Atieh Jibbe, MD

Clinical Challenge

An odontogenic cutaneous sinus tract (OCST) of dental origin is an uncommon occurrence and is most commonly caused by chronic periodontitis, specifically a periapical abscess due to chronic dental infection.^1,2 Odontogenic cutaneous sinus tract commonly is misdiagnosed due to a lack of symptoms on presentation, location, and variations in clinical appearance mimicking other lesions. Patients with OCSTs typically present with a fixed, erythematous, crusty, and nontender nodule with periodic drainage that easily can be mistaken for a pustule, furuncle, cyst, foreign-body lesion, squamous cell carcinoma (SCC), basal cell carcinoma, or granulomatous disorder.³ It becomes challenging for dermatologists to correctly diagnose these lesions and refer for proper evaluation and treatment.

Practice Gap

It is estimated that half of patients with an extraoral fistula are treated with multiple dermatologic surgical operations, radiotherapy, antibiotic therapy, and chemotherapy before the correct diagnosis is made.¹ Thus, proper identification of these lesions is crucial for prognosis and treatment. The most common locations for OCSTs are the mandibular, submandibular, and cervical skin.^1,2 Given these locations, patients with OCSTs commonly present to the dermatology office for evaluation. Education regarding the clinical presentation, histopathology, and proper evaluation and further referral for treatment is essential for dermatologists.

Tools and Technique for Diagnosis

We present 2 patients with OCSTs who were referred for cutaneous surgery for an SCC and epidermal cyst, but the proper diagnosis was rendered after an index of suspicion and clinicopathologic correlation led to additional testing and eventual referral for imaging.

Patient 1
A 68-year-old woman presented for Mohs micrographic surgery (MMS) of a biopsy-proven SCC on the chin. The tumor cleared after 2 MMS stages (Figure 1A). Due to notable inflammation in each stage, the slides were sent to a pathologist who confirmed clear margins. Within 2 weeks of MMS, the wound began to dehisce (Figure 1B). The patient presented 4 months later with a crusted ulcerated nodule at the MMS site (Figure 1C). A biopsy showed likely recurrence of SCC. Upon presentation to the Mohs surgeon, the nodule felt fixed to the underlying jaw, and the patient was noted to have poor dentition. The patient was sent for computed tomography (CT), which showed focal thinning of the mandible, likely postsurgical, and clear maxillary sinuses. Due to the clinical appearance and anatomic location of the lesion, a request was made for a second read of the CT, specifically looking for an OCST at the prior surgical site. With this information, the radiologist noted an OCST extending from the mandible to the lesion, reported as a periapical lucency (representing a periapical abscess) at a mandibular tooth with a dental sinus draining into the soft tissues. The patient was started on antibiotics and referred to an oral surgeon for OCST excision.

Practice Implications

Odontogenic cutaneous sinus tracts commonly are misdiagnosed due to variations in clinical presentations resembling more common cutaneous diagnoses, nonspecific histopathologic findings, and lack of dental symptoms or concerns about dentition. Clinically, an OCST presents as a fixed, red, crusty, nontender nodule with intermittent draining. With palpation of the involved area, the clinician may feel a cord of tissue connecting the skin lesion intraorally.^2,4 A clinician should have a high index of suspicion for an OCST when evaluating fixed lesions of the lower face, jawline, and neck due to the possibility of a dental origin,¹ which is important because an OCST can have similar clinical findings to lesions such as congenital fistulas, pustules, cysts, osteomyelitis, foreign-body granulomas, pyogenic granulomas, syphilis, metastatic carcinomas, basal cell carcinomas, and SCCs.^2,4 A PubMed search of articles indexed for MEDLINE using the terms Mohs, MMS, chemosurgery, odontogenic sinus, odontogenic cutaneous sinus tract, and dental sinus yielded only 2 OCSTs that were referred for MMS in the last 30 years, both of which were in the nasolabial fold/medial malar cheek.^2,4 Histopathologic findings of an OCST are nonspecific; a mixed or granulomatous inflammatory infiltrate, granulation tissue, and scarring can be seen.¹ Pseudocarcinomatous/pseudoepitheliomatous hyperplasia of the epidermis can be seen and cause histologic misinterpretation for an SCC.² Given that these findings are nonspecific without a clinical context, even with a histopathologic diagnosis of SCC or cyst, a clinical suspicion for an OCST should lead to an intraoral examination. Imaging can be ordered to look for an OCST in the area of interest. Although panoramic or periapical radiography with or without dental probes/radiopaque markers commonly have been used, more recent literature has suggested that CT may be superior to radiographs for making an OCST diagnosis.^1,3 If imaging is not consistent with the clinically suspected OCST, we recommend directly contacting the radiologist to explain the clinical history and even refresh his/her suspicion for this diagnosis.

If a diagnosis of an OCST is made, oral antibiotics can be prescribed, though the use of antibiotics has been controversial. For severe odontogenic infections, typically beta-lactam antibiotics, cephalosporins, metronidazole, clindamycin, moxifloxacin, or erythromycin can be given for 7 days or until 3 days after symptoms have resolved.⁵ Although antibiotics can bring temporary resolution, it is imperative to treat the source of infection to prevent recurrence. It is crucial for these patients to be referred to an oral surgeon for evaluation and treatment of OCST by either a root canal or tooth extraction.

Final Thoughts

We present this pearl on the diagnosis and management of an OCST, also known as a dental sinus, to better assist clinicians in making this diagnosis. With an index of suspicion as well as intraoral and radiologic evaluations, a proper diagnosis may be rendered, potentially avoiding unnecessary cutaneous surgery. In addition, we highlight the importance of communication between the clinician and the radiologist to directly look for OCST in the area of concern and consider a re-read of the images when clinical suspicion does not correlate with the radiology report.

Clinical Challenge

An odontogenic cutaneous sinus tract (OCST) of dental origin is an uncommon occurrence and is most commonly caused by chronic periodontitis, specifically a periapical abscess due to chronic dental infection.^1,2 Odontogenic cutaneous sinus tract commonly is misdiagnosed due to a lack of symptoms on presentation, location, and variations in clinical appearance mimicking other lesions. Patients with OCSTs typically present with a fixed, erythematous, crusty, and nontender nodule with periodic drainage that easily can be mistaken for a pustule, furuncle, cyst, foreign-body lesion, squamous cell carcinoma (SCC), basal cell carcinoma, or granulomatous disorder.³ It becomes challenging for dermatologists to correctly diagnose these lesions and refer for proper evaluation and treatment.

Practice Gap

It is estimated that half of patients with an extraoral fistula are treated with multiple dermatologic surgical operations, radiotherapy, antibiotic therapy, and chemotherapy before the correct diagnosis is made.¹ Thus, proper identification of these lesions is crucial for prognosis and treatment. The most common locations for OCSTs are the mandibular, submandibular, and cervical skin.^1,2 Given these locations, patients with OCSTs commonly present to the dermatology office for evaluation. Education regarding the clinical presentation, histopathology, and proper evaluation and further referral for treatment is essential for dermatologists.

Tools and Technique for Diagnosis

We present 2 patients with OCSTs who were referred for cutaneous surgery for an SCC and epidermal cyst, but the proper diagnosis was rendered after an index of suspicion and clinicopathologic correlation led to additional testing and eventual referral for imaging.

Patient 1
A 68-year-old woman presented for Mohs micrographic surgery (MMS) of a biopsy-proven SCC on the chin. The tumor cleared after 2 MMS stages (Figure 1A). Due to notable inflammation in each stage, the slides were sent to a pathologist who confirmed clear margins. Within 2 weeks of MMS, the wound began to dehisce (Figure 1B). The patient presented 4 months later with a crusted ulcerated nodule at the MMS site (Figure 1C). A biopsy showed likely recurrence of SCC. Upon presentation to the Mohs surgeon, the nodule felt fixed to the underlying jaw, and the patient was noted to have poor dentition. The patient was sent for computed tomography (CT), which showed focal thinning of the mandible, likely postsurgical, and clear maxillary sinuses. Due to the clinical appearance and anatomic location of the lesion, a request was made for a second read of the CT, specifically looking for an OCST at the prior surgical site. With this information, the radiologist noted an OCST extending from the mandible to the lesion, reported as a periapical lucency (representing a periapical abscess) at a mandibular tooth with a dental sinus draining into the soft tissues. The patient was started on antibiotics and referred to an oral surgeon for OCST excision.

Practice Implications

Odontogenic cutaneous sinus tracts commonly are misdiagnosed due to variations in clinical presentations resembling more common cutaneous diagnoses, nonspecific histopathologic findings, and lack of dental symptoms or concerns about dentition. Clinically, an OCST presents as a fixed, red, crusty, nontender nodule with intermittent draining. With palpation of the involved area, the clinician may feel a cord of tissue connecting the skin lesion intraorally.^2,4 A clinician should have a high index of suspicion for an OCST when evaluating fixed lesions of the lower face, jawline, and neck due to the possibility of a dental origin,¹ which is important because an OCST can have similar clinical findings to lesions such as congenital fistulas, pustules, cysts, osteomyelitis, foreign-body granulomas, pyogenic granulomas, syphilis, metastatic carcinomas, basal cell carcinomas, and SCCs.^2,4 A PubMed search of articles indexed for MEDLINE using the terms Mohs, MMS, chemosurgery, odontogenic sinus, odontogenic cutaneous sinus tract, and dental sinus yielded only 2 OCSTs that were referred for MMS in the last 30 years, both of which were in the nasolabial fold/medial malar cheek.^2,4 Histopathologic findings of an OCST are nonspecific; a mixed or granulomatous inflammatory infiltrate, granulation tissue, and scarring can be seen.¹ Pseudocarcinomatous/pseudoepitheliomatous hyperplasia of the epidermis can be seen and cause histologic misinterpretation for an SCC.² Given that these findings are nonspecific without a clinical context, even with a histopathologic diagnosis of SCC or cyst, a clinical suspicion for an OCST should lead to an intraoral examination. Imaging can be ordered to look for an OCST in the area of interest. Although panoramic or periapical radiography with or without dental probes/radiopaque markers commonly have been used, more recent literature has suggested that CT may be superior to radiographs for making an OCST diagnosis.^1,3 If imaging is not consistent with the clinically suspected OCST, we recommend directly contacting the radiologist to explain the clinical history and even refresh his/her suspicion for this diagnosis.

If a diagnosis of an OCST is made, oral antibiotics can be prescribed, though the use of antibiotics has been controversial. For severe odontogenic infections, typically beta-lactam antibiotics, cephalosporins, metronidazole, clindamycin, moxifloxacin, or erythromycin can be given for 7 days or until 3 days after symptoms have resolved.⁵ Although antibiotics can bring temporary resolution, it is imperative to treat the source of infection to prevent recurrence. It is crucial for these patients to be referred to an oral surgeon for evaluation and treatment of OCST by either a root canal or tooth extraction.

Final Thoughts

We present this pearl on the diagnosis and management of an OCST, also known as a dental sinus, to better assist clinicians in making this diagnosis. With an index of suspicion as well as intraoral and radiologic evaluations, a proper diagnosis may be rendered, potentially avoiding unnecessary cutaneous surgery. In addition, we highlight the importance of communication between the clinician and the radiologist to directly look for OCST in the area of concern and consider a re-read of the images when clinical suspicion does not correlate with the radiology report.

Clinical Challenge

An odontogenic cutaneous sinus tract (OCST) of dental origin is an uncommon occurrence and is most commonly caused by chronic periodontitis, specifically a periapical abscess due to chronic dental infection.^1,2 Odontogenic cutaneous sinus tract commonly is misdiagnosed due to a lack of symptoms on presentation, location, and variations in clinical appearance mimicking other lesions. Patients with OCSTs typically present with a fixed, erythematous, crusty, and nontender nodule with periodic drainage that easily can be mistaken for a pustule, furuncle, cyst, foreign-body lesion, squamous cell carcinoma (SCC), basal cell carcinoma, or granulomatous disorder.³ It becomes challenging for dermatologists to correctly diagnose these lesions and refer for proper evaluation and treatment.

Practice Gap

It is estimated that half of patients with an extraoral fistula are treated with multiple dermatologic surgical operations, radiotherapy, antibiotic therapy, and chemotherapy before the correct diagnosis is made.¹ Thus, proper identification of these lesions is crucial for prognosis and treatment. The most common locations for OCSTs are the mandibular, submandibular, and cervical skin.^1,2 Given these locations, patients with OCSTs commonly present to the dermatology office for evaluation. Education regarding the clinical presentation, histopathology, and proper evaluation and further referral for treatment is essential for dermatologists.

Tools and Technique for Diagnosis

We present 2 patients with OCSTs who were referred for cutaneous surgery for an SCC and epidermal cyst, but the proper diagnosis was rendered after an index of suspicion and clinicopathologic correlation led to additional testing and eventual referral for imaging.

Patient 1
A 68-year-old woman presented for Mohs micrographic surgery (MMS) of a biopsy-proven SCC on the chin. The tumor cleared after 2 MMS stages (Figure 1A). Due to notable inflammation in each stage, the slides were sent to a pathologist who confirmed clear margins. Within 2 weeks of MMS, the wound began to dehisce (Figure 1B). The patient presented 4 months later with a crusted ulcerated nodule at the MMS site (Figure 1C). A biopsy showed likely recurrence of SCC. Upon presentation to the Mohs surgeon, the nodule felt fixed to the underlying jaw, and the patient was noted to have poor dentition. The patient was sent for computed tomography (CT), which showed focal thinning of the mandible, likely postsurgical, and clear maxillary sinuses. Due to the clinical appearance and anatomic location of the lesion, a request was made for a second read of the CT, specifically looking for an OCST at the prior surgical site. With this information, the radiologist noted an OCST extending from the mandible to the lesion, reported as a periapical lucency (representing a periapical abscess) at a mandibular tooth with a dental sinus draining into the soft tissues. The patient was started on antibiotics and referred to an oral surgeon for OCST excision.

Practice Implications

Odontogenic cutaneous sinus tracts commonly are misdiagnosed due to variations in clinical presentations resembling more common cutaneous diagnoses, nonspecific histopathologic findings, and lack of dental symptoms or concerns about dentition. Clinically, an OCST presents as a fixed, red, crusty, nontender nodule with intermittent draining. With palpation of the involved area, the clinician may feel a cord of tissue connecting the skin lesion intraorally.^2,4 A clinician should have a high index of suspicion for an OCST when evaluating fixed lesions of the lower face, jawline, and neck due to the possibility of a dental origin,¹ which is important because an OCST can have similar clinical findings to lesions such as congenital fistulas, pustules, cysts, osteomyelitis, foreign-body granulomas, pyogenic granulomas, syphilis, metastatic carcinomas, basal cell carcinomas, and SCCs.^2,4 A PubMed search of articles indexed for MEDLINE using the terms Mohs, MMS, chemosurgery, odontogenic sinus, odontogenic cutaneous sinus tract, and dental sinus yielded only 2 OCSTs that were referred for MMS in the last 30 years, both of which were in the nasolabial fold/medial malar cheek.^2,4 Histopathologic findings of an OCST are nonspecific; a mixed or granulomatous inflammatory infiltrate, granulation tissue, and scarring can be seen.¹ Pseudocarcinomatous/pseudoepitheliomatous hyperplasia of the epidermis can be seen and cause histologic misinterpretation for an SCC.² Given that these findings are nonspecific without a clinical context, even with a histopathologic diagnosis of SCC or cyst, a clinical suspicion for an OCST should lead to an intraoral examination. Imaging can be ordered to look for an OCST in the area of interest. Although panoramic or periapical radiography with or without dental probes/radiopaque markers commonly have been used, more recent literature has suggested that CT may be superior to radiographs for making an OCST diagnosis.^1,3 If imaging is not consistent with the clinically suspected OCST, we recommend directly contacting the radiologist to explain the clinical history and even refresh his/her suspicion for this diagnosis.

If a diagnosis of an OCST is made, oral antibiotics can be prescribed, though the use of antibiotics has been controversial. For severe odontogenic infections, typically beta-lactam antibiotics, cephalosporins, metronidazole, clindamycin, moxifloxacin, or erythromycin can be given for 7 days or until 3 days after symptoms have resolved.⁵ Although antibiotics can bring temporary resolution, it is imperative to treat the source of infection to prevent recurrence. It is crucial for these patients to be referred to an oral surgeon for evaluation and treatment of OCST by either a root canal or tooth extraction.

Final Thoughts

We present this pearl on the diagnosis and management of an OCST, also known as a dental sinus, to better assist clinicians in making this diagnosis. With an index of suspicion as well as intraoral and radiologic evaluations, a proper diagnosis may be rendered, potentially avoiding unnecessary cutaneous surgery. In addition, we highlight the importance of communication between the clinician and the radiologist to directly look for OCST in the area of concern and consider a re-read of the images when clinical suspicion does not correlate with the radiology report.

The Diagnosis: Epidermodysplasia Verruciformis 

Histopathologic examination demonstrated acanthosis and coarse hypergranulosis with enlarged keratinocytes exhibiting blue cytoplasmic discoloration (Figure), which was suggestive of acquired epidermodysplasia verruciformis (EV).  

Acquired EV is a rare dermatologic condition associated with specific human papillomavirus (HPV) types that presents with recalcitrant lesions most commonly in the setting of immunosuppression.¹ The most common HPV types associated with EV are HPV-5 and -8, but associations with HPV-3, -9, -10, -12, -14, -15, -17, -19 to -25, -36 to -38, -47, and -50 also have been reported.^1,2 Acquired EV has been identified in individuals with human immunodeficiency virus, as well as in immunosuppressed patients with organ transplantation, Hodgkin lymphoma, systemic lupus erythematosus, and IgM deficiency, and in patients taking immunosuppressive medications such as tumor necrosis factor α inhibitors.^1,3 The diagnosis is clinicopathological with potential polymerase chain reaction studies to identify underlying HPV types. 

Acquired EV presents as hypopigmented to red, tinea versicolor-like macules or as verrucous, flat-topped papules on the trunk, arms, and/or legs.⁴ Histopathology reveals viral epidermal cytopathic changes, blue cytoplasm, and coarse hypogranulosis.⁴ 

There is no standardized treatment regimen for acquired EV, and no single approach has proven to yield an efficacious clinical outcome. Topical treatment options include steroids, retinoids, immunomodulators, cryotherapy, and electrosurgery, whereas retinoids or interferon alfa have been used as oral systemic therapy. Photodynamic therapy also has been shown to improve symptoms.³ Combination therapy such as interferon alfa with zidovudine or imiquimod with oral isotretinoin has shown better results than any single treatment.⁴ Due to the underlying HPV infection and its role in promotion of skin cancer development, lesions can characteristically undergo malignant transformations into Bowen disease but most commonly invasive squamous cell carcinoma (SCC), with initial lesions preferentially affecting sun-exposed areas due to the synergistic effect of UV light with EV-HPV lesions. The EV-HPV strains ^{5, 8,} and 41 carry the highest oncogenic potential.5 Little is known of the true incidence of oncogenicity for acquired EV. Regardless, consistent sun protection and lifelong clinical examinations are critical for prognosis.⁵  

The differential diagnosis of EV presenting in a tattoo includes allergic contact dermatitis, cutaneous sarcoidosis, pityriasis versicolor, and SCC. The pathology is critical to differentiate between these entities. The most frequently reported skin reactions to tattoo ink include inflammatory diseases (eg, allergic contact dermatitis, granulomatous reaction) or infectious diseases (eg, bacterial, viral, fungal).⁶ Allergic contact dermatitis, typically red pigment, is a common tattoo reaction. The most common histologic feature, however, is spongiosis, which results from intercellular edema. It often is limited to the lower epidermis but may affect the upper layers if the reaction is severe.⁷ Cutaneous sarcoidosis is a great masquerader that can present in various ways; however, its salient features on pathology are noncaseating granuloma involving the basal cell layer and epithelioid granuloma consisting of Langerhans giant cells.⁸ Although pityriasis versicolor can present in young immunocompromised adults, histologically salient features are the presence of both spores and hyphae in the stratum corneum.⁹ Although immunosuppression is a known risk factor for SCC, it is characterized histologically by hyperkeratosis, parakeratosis, and acanthosis with thickened and elongated rete ridges. Scattered atypical cells and frequent mitoses are present.¹⁰ 

The Diagnosis: Epidermodysplasia Verruciformis 

Histopathologic examination demonstrated acanthosis and coarse hypergranulosis with enlarged keratinocytes exhibiting blue cytoplasmic discoloration (Figure), which was suggestive of acquired epidermodysplasia verruciformis (EV).  

Acquired EV is a rare dermatologic condition associated with specific human papillomavirus (HPV) types that presents with recalcitrant lesions most commonly in the setting of immunosuppression.¹ The most common HPV types associated with EV are HPV-5 and -8, but associations with HPV-3, -9, -10, -12, -14, -15, -17, -19 to -25, -36 to -38, -47, and -50 also have been reported.^1,2 Acquired EV has been identified in individuals with human immunodeficiency virus, as well as in immunosuppressed patients with organ transplantation, Hodgkin lymphoma, systemic lupus erythematosus, and IgM deficiency, and in patients taking immunosuppressive medications such as tumor necrosis factor α inhibitors.^1,3 The diagnosis is clinicopathological with potential polymerase chain reaction studies to identify underlying HPV types. 

Acquired EV presents as hypopigmented to red, tinea versicolor-like macules or as verrucous, flat-topped papules on the trunk, arms, and/or legs.⁴ Histopathology reveals viral epidermal cytopathic changes, blue cytoplasm, and coarse hypogranulosis.⁴ 

There is no standardized treatment regimen for acquired EV, and no single approach has proven to yield an efficacious clinical outcome. Topical treatment options include steroids, retinoids, immunomodulators, cryotherapy, and electrosurgery, whereas retinoids or interferon alfa have been used as oral systemic therapy. Photodynamic therapy also has been shown to improve symptoms.³ Combination therapy such as interferon alfa with zidovudine or imiquimod with oral isotretinoin has shown better results than any single treatment.⁴ Due to the underlying HPV infection and its role in promotion of skin cancer development, lesions can characteristically undergo malignant transformations into Bowen disease but most commonly invasive squamous cell carcinoma (SCC), with initial lesions preferentially affecting sun-exposed areas due to the synergistic effect of UV light with EV-HPV lesions. The EV-HPV strains ^{5, 8,} and 41 carry the highest oncogenic potential.5 Little is known of the true incidence of oncogenicity for acquired EV. Regardless, consistent sun protection and lifelong clinical examinations are critical for prognosis.⁵  

The differential diagnosis of EV presenting in a tattoo includes allergic contact dermatitis, cutaneous sarcoidosis, pityriasis versicolor, and SCC. The pathology is critical to differentiate between these entities. The most frequently reported skin reactions to tattoo ink include inflammatory diseases (eg, allergic contact dermatitis, granulomatous reaction) or infectious diseases (eg, bacterial, viral, fungal).⁶ Allergic contact dermatitis, typically red pigment, is a common tattoo reaction. The most common histologic feature, however, is spongiosis, which results from intercellular edema. It often is limited to the lower epidermis but may affect the upper layers if the reaction is severe.⁷ Cutaneous sarcoidosis is a great masquerader that can present in various ways; however, its salient features on pathology are noncaseating granuloma involving the basal cell layer and epithelioid granuloma consisting of Langerhans giant cells.⁸ Although pityriasis versicolor can present in young immunocompromised adults, histologically salient features are the presence of both spores and hyphae in the stratum corneum.⁹ Although immunosuppression is a known risk factor for SCC, it is characterized histologically by hyperkeratosis, parakeratosis, and acanthosis with thickened and elongated rete ridges. Scattered atypical cells and frequent mitoses are present.¹⁰ 

The Diagnosis: Epidermodysplasia Verruciformis 

Histopathologic examination demonstrated acanthosis and coarse hypergranulosis with enlarged keratinocytes exhibiting blue cytoplasmic discoloration (Figure), which was suggestive of acquired epidermodysplasia verruciformis (EV).  

Acquired EV is a rare dermatologic condition associated with specific human papillomavirus (HPV) types that presents with recalcitrant lesions most commonly in the setting of immunosuppression.¹ The most common HPV types associated with EV are HPV-5 and -8, but associations with HPV-3, -9, -10, -12, -14, -15, -17, -19 to -25, -36 to -38, -47, and -50 also have been reported.^1,2 Acquired EV has been identified in individuals with human immunodeficiency virus, as well as in immunosuppressed patients with organ transplantation, Hodgkin lymphoma, systemic lupus erythematosus, and IgM deficiency, and in patients taking immunosuppressive medications such as tumor necrosis factor α inhibitors.^1,3 The diagnosis is clinicopathological with potential polymerase chain reaction studies to identify underlying HPV types. 

Acquired EV presents as hypopigmented to red, tinea versicolor-like macules or as verrucous, flat-topped papules on the trunk, arms, and/or legs.⁴ Histopathology reveals viral epidermal cytopathic changes, blue cytoplasm, and coarse hypogranulosis.⁴ 

There is no standardized treatment regimen for acquired EV, and no single approach has proven to yield an efficacious clinical outcome. Topical treatment options include steroids, retinoids, immunomodulators, cryotherapy, and electrosurgery, whereas retinoids or interferon alfa have been used as oral systemic therapy. Photodynamic therapy also has been shown to improve symptoms.³ Combination therapy such as interferon alfa with zidovudine or imiquimod with oral isotretinoin has shown better results than any single treatment.⁴ Due to the underlying HPV infection and its role in promotion of skin cancer development, lesions can characteristically undergo malignant transformations into Bowen disease but most commonly invasive squamous cell carcinoma (SCC), with initial lesions preferentially affecting sun-exposed areas due to the synergistic effect of UV light with EV-HPV lesions. The EV-HPV strains ^{5, 8,} and 41 carry the highest oncogenic potential.5 Little is known of the true incidence of oncogenicity for acquired EV. Regardless, consistent sun protection and lifelong clinical examinations are critical for prognosis.⁵  

The differential diagnosis of EV presenting in a tattoo includes allergic contact dermatitis, cutaneous sarcoidosis, pityriasis versicolor, and SCC. The pathology is critical to differentiate between these entities. The most frequently reported skin reactions to tattoo ink include inflammatory diseases (eg, allergic contact dermatitis, granulomatous reaction) or infectious diseases (eg, bacterial, viral, fungal).⁶ Allergic contact dermatitis, typically red pigment, is a common tattoo reaction. The most common histologic feature, however, is spongiosis, which results from intercellular edema. It often is limited to the lower epidermis but may affect the upper layers if the reaction is severe.⁷ Cutaneous sarcoidosis is a great masquerader that can present in various ways; however, its salient features on pathology are noncaseating granuloma involving the basal cell layer and epithelioid granuloma consisting of Langerhans giant cells.⁸ Although pityriasis versicolor can present in young immunocompromised adults, histologically salient features are the presence of both spores and hyphae in the stratum corneum.⁹ Although immunosuppression is a known risk factor for SCC, it is characterized histologically by hyperkeratosis, parakeratosis, and acanthosis with thickened and elongated rete ridges. Scattered atypical cells and frequent mitoses are present.¹⁰ 

To the Editor:

A thorough full-body skin examination (FBSE) is an integral component of a dermatologic encounter and helps identify potentially malignant and high-risk lesions, particularly in areas that are difficult for the patient to visualize.¹ Despite these benefits, many patients experience discomfort and anxiety about this examination because it involves sensitive anatomical areas. The true psychological impact of an FBSE is not clearly understood; however, research into improving patient comfort in these circumstances can have a broad positive impact.² The purpose