure in conjunction with arthroscopic Bankart repair have suggested it has an additive effect on anterior shoulder stability without limiting motion.^24,25

In our study, arthroscopic closure of the rotator interval with 2 superior-to-inferior stitches reduced intracapsular volume by 45%. Even though open capsular shifts use different surgical techniques, similar technique volume reduction studies have reported reductions between 34% and 54% with open shifts.^27,30 It is unknown if the stability resulting from decreased GHV is primarily from increasing intra-articular pressures or from restricting ROM, or from a combination of both. In shoulders with multidirectional instability, the joint volume may be increased, the joint capsule may be enlarged, or the glenohumeral ligaments may be lax and thin.^4,6,32,33 Yamamoto and colleagues¹⁹ stated that intra-articular pressure is determined by 3 factors: load, joint volume, and material properties of the capsule. Load is a constant; joint volume and material properties can be changed.¹⁹ In our study, material properties were controlled by using a majority of matched specimens. Regardless of the stabilizing mechanism, our study results demonstrated that arthroscopic rotator interval closure may be a powerful tool in reducing shoulder volume, a consistent principle of surgical techniques used in reestablishing shoulder stability.^19,20

When a single rotator interval closure stitch was used, volume reduction with a lateral stitch was superior to that with a medial stitch. This finding is logical, as anatomically the dimensions of the rotator interval are larger laterally as the CHL fans out to insert on the greater and lesser tuberosities.¹⁴ This finding has also been reported in open capsular shifts for multidirectional instability, with a lateral humeral shift having a larger volume reduction than a medial glenoid shift.²⁷ Miller and colleagues²⁷ used the image of a cone, with its larger opening facing the humerus and narrower side facing the glenoid, to illustrate this difference in open capsular shifts.

Our study also showed a larger volume reduction with 2 rotator interval closure stitches than with a single interval stitch. As ROM testing has not shown a difference between results with 1 and 2 sutures, we recommend a minimum of 2 sutures for arthroscopic rotator interval closure.¹⁵ If a single plication stitch is preferred, a lateral stitch (vs a medial stitch) can be used for a significantly larger reduction in shoulder volume. We think this is because of a larger amount of capsule being purchased with lateral closure (Figure 5). However, if a medial stitch is used, it is important to not place it too near the glenoid to avoid CHL tethering and subsequent excessive loss of external rotation.¹⁵

This study had several weaknesses. First, it was a cadaveric study, and use of specimens not known to have instability or specific rotator interval injury may make generalization to a clinical situation difficult. Second, although our power analysis called for 5 shoulders in each group, full-thickness rotator cuff tears rendered 2 shoulders unusable. This reduced our sample sizes and potentially decreased the power of the study, though the data demonstrated statistically significant differences. Third, we did not compare the effects of an open medial-to-lateral imbrication of the rotator interval on intracapsular volume with the effects of our arthroscopic method. We also did not assess our specimens’ ROM, effects of interval closure stitches on shoulder stability, or glenohumeral contact surface pressures, as these factors have already been studied.^13-19 Instead, we focused on the effects of rotator interval closure on intracapsular volume, which had not been quantified until now. The clinical significance of such a volume reduction is unknown, especially with respect to influence on ROM, but the degree of volume reduction was larger than with previously reported arthroscopic instability repairs and smaller than with open capsular shifts, demonstrating that it may be a powerful tool in restoring stability in an unstable shoulder.^26-30,34 Fourth, the role of isolated rotator interval closure is poorly defined, as only 1 clinical series of isolated rotator interval closure has been reported thus far.¹² It has been far more common for rotator interval closure to be used with Bankart repair or capsulorrhaphy.^1-3,7-9

In a cadaveric study by Provencher and colleagues,¹⁶ open rotator interval closure with medial-to-lateral imbrication of the interval altered shoulder kinematics differently from what occurred with arthroscopic closure of the MGHL to the SGHL, resulting in superior-to-inferior shift. Comparing the 2 methods may therefore be inappropriate. Currently we reserve rotator interval closure for infrequent cases of revision instability and cases in which glenoid bone loss is marginal (5%-15%) and there is a willingness to potentially sacrifice ROM to restore stability and avoid an open stabilization procedure. Continued investigation into the clinical role of rotator interval closure in shoulder stability is needed. We should identify the pathology in a patient with instability and use this technique as an adjuvant to other stabilization procedures. 

Conclusion

Arthroscopic rotator interval closure with 2 plication stitches is a powerful tool in reducing the intracapsular volume of the shoulder. If a single plication stitch is preferred, a lateral rotator interval closure stitch (vs a medial stitch) can be used for a larger reduction in shoulder volume.

The term spontaneous osteonecrosis of the knee was first used by Ahlbäck¹ in 1968. This term, and the acronym SONK (sometimes SPONK²), has subsequently been used by other authors to refer to an apparent osteonecrosis of the knee, most commonly occurring within the medial femoral condyle. SONK typically occurs in older women who usually do not have the typical osteonecrosis risk factors, such as steroid use, sickle-cell anemia, and excessive alcohol intake. Furthermore, the radiologic appearance of SONK differs from the typical avascular necrosis findings seen with radiography and magnetic resonance imaging (MRI). In particular, on MRI, the abnormality of SONK does not have the typical serpiginous margin of bone infarction, or the double-line sign indicating both sclerosis and granulation tissue.³ SONK is normally seen as a line of signal intensity on T1- and T2-weighted sequences; this line is adjacent to or parallels the subchondral bone with an adjacent area of extensive edema.

There is dispute over the cause of SONK. Yamamoto and Bullough⁴ proposed the lesion is in part a subchondral insufficiency fracture and staged it into 4 parts. Histologic findings suggest at least some SONK lesions are subchondral insufficiency fractures.⁵ Brahme and colleagues⁶ were the first to describe SONK occurring after arthroscopy, and others have documented this finding. The condition has also been referred to as osteonecrosis in the postoperative knee.^7-13 An association of postoperative SONK with cartilage loss and meniscal tear has been proposed.^7-13

We reviewed the clinical, radiologic, and MRI findings in 11 patients with evidence of postarthroscopy SONK to try to identify any risk factors that might predispose them to poor outcomes. Our study population consisted of 11 patients (12 knees) with SONK; 6 of the knees had the lesion before knee arthroscopy, and the other 6 developed the lesion after arthroscopy. We also considered MRI findings in a group of 11 age- and sex-matched patients who underwent knee arthroscopy and did not have or develop SONK. We reviewed the preoperative MRI findings of both groups for meniscal tear, meniscal extrusion, and cartilage loss. We had 2 hypotheses. First, patients with preoperative MRI findings of SONK would have articular cartilage changes, posterior root degeneration, and meniscal extrusion similar to those of patients who developed SONK after arthroscopy. Second, an age- and sex-matched group of patients who underwent arthroscopy and did not develop SONK would be similar in articular cartilage changes, posterior root degeneration or tear, and meniscal extrusion.

Materials and Methods

With institutional review board approval and waived informed consent, we reviewed all imaging studies, particularly the radiographs and MRI studies, of 11 patients (12 knees) who either had SONK before arthroscopy or developed it after arthroscopy. In all these cases, arthroscopy was performed to alleviate mechanical symptoms associated with meniscal tear.

On subsequent review by a musculoskeletal radiologist, 6 patients with SONK had an identifiable lesion before surgery. All patients’ symptoms had not improved with an earlier trial of conservative management. All preoperative and postoperative radiologic and MRI findings were reviewed. The patient group was assembled by writing to all the orthopedic surgeons who performed arthroscopy at our institution and asking for SONK cases seen in their practices. All but 2 cases were performed by a surgeon who treated a predominantly older, less active population. Clinical notes were reviewed for outcomes, and the musculoskeletal radiologist reviewed all radiologic studies. The 4 men and 7 women in the SONK group (1 woman had bilateral knee lesions) ranged in age from 43 to 74 years (mean, 63.8 years), and the 4 men and 7 women in the control group were age-matched to 43 to 75 years (mean, 63.6 years). The controls were chosen from a pool of patients who underwent knee arthroscopy at our institution.

MRI was performed using General Electric 1-T, 1.5-T, or 3-T magnets (GE Healthcare, Milwaukee, Wisconsin) or using Philips 1.5-T or open 0.7-T magnets (Philips Healthcare, Andover, Massachusetts). Imaging included sagittal and coronal proton density–weighted sequences and coronal and axial fat-suppressed T2-weighted sequences. SONK was diagnosed when a low signal line adjacent to the subchondral bone plate on the femoral or tibial condyles was present with an adjacent area of bone marrow edema in the respective condyle or when there was depression of the subchondral bone plate with adjacent edema. The MRI studies were reviewed for lesion location, and medial meniscus and lateral meniscus were reviewed for tear. Type of meniscal tear (horizontal cleavage, radial, complex degenerative) was documented, as was meniscal extrusion. The meniscus was regarded as extruded if the body extended more than 3 mm from the joint margin. Cartilage in the medial and lateral compartment was reviewed according to a modified Noyes scale listing 0 as normal, 1 as internal changes only, 2A as 1% to 49% cartilage loss, 2B as 50% to 90% loss of articular cartilage, 3A as 100% articular cartilage loss with subchondral bone plate intact, and 3B as 100% articular cartilage loss with ulcerated subchondral bone plate.¹⁴ Osteoarthritic severity was similarly classified using the Kellgren-Lawrence scale,¹⁵ where grade 0 is normal; grade 1 is unlikely to have narrowing of the joint space but potentially has osteophytic lipping; grade 2 has both definite narrowing of the joint space and osteophytes; grade 3 has narrowing of the joint space and multiple osteophytes, some sclerosis, and possible deformity of bone contour; and grade 4 has marked narrowing of the joint space, large osteophytes, severe sclerosis, and definite deformity of bone contour. Follow-up clinical notes and radiologic studies were reviewed in the assessment of patient outcomes.

All statistical analyses were performed with SAS 9.2 software (SAS Institute, Cary, North Carolina). Age data were evaluated with the Shapiro-Wilk test and graphical displays and were found to violate normality assumptions, so they are presented as medians and ranges; other variables are presented as count and column percentages. The Wilcoxon rank sum test was used to compare the 2 groups’ age distributions. Fisher exact tests were used to compare proportions between the 2 groups for the other variables. Statistical significance was set at P < .05.

Results

Table 1 lists the demographics and imaging characteristics of the 11 patients—6 had SONK before arthroscopy and 6 developed it after arthroscopy. Comparison of the 11 patients with SONK and the 11 controls is summarized with P values in Table 2. Representative cases that either presented before surgery or developed after surgery are shown in Figures 1 to 4. There were 6 prearthroscopy lesions and 6 postarthroscopy lesions—all 12 in the medial femoral condyle. Eleven of the 12 knees had a medial meniscal tear, and 1 knee had both medial and lateral meniscal tears. In 8 of the 12 knees, the lateral meniscus was normal; in 2 knees, it had mild degeneration; and, in 1 knee, it had a complex tear. Assessment of hyaline cartilage revealed medial cartilage loss ranging from 2A to 3B (median, 2B) in the patients with SONK, and lateral cartilage loss ranging from 0 to 2A (median, 0). At surgery, all knees had a partial medial meniscectomy, and 6 had a partial lateral meniscectomy. Ten of the 12 knees had chondroplasty, 9 patellar and 5 of the medial femoral condyle. Only 4 of the 11 patients with follow-up of more than 1 year went on to joint replacement. Six of the 12 had follow-up of more than 2 years. Of the 6 patients without an identifiable SONK lesion on MRI before arthroscopy, 4 had mild to moderate knee pain 0.5, 2.4, 3.5, and 4 years after surgery. For the other 2 patients, knee replacement was performed 1.5 and 1.8 years after surgery. Of the 6 patients with prearthroscopy SONK, 4 had mild to moderate knee pain 1.5, 3.7, 6.5, and 6.8 years after surgery; the other 2 had knee replacement 0.5 and 1.8 years after surgery. Articular cartilage degeneration and meniscal extrusion were similar (Table 1). In the control group, there was only 1 knee replacement, at 3 years, and the other 11 were functioning 2.6 to 5 years later. The longer follow-up resulted from selection of appropriate controls from the same year. Of the 6 SONK lesions found on preoperative MRI, 3 were read by the interpreting radiologist before surgery as possible SONK lesions, 2 were read as insufficiency fractures, and 1 was read as a possible insufficiency fracture.

Discussion

SONK is well described as a complication of arthroscopic knee surgery. However, this condition more commonly appears spontaneously in a population that has not had surgery. It has become clear that the term SONK may be misleading.¹⁶ In a recent series of postoperative subchondral fractures reported by MacDessi and colleagues,⁵ the average age of patients included in their study was 64 years. Pathologic analysis revealed subchondral fracture with callus formation in all cases. Only 2 knees had evidence of osteonecrosis, which appeared to be secondary to the fracture. Based on these findings, the authors concluded that “further investigation into the etiology of this condition is warranted.” A prominent association with medial meniscal tear has been noted, with the medial femoral condyle predominantly affected. As already mentioned, SONK differs from classical avascular necrosis on several points, including lack of the typical avascular osteonecrosis risk factors and absence of the serpiginous margin and double-line sign seen with typical bone infarction. In addition, the SONK lesions seen on radiographs and MRIs of the knee typically are in the medial femoral condyle and are very different from the typical area of infarction seen in patients with known risk factors for secondary osteonecrosis.

The cause of SONK is not known. Of more importance from a medicolegal standpoint is that these lesions are not necessarily related to arthroscopy.¹⁷ Interestingly, Pape and colleagues¹⁷ noted that some of the lesions they studied may have been present before surgery, which is what we found in 6 (50%) of the SONK knees in our study. Our data thus support the proposition that some SONK lesions are present before arthroscopy, and some cases of so-called postarthroscopy SONK may in fact have been progressing before surgery.

Our data also reinforce the importance of radiologist–orthopedic surgeon communication regarding the presence of SONK. We emphasize the importance of communicating the MRI findings clearly, whether the lesion is called SONK, SPONK, or insufficiency fracture. The orthopedic surgeons in our series may have been unaware of the presence of these lesions before arthroscopic meniscectomy, given the wide variety of terms being used in radiologic reports.

The natural history of spontaneous osteonecrosis of the medial tibial plateau has also been studied.¹⁸ There were 3 outcome patterns—acute extensive collapse of the medial tibial plateau, rapid progression to varying degrees of osteoarthritis, and complete resolution. It has been shown that resolution of SONK can occur in the early stages of the disease, within several months, but often the changes progress to bone destruction and articular cartilage collapse.¹⁹

In our series of patients, there was a female predominance, and mean age was 64 years. We investigated cartilage loss, meniscal tear, and meniscal extrusion to see if we could predict outcomes in patients who had the lesion before arthroscopy and if we could predict who might be at risk for developing the lesion after arthroscopy. Type of surgical procedure was also reviewed. For the sake of simplicity, we divided the follow-up patients into 2 groups: those managed with conservative treatment, which we deemed a reasonable outcome, and those who subsequently required knee joint replacement, which we deemed a poor outcome. As seen from our representative cases, both groups had patients with cartilage loss, meniscal tear, and meniscal extrusion to varying degrees. There were no risk factors pointing to a reasonable or poor outcome. In the group of patients with prearthroscopy lesions, we found the same problem. We were unable to identify a risk factor that might suggest a poor rather than a reasonable outcome. We must also emphasize that, in our review of patient charts, we could find no other causes for osteonecrosis. In particular, arthroscopic causes of acute chondral loss (eg, thermal wash, laser, bupivacaine pain pumps, epinephrine in irrigant) were not identified.

This study consisted of a series of cases managed at our institution over the past 8 years. Our data and this study had several limitations:

We may have been unable to identify other SONK cases that belonged in the group from our institution. In addition, we had only 11 patients for comparison with patients without SONK. Likewise, there were only 6 knees each in the prearthroscopy and postarthroscopy SONK groups. We also used images obtained from 1-T, 1.5-T, and 3-T closed MRI devices and one 0.7-T open device. These were, however, at the same institution.

Timing of our imaging was not uniform. In particular, in 3 of the patients who developed SONK after arthroscopy, preoperative MRI studies were performed quite some time before surgery. However, in these patients, more recent preoperative radiographs did not show any evidence of lesions. It can also be seen that postarthroscopy follow-up of patients varied. It is possible that, on longer follow-up, some of the cases we classified as having a reasonable outcome may have gone on to require total knee arthroplasty. One could argue that, in the patient who developed SONK within 1 year after surgery (Figure 4), the lesion was not related to the surgery. However, this patient’s radiographs 3 months after surgery did not show the SONK lesion but clearly showed prominent medial joint space narrowing—a new finding.

Only 1 musculoskeletal radiologist evaluated the radiographs, MRIs, and tomosynthesis (similar to computed tomography) studies for this investigation.

This lesion is not common, thus giving us a small group to analyze.

Despite our data limitations and the retrospective nature of this study, we compiled a reasonably representative sample of surgical SONK patients that matches other samples reported in the literature. Unfortunately, we could not identify any risk factors pointing to the likelihood of developing SONK or any risk factors pointing to either a reasonable or a poor prognosis in these patients. The etiology of the lesion remains an enigma. Our finding 6 cases of prearthroscopy lesions that did not necessarily result in a poor outcome, combined with our inability to identify any risk factors for SONK, points to the lack of a causal relationship with arthroscopy.

The term spontaneous osteonecrosis of the knee was first used by Ahlbäck¹ in 1968. This term, and the acronym SONK (sometimes SPONK²), has subsequently been used by other authors to refer to an apparent osteonecrosis of the knee, most commonly occurring within the medial femoral condyle. SONK typically occurs in older women who usually do not have the typical osteonecrosis risk factors, such as steroid use, sickle-cell anemia, and excessive alcohol intake. Furthermore, the radiologic appearance of SONK differs from the typical avascular necrosis findings seen with radiography and magnetic resonance imaging (MRI). In particular, on MRI, the abnormality of SONK does not have the typical serpiginous margin of bone infarction, or the double-line sign indicating both sclerosis and granulation tissue.³ SONK is normally seen as a line of signal intensity on T1- and T2-weighted sequences; this line is adjacent to or parallels the subchondral bone with an adjacent area of extensive edema.

There is dispute over the cause of SONK. Yamamoto and Bullough⁴ proposed the lesion is in part a subchondral insufficiency fracture and staged it into 4 parts. Histologic findings suggest at least some SONK lesions are subchondral insufficiency fractures.⁵ Brahme and colleagues⁶ were the first to describe SONK occurring after arthroscopy, and others have documented this finding. The condition has also been referred to as osteonecrosis in the postoperative knee.^7-13 An association of postoperative SONK with cartilage loss and meniscal tear has been proposed.^7-13

We reviewed the clinical, radiologic, and MRI findings in 11 patients with evidence of postarthroscopy SONK to try to identify any risk factors that might predispose them to poor outcomes. Our study population consisted of 11 patients (12 knees) with SONK; 6 of the knees had the lesion before knee arthroscopy, and the other 6 developed the lesion after arthroscopy. We also considered MRI findings in a group of 11 age- and sex-matched patients who underwent knee arthroscopy and did not have or develop SONK. We reviewed the preoperative MRI findings of both groups for meniscal tear, meniscal extrusion, and cartilage loss. We had 2 hypotheses. First, patients with preoperative MRI findings of SONK would have articular cartilage changes, posterior root degeneration, and meniscal extrusion similar to those of patients who developed SONK after arthroscopy. Second, an age- and sex-matched group of patients who underwent arthroscopy and did not develop SONK would be similar in articular cartilage changes, posterior root degeneration or tear, and meniscal extrusion.

Materials and Methods

With institutional review board approval and waived informed consent, we reviewed all imaging studies, particularly the radiographs and MRI studies, of 11 patients (12 knees) who either had SONK before arthroscopy or developed it after arthroscopy. In all these cases, arthroscopy was performed to alleviate mechanical symptoms associated with meniscal tear.

On subsequent review by a musculoskeletal radiologist, 6 patients with SONK had an identifiable lesion before surgery. All patients’ symptoms had not improved with an earlier trial of conservative management. All preoperative and postoperative radiologic and MRI findings were reviewed. The patient group was assembled by writing to all the orthopedic surgeons who performed arthroscopy at our institution and asking for SONK cases seen in their practices. All but 2 cases were performed by a surgeon who treated a predominantly older, less active population. Clinical notes were reviewed for outcomes, and the musculoskeletal radiologist reviewed all radiologic studies. The 4 men and 7 women in the SONK group (1 woman had bilateral knee lesions) ranged in age from 43 to 74 years (mean, 63.8 years), and the 4 men and 7 women in the control group were age-matched to 43 to 75 years (mean, 63.6 years). The controls were chosen from a pool of patients who underwent knee arthroscopy at our institution.

MRI was performed using General Electric 1-T, 1.5-T, or 3-T magnets (GE Healthcare, Milwaukee, Wisconsin) or using Philips 1.5-T or open 0.7-T magnets (Philips Healthcare, Andover, Massachusetts). Imaging included sagittal and coronal proton density–weighted sequences and coronal and axial fat-suppressed T2-weighted sequences. SONK was diagnosed when a low signal line adjacent to the subchondral bone plate on the femoral or tibial condyles was present with an adjacent area of bone marrow edema in the respective condyle or when there was depression of the subchondral bone plate with adjacent edema. The MRI studies were reviewed for lesion location, and medial meniscus and lateral meniscus were reviewed for tear. Type of meniscal tear (horizontal cleavage, radial, complex degenerative) was documented, as was meniscal extrusion. The meniscus was regarded as extruded if the body extended more than 3 mm from the joint margin. Cartilage in the medial and lateral compartment was reviewed according to a modified Noyes scale listing 0 as normal, 1 as internal changes only, 2A as 1% to 49% cartilage loss, 2B as 50% to 90% loss of articular cartilage, 3A as 100% articular cartilage loss with subchondral bone plate intact, and 3B as 100% articular cartilage loss with ulcerated subchondral bone plate.¹⁴ Osteoarthritic severity was similarly classified using the Kellgren-Lawrence scale,¹⁵ where grade 0 is normal; grade 1 is unlikely to have narrowing of the joint space but potentially has osteophytic lipping; grade 2 has both definite narrowing of the joint space and osteophytes; grade 3 has narrowing of the joint space and multiple osteophytes, some sclerosis, and possible deformity of bone contour; and grade 4 has marked narrowing of the joint space, large osteophytes, severe sclerosis, and definite deformity of bone contour. Follow-up clinical notes and radiologic studies were reviewed in the assessment of patient outcomes.

All statistical analyses were performed with SAS 9.2 software (SAS Institute, Cary, North Carolina). Age data were evaluated with the Shapiro-Wilk test and graphical displays and were found to violate normality assumptions, so they are presented as medians and ranges; other variables are presented as count and column percentages. The Wilcoxon rank sum test was used to compare the 2 groups’ age distributions. Fisher exact tests were used to compare proportions between the 2 groups for the other variables. Statistical significance was set at P < .05.

Results

Table 1 lists the demographics and imaging characteristics of the 11 patients—6 had SONK before arthroscopy and 6 developed it after arthroscopy. Comparison of the 11 patients with SONK and the 11 controls is summarized with P values in Table 2. Representative cases that either presented before surgery or developed after surgery are shown in Figures 1 to 4. There were 6 prearthroscopy lesions and 6 postarthroscopy lesions—all 12 in the medial femoral condyle. Eleven of the 12 knees had a medial meniscal tear, and 1 knee had both medial and lateral meniscal tears. In 8 of the 12 knees, the lateral meniscus was normal; in 2 knees, it had mild degeneration; and, in 1 knee, it had a complex tear. Assessment of hyaline cartilage revealed medial cartilage loss ranging from 2A to 3B (median, 2B) in the patients with SONK, and lateral cartilage loss ranging from 0 to 2A (median, 0). At surgery, all knees had a partial medial meniscectomy, and 6 had a partial lateral meniscectomy. Ten of the 12 knees had chondroplasty, 9 patellar and 5 of the medial femoral condyle. Only 4 of the 11 patients with follow-up of more than 1 year went on to joint replacement. Six of the 12 had follow-up of more than 2 years. Of the 6 patients without an identifiable SONK lesion on MRI before arthroscopy, 4 had mild to moderate knee pain 0.5, 2.4, 3.5, and 4 years after surgery. For the other 2 patients, knee replacement was performed 1.5 and 1.8 years after surgery. Of the 6 patients with prearthroscopy SONK, 4 had mild to moderate knee pain 1.5, 3.7, 6.5, and 6.8 years after surgery; the other 2 had knee replacement 0.5 and 1.8 years after surgery. Articular cartilage degeneration and meniscal extrusion were similar (Table 1). In the control group, there was only 1 knee replacement, at 3 years, and the other 11 were functioning 2.6 to 5 years later. The longer follow-up resulted from selection of appropriate controls from the same year. Of the 6 SONK lesions found on preoperative MRI, 3 were read by the interpreting radiologist before surgery as possible SONK lesions, 2 were read as insufficiency fractures, and 1 was read as a possible insufficiency fracture.

Discussion

SONK is well described as a complication of arthroscopic knee surgery. However, this condition more commonly appears spontaneously in a population that has not had surgery. It has become clear that the term SONK may be misleading.¹⁶ In a recent series of postoperative subchondral fractures reported by MacDessi and colleagues,⁵ the average age of patients included in their study was 64 years. Pathologic analysis revealed subchondral fracture with callus formation in all cases. Only 2 knees had evidence of osteonecrosis, which appeared to be secondary to the fracture. Based on these findings, the authors concluded that “further investigation into the etiology of this condition is warranted.” A prominent association with medial meniscal tear has been noted, with the medial femoral condyle predominantly affected. As already mentioned, SONK differs from classical avascular necrosis on several points, including lack of the typical avascular osteonecrosis risk factors and absence of the serpiginous margin and double-line sign seen with typical bone infarction. In addition, the SONK lesions seen on radiographs and MRIs of the knee typically are in the medial femoral condyle and are very different from the typical area of infarction seen in patients with known risk factors for secondary osteonecrosis.

The cause of SONK is not known. Of more importance from a medicolegal standpoint is that these lesions are not necessarily related to arthroscopy.¹⁷ Interestingly, Pape and colleagues¹⁷ noted that some of the lesions they studied may have been present before surgery, which is what we found in 6 (50%) of the SONK knees in our study. Our data thus support the proposition that some SONK lesions are present before arthroscopy, and some cases of so-called postarthroscopy SONK may in fact have been progressing before surgery.

Our data also reinforce the importance of radiologist–orthopedic surgeon communication regarding the presence of SONK. We emphasize the importance of communicating the MRI findings clearly, whether the lesion is called SONK, SPONK, or insufficiency fracture. The orthopedic surgeons in our series may have been unaware of the presence of these lesions before arthroscopic meniscectomy, given the wide variety of terms being used in radiologic reports.

The natural history of spontaneous osteonecrosis of the medial tibial plateau has also been studied.¹⁸ There were 3 outcome patterns—acute extensive collapse of the medial tibial plateau, rapid progression to varying degrees of osteoarthritis, and complete resolution. It has been shown that resolution of SONK can occur in the early stages of the disease, within several months, but often the changes progress to bone destruction and articular cartilage collapse.¹⁹

In our series of patients, there was a female predominance, and mean age was 64 years. We investigated cartilage loss, meniscal tear, and meniscal extrusion to see if we could predict outcomes in patients who had the lesion before arthroscopy and if we could predict who might be at risk for developing the lesion after arthroscopy. Type of surgical procedure was also reviewed. For the sake of simplicity, we divided the follow-up patients into 2 groups: those managed with conservative treatment, which we deemed a reasonable outcome, and those who subsequently required knee joint replacement, which we deemed a poor outcome. As seen from our representative cases, both groups had patients with cartilage loss, meniscal tear, and meniscal extrusion to varying degrees. There were no risk factors pointing to a reasonable or poor outcome. In the group of patients with prearthroscopy lesions, we found the same problem. We were unable to identify a risk factor that might suggest a poor rather than a reasonable outcome. We must also emphasize that, in our review of patient charts, we could find no other causes for osteonecrosis. In particular, arthroscopic causes of acute chondral loss (eg, thermal wash, laser, bupivacaine pain pumps, epinephrine in irrigant) were not identified.

This study consisted of a series of cases managed at our institution over the past 8 years. Our data and this study had several limitations:

We may have been unable to identify other SONK cases that belonged in the group from our institution. In addition, we had only 11 patients for comparison with patients without SONK. Likewise, there were only 6 knees each in the prearthroscopy and postarthroscopy SONK groups. We also used images obtained from 1-T, 1.5-T, and 3-T closed MRI devices and one 0.7-T open device. These were, however, at the same institution.

Timing of our imaging was not uniform. In particular, in 3 of the patients who developed SONK after arthroscopy, preoperative MRI studies were performed quite some time before surgery. However, in these patients, more recent preoperative radiographs did not show any evidence of lesions. It can also be seen that postarthroscopy follow-up of patients varied. It is possible that, on longer follow-up, some of the cases we classified as having a reasonable outcome may have gone on to require total knee arthroplasty. One could argue that, in the patient who developed SONK within 1 year after surgery (Figure 4), the lesion was not related to the surgery. However, this patient’s radiographs 3 months after surgery did not show the SONK lesion but clearly showed prominent medial joint space narrowing—a new finding.

Only 1 musculoskeletal radiologist evaluated the radiographs, MRIs, and tomosynthesis (similar to computed tomography) studies for this investigation.

This lesion is not common, thus giving us a small group to analyze.

Despite our data limitations and the retrospective nature of this study, we compiled a reasonably representative sample of surgical SONK patients that matches other samples reported in the literature. Unfortunately, we could not identify any risk factors pointing to the likelihood of developing SONK or any risk factors pointing to either a reasonable or a poor prognosis in these patients. The etiology of the lesion remains an enigma. Our finding 6 cases of prearthroscopy lesions that did not necessarily result in a poor outcome, combined with our inability to identify any risk factors for SONK, points to the lack of a causal relationship with arthroscopy.

The term spontaneous osteonecrosis of the knee was first used by Ahlbäck¹ in 1968. This term, and the acronym SONK (sometimes SPONK²), has subsequently been used by other authors to refer to an apparent osteonecrosis of the knee, most commonly occurring within the medial femoral condyle. SONK typically occurs in older women who usually do not have the typical osteonecrosis risk factors, such as steroid use, sickle-cell anemia, and excessive alcohol intake. Furthermore, the radiologic appearance of SONK differs from the typical avascular necrosis findings seen with radiography and magnetic resonance imaging (MRI). In particular, on MRI, the abnormality of SONK does not have the typical serpiginous margin of bone infarction, or the double-line sign indicating both sclerosis and granulation tissue.³ SONK is normally seen as a line of signal intensity on T1- and T2-weighted sequences; this line is adjacent to or parallels the subchondral bone with an adjacent area of extensive edema.

There is dispute over the cause of SONK. Yamamoto and Bullough⁴ proposed the lesion is in part a subchondral insufficiency fracture and staged it into 4 parts. Histologic findings suggest at least some SONK lesions are subchondral insufficiency fractures.⁵ Brahme and colleagues⁶ were the first to describe SONK occurring after arthroscopy, and others have documented this finding. The condition has also been referred to as osteonecrosis in the postoperative knee.^7-13 An association of postoperative SONK with cartilage loss and meniscal tear has been proposed.^7-13

We reviewed the clinical, radiologic, and MRI findings in 11 patients with evidence of postarthroscopy SONK to try to identify any risk factors that might predispose them to poor outcomes. Our study population consisted of 11 patients (12 knees) with SONK; 6 of the knees had the lesion before knee arthroscopy, and the other 6 developed the lesion after arthroscopy. We also considered MRI findings in a group of 11 age- and sex-matched patients who underwent knee arthroscopy and did not have or develop SONK. We reviewed the preoperative MRI findings of both groups for meniscal tear, meniscal extrusion, and cartilage loss. We had 2 hypotheses. First, patients with preoperative MRI findings of SONK would have articular cartilage changes, posterior root degeneration, and meniscal extrusion similar to those of patients who developed SONK after arthroscopy. Second, an age- and sex-matched group of patients who underwent arthroscopy and did not develop SONK would be similar in articular cartilage changes, posterior root degeneration or tear, and meniscal extrusion.

Materials and Methods

With institutional review board approval and waived informed consent, we reviewed all imaging studies, particularly the radiographs and MRI studies, of 11 patients (12 knees) who either had SONK before arthroscopy or developed it after arthroscopy. In all these cases, arthroscopy was performed to alleviate mechanical symptoms associated with meniscal tear.

On subsequent review by a musculoskeletal radiologist, 6 patients with SONK had an identifiable lesion before surgery. All patients’ symptoms had not improved with an earlier trial of conservative management. All preoperative and postoperative radiologic and MRI findings were reviewed. The patient group was assembled by writing to all the orthopedic surgeons who performed arthroscopy at our institution and asking for SONK cases seen in their practices. All but 2 cases were performed by a surgeon who treated a predominantly older, less active population. Clinical notes were reviewed for outcomes, and the musculoskeletal radiologist reviewed all radiologic studies. The 4 men and 7 women in the SONK group (1 woman had bilateral knee lesions) ranged in age from 43 to 74 years (mean, 63.8 years), and the 4 men and 7 women in the control group were age-matched to 43 to 75 years (mean, 63.6 years). The controls were chosen from a pool of patients who underwent knee arthroscopy at our institution.

MRI was performed using General Electric 1-T, 1.5-T, or 3-T magnets (GE Healthcare, Milwaukee, Wisconsin) or using Philips 1.5-T or open 0.7-T magnets (Philips Healthcare, Andover, Massachusetts). Imaging included sagittal and coronal proton density–weighted sequences and coronal and axial fat-suppressed T2-weighted sequences. SONK was diagnosed when a low signal line adjacent to the subchondral bone plate on the femoral or tibial condyles was present with an adjacent area of bone marrow edema in the respective condyle or when there was depression of the subchondral bone plate with adjacent edema. The MRI studies were reviewed for lesion location, and medial meniscus and lateral meniscus were reviewed for tear. Type of meniscal tear (horizontal cleavage, radial, complex degenerative) was documented, as was meniscal extrusion. The meniscus was regarded as extruded if the body extended more than 3 mm from the joint margin. Cartilage in the medial and lateral compartment was reviewed according to a modified Noyes scale listing 0 as normal, 1 as internal changes only, 2A as 1% to 49% cartilage loss, 2B as 50% to 90% loss of articular cartilage, 3A as 100% articular cartilage loss with subchondral bone plate intact, and 3B as 100% articular cartilage loss with ulcerated subchondral bone plate.¹⁴ Osteoarthritic severity was similarly classified using the Kellgren-Lawrence scale,¹⁵ where grade 0 is normal; grade 1 is unlikely to have narrowing of the joint space but potentially has osteophytic lipping; grade 2 has both definite narrowing of the joint space and osteophytes; grade 3 has narrowing of the joint space and multiple osteophytes, some sclerosis, and possible deformity of bone contour; and grade 4 has marked narrowing of the joint space, large osteophytes, severe sclerosis, and definite deformity of bone contour. Follow-up clinical notes and radiologic studies were reviewed in the assessment of patient outcomes.

All statistical analyses were performed with SAS 9.2 software (SAS Institute, Cary, North Carolina). Age data were evaluated with the Shapiro-Wilk test and graphical displays and were found to violate normality assumptions, so they are presented as medians and ranges; other variables are presented as count and column percentages. The Wilcoxon rank sum test was used to compare the 2 groups’ age distributions. Fisher exact tests were used to compare proportions between the 2 groups for the other variables. Statistical significance was set at P < .05.

Results

Table 1 lists the demographics and imaging characteristics of the 11 patients—6 had SONK before arthroscopy and 6 developed it after arthroscopy. Comparison of the 11 patients with SONK and the 11 controls is summarized with P values in Table 2. Representative cases that either presented before surgery or developed after surgery are shown in Figures 1 to 4. There were 6 prearthroscopy lesions and 6 postarthroscopy lesions—all 12 in the medial femoral condyle. Eleven of the 12 knees had a medial meniscal tear, and 1 knee had both medial and lateral meniscal tears. In 8 of the 12 knees, the lateral meniscus was normal; in 2 knees, it had mild degeneration; and, in 1 knee, it had a complex tear. Assessment of hyaline cartilage revealed medial cartilage loss ranging from 2A to 3B (median, 2B) in the patients with SONK, and lateral cartilage loss ranging from 0 to 2A (median, 0). At surgery, all knees had a partial medial meniscectomy, and 6 had a partial lateral meniscectomy. Ten of the 12 knees had chondroplasty, 9 patellar and 5 of the medial femoral condyle. Only 4 of the 11 patients with follow-up of more than 1 year went on to joint replacement. Six of the 12 had follow-up of more than 2 years. Of the 6 patients without an identifiable SONK lesion on MRI before arthroscopy, 4 had mild to moderate knee pain 0.5, 2.4, 3.5, and 4 years after surgery. For the other 2 patients, knee replacement was performed 1.5 and 1.8 years after surgery. Of the 6 patients with prearthroscopy SONK, 4 had mild to moderate knee pain 1.5, 3.7, 6.5, and 6.8 years after surgery; the other 2 had knee replacement 0.5 and 1.8 years after surgery. Articular cartilage degeneration and meniscal extrusion were similar (Table 1). In the control group, there was only 1 knee replacement, at 3 years, and the other 11 were functioning 2.6 to 5 years later. The longer follow-up resulted from selection of appropriate controls from the same year. Of the 6 SONK lesions found on preoperative MRI, 3 were read by the interpreting radiologist before surgery as possible SONK lesions, 2 were read as insufficiency fractures, and 1 was read as a possible insufficiency fracture.

Discussion

SONK is well described as a complication of arthroscopic knee surgery. However, this condition more commonly appears spontaneously in a population that has not had surgery. It has become clear that the term SONK may be misleading.¹⁶ In a recent series of postoperative subchondral fractures reported by MacDessi and colleagues,⁵ the average age of patients included in their study was 64 years. Pathologic analysis revealed subchondral fracture with callus formation in all cases. Only 2 knees had evidence of osteonecrosis, which appeared to be secondary to the fracture. Based on these findings, the authors concluded that “further investigation into the etiology of this condition is warranted.” A prominent association with medial meniscal tear has been noted, with the medial femoral condyle predominantly affected. As already mentioned, SONK differs from classical avascular necrosis on several points, including lack of the typical avascular osteonecrosis risk factors and absence of the serpiginous margin and double-line sign seen with typical bone infarction. In addition, the SONK lesions seen on radiographs and MRIs of the knee typically are in the medial femoral condyle and are very different from the typical area of infarction seen in patients with known risk factors for secondary osteonecrosis.

The cause of SONK is not known. Of more importance from a medicolegal standpoint is that these lesions are not necessarily related to arthroscopy.¹⁷ Interestingly, Pape and colleagues¹⁷ noted that some of the lesions they studied may have been present before surgery, which is what we found in 6 (50%) of the SONK knees in our study. Our data thus support the proposition that some SONK lesions are present before arthroscopy, and some cases of so-called postarthroscopy SONK may in fact have been progressing before surgery.

Our data also reinforce the importance of radiologist–orthopedic surgeon communication regarding the presence of SONK. We emphasize the importance of communicating the MRI findings clearly, whether the lesion is called SONK, SPONK, or insufficiency fracture. The orthopedic surgeons in our series may have been unaware of the presence of these lesions before arthroscopic meniscectomy, given the wide variety of terms being used in radiologic reports.

The natural history of spontaneous osteonecrosis of the medial tibial plateau has also been studied.¹⁸ There were 3 outcome patterns—acute extensive collapse of the medial tibial plateau, rapid progression to varying degrees of osteoarthritis, and complete resolution. It has been shown that resolution of SONK can occur in the early stages of the disease, within several months, but often the changes progress to bone destruction and articular cartilage collapse.¹⁹

In our series of patients, there was a female predominance, and mean age was 64 years. We investigated cartilage loss, meniscal tear, and meniscal extrusion to see if we could predict outcomes in patients who had the lesion before arthroscopy and if we could predict who might be at risk for developing the lesion after arthroscopy. Type of surgical procedure was also reviewed. For the sake of simplicity, we divided the follow-up patients into 2 groups: those managed with conservative treatment, which we deemed a reasonable outcome, and those who subsequently required knee joint replacement, which we deemed a poor outcome. As seen from our representative cases, both groups had patients with cartilage loss, meniscal tear, and meniscal extrusion to varying degrees. There were no risk factors pointing to a reasonable or poor outcome. In the group of patients with prearthroscopy lesions, we found the same problem. We were unable to identify a risk factor that might suggest a poor rather than a reasonable outcome. We must also emphasize that, in our review of patient charts, we could find no other causes for osteonecrosis. In particular, arthroscopic causes of acute chondral loss (eg, thermal wash, laser, bupivacaine pain pumps, epinephrine in irrigant) were not identified.

This study consisted of a series of cases managed at our institution over the past 8 years. Our data and this study had several limitations:

We may have been unable to identify other SONK cases that belonged in the group from our institution. In addition, we had only 11 patients for comparison with patients without SONK. Likewise, there were only 6 knees each in the prearthroscopy and postarthroscopy SONK groups. We also used images obtained from 1-T, 1.5-T, and 3-T closed MRI devices and one 0.7-T open device. These were, however, at the same institution.

Timing of our imaging was not uniform. In particular, in 3 of the patients who developed SONK after arthroscopy, preoperative MRI studies were performed quite some time before surgery. However, in these patients, more recent preoperative radiographs did not show any evidence of lesions. It can also be seen that postarthroscopy follow-up of patients varied. It is possible that, on longer follow-up, some of the cases we classified as having a reasonable outcome may have gone on to require total knee arthroplasty. One could argue that, in the patient who developed SONK within 1 year after surgery (Figure 4), the lesion was not related to the surgery. However, this patient’s radiographs 3 months after surgery did not show the SONK lesion but clearly showed prominent medial joint space narrowing—a new finding.

Only 1 musculoskeletal radiologist evaluated the radiographs, MRIs, and tomosynthesis (similar to computed tomography) studies for this investigation.

This lesion is not common, thus giving us a small group to analyze.

Despite our data limitations and the retrospective nature of this study, we compiled a reasonably representative sample of surgical SONK patients that matches other samples reported in the literature. Unfortunately, we could not identify any risk factors pointing to the likelihood of developing SONK or any risk factors pointing to either a reasonable or a poor prognosis in these patients. The etiology of the lesion remains an enigma. Our finding 6 cases of prearthroscopy lesions that did not necessarily result in a poor outcome, combined with our inability to identify any risk factors for SONK, points to the lack of a causal relationship with arthroscopy.