Francesca Pezzetta, MD

To the Editor: Buencamino and colleagues¹ reviewed the association between menopause and periodontal disease. However, they did not mention the role of vitamin D status in this setting.

Vitamin D status is usually divided into three categories based on serum 25-hydroxyvitamin D levels: “deficient” (≤ 15 ng/mL), “insufficient” (15.1–29.9 ng/mL), and “sufficient” (≥ 30 ng/mL). Serum 25-hydroxyvitamin D levels have been decreasing significantly for more than a decade, and as a result, a majority of the US population has a vitamin D insufficiency.

In the third National Health and Nutrition Examination Survey (NHANES III), a large US population survey, a low serum 25-hydroxyvitamin D concentration was independently associated with periodontal disease.² In particular, it was significantly associated with loss of alveolar attachment in persons older than 50 years of both sexes, independent of race or ethnicity; women in the highest 25-hydroxyvitamin D quintile had, on average, 0.26 mm (95% confidence interval 0.09–0.43 mm) less mean attachment loss than did women in the lowest quintile. Furthermore, in a randomized trial, supplementation with vitamin D (700 IU/day) plus calcium (500 mg/day) has been shown to significantly reduce tooth loss in older persons over a 3-year treatment period.³

Osteoporosis and periodontal disease share several risk factors, and it might be speculated that these pathologic conditions are biologically intertwined.⁴ The decreased bone mineral density of osteoporosis can lead to an altered trabecular pattern and more rapid alveolar bone resorption, thus predisposing to periodontal disease. On the other hand, periodontal infections can increase the systemic release of inflammatory cytokines, which accelerate systemic bone resorption. Indeed, vitamin D deficiency has been associated with a cytokine profile that favors greater inflammation (eg, higher levels of C-reactive protein and interleukin 6, and lower levels of interleukin 10), and vitamin D supplementation decreases circulating inflammatory markers.⁵ This might break the vicious circle of osteoporosis, periodontal disease development, and further systemic bone resorption.

Therefore, we suggest that menopausal women should maintain an adequate vitamin D status in order to prevent and treat osteoporosis-associated periodontal disease.

To the Editor: Buencamino and colleagues¹ reviewed the association between menopause and periodontal disease. However, they did not mention the role of vitamin D status in this setting.

Vitamin D status is usually divided into three categories based on serum 25-hydroxyvitamin D levels: “deficient” (≤ 15 ng/mL), “insufficient” (15.1–29.9 ng/mL), and “sufficient” (≥ 30 ng/mL). Serum 25-hydroxyvitamin D levels have been decreasing significantly for more than a decade, and as a result, a majority of the US population has a vitamin D insufficiency.

In the third National Health and Nutrition Examination Survey (NHANES III), a large US population survey, a low serum 25-hydroxyvitamin D concentration was independently associated with periodontal disease.² In particular, it was significantly associated with loss of alveolar attachment in persons older than 50 years of both sexes, independent of race or ethnicity; women in the highest 25-hydroxyvitamin D quintile had, on average, 0.26 mm (95% confidence interval 0.09–0.43 mm) less mean attachment loss than did women in the lowest quintile. Furthermore, in a randomized trial, supplementation with vitamin D (700 IU/day) plus calcium (500 mg/day) has been shown to significantly reduce tooth loss in older persons over a 3-year treatment period.³

Osteoporosis and periodontal disease share several risk factors, and it might be speculated that these pathologic conditions are biologically intertwined.⁴ The decreased bone mineral density of osteoporosis can lead to an altered trabecular pattern and more rapid alveolar bone resorption, thus predisposing to periodontal disease. On the other hand, periodontal infections can increase the systemic release of inflammatory cytokines, which accelerate systemic bone resorption. Indeed, vitamin D deficiency has been associated with a cytokine profile that favors greater inflammation (eg, higher levels of C-reactive protein and interleukin 6, and lower levels of interleukin 10), and vitamin D supplementation decreases circulating inflammatory markers.⁵ This might break the vicious circle of osteoporosis, periodontal disease development, and further systemic bone resorption.

Therefore, we suggest that menopausal women should maintain an adequate vitamin D status in order to prevent and treat osteoporosis-associated periodontal disease.

To the Editor: Buencamino and colleagues¹ reviewed the association between menopause and periodontal disease. However, they did not mention the role of vitamin D status in this setting.

Vitamin D status is usually divided into three categories based on serum 25-hydroxyvitamin D levels: “deficient” (≤ 15 ng/mL), “insufficient” (15.1–29.9 ng/mL), and “sufficient” (≥ 30 ng/mL). Serum 25-hydroxyvitamin D levels have been decreasing significantly for more than a decade, and as a result, a majority of the US population has a vitamin D insufficiency.

In the third National Health and Nutrition Examination Survey (NHANES III), a large US population survey, a low serum 25-hydroxyvitamin D concentration was independently associated with periodontal disease.² In particular, it was significantly associated with loss of alveolar attachment in persons older than 50 years of both sexes, independent of race or ethnicity; women in the highest 25-hydroxyvitamin D quintile had, on average, 0.26 mm (95% confidence interval 0.09–0.43 mm) less mean attachment loss than did women in the lowest quintile. Furthermore, in a randomized trial, supplementation with vitamin D (700 IU/day) plus calcium (500 mg/day) has been shown to significantly reduce tooth loss in older persons over a 3-year treatment period.³

Osteoporosis and periodontal disease share several risk factors, and it might be speculated that these pathologic conditions are biologically intertwined.⁴ The decreased bone mineral density of osteoporosis can lead to an altered trabecular pattern and more rapid alveolar bone resorption, thus predisposing to periodontal disease. On the other hand, periodontal infections can increase the systemic release of inflammatory cytokines, which accelerate systemic bone resorption. Indeed, vitamin D deficiency has been associated with a cytokine profile that favors greater inflammation (eg, higher levels of C-reactive protein and interleukin 6, and lower levels of interleukin 10), and vitamin D supplementation decreases circulating inflammatory markers.⁵ This might break the vicious circle of osteoporosis, periodontal disease development, and further systemic bone resorption.

Therefore, we suggest that menopausal women should maintain an adequate vitamin D status in order to prevent and treat osteoporosis-associated periodontal disease.

To the Editor: We read the interesting paper by Dr. Susan Rehm on the recently changing epidemiology and increasing incidence of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia.¹ We feel these trends may be related in part to the increasing use of statin therapy in both outpatient and hospital settings.

In a case-control study,² skin and soft tissue infections as the source of bacteremia were significantly more prevalent among patients treated with statins compared with patients not receiving statin therapy. Additionally, there have been isolated reports of recurrent community-acquired MRSA skin infections in subjects on therapy with high-dose statins and no obvious risk factors for skin infection.³

The epidermis is a very active site of cholesterol synthesis, and after barrier disruption in the murine model, there is a brisk increase in epidermal cholesterol synthesis.⁴ Moreover, if the increase in epidermal cholesterol synthesis is inhibited by the topical application of statins, barrier function is impaired.⁴

Therefore, it is plausible that systemic statin therapy alters epidermal cholesterol homeostasis, resulting in barrier inadequacy and impaired innate immune function of the skin,⁵ leaving it more vulnerable to external pathogens and resulting bacteremia. Importantly, this needs to be investigated, particularly in light of the increasing and widespread use of high-dose statin therapy.

To the Editor: We read the interesting paper by Dr. Susan Rehm on the recently changing epidemiology and increasing incidence of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia.¹ We feel these trends may be related in part to the increasing use of statin therapy in both outpatient and hospital settings.

In a case-control study,² skin and soft tissue infections as the source of bacteremia were significantly more prevalent among patients treated with statins compared with patients not receiving statin therapy. Additionally, there have been isolated reports of recurrent community-acquired MRSA skin infections in subjects on therapy with high-dose statins and no obvious risk factors for skin infection.³

The epidermis is a very active site of cholesterol synthesis, and after barrier disruption in the murine model, there is a brisk increase in epidermal cholesterol synthesis.⁴ Moreover, if the increase in epidermal cholesterol synthesis is inhibited by the topical application of statins, barrier function is impaired.⁴

Therefore, it is plausible that systemic statin therapy alters epidermal cholesterol homeostasis, resulting in barrier inadequacy and impaired innate immune function of the skin,⁵ leaving it more vulnerable to external pathogens and resulting bacteremia. Importantly, this needs to be investigated, particularly in light of the increasing and widespread use of high-dose statin therapy.

To the Editor: We read the interesting paper by Dr. Susan Rehm on the recently changing epidemiology and increasing incidence of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia.¹ We feel these trends may be related in part to the increasing use of statin therapy in both outpatient and hospital settings.

In a case-control study,² skin and soft tissue infections as the source of bacteremia were significantly more prevalent among patients treated with statins compared with patients not receiving statin therapy. Additionally, there have been isolated reports of recurrent community-acquired MRSA skin infections in subjects on therapy with high-dose statins and no obvious risk factors for skin infection.³

The epidermis is a very active site of cholesterol synthesis, and after barrier disruption in the murine model, there is a brisk increase in epidermal cholesterol synthesis.⁴ Moreover, if the increase in epidermal cholesterol synthesis is inhibited by the topical application of statins, barrier function is impaired.⁴

Therefore, it is plausible that systemic statin therapy alters epidermal cholesterol homeostasis, resulting in barrier inadequacy and impaired innate immune function of the skin,⁵ leaving it more vulnerable to external pathogens and resulting bacteremia. Importantly, this needs to be investigated, particularly in light of the increasing and widespread use of high-dose statin therapy.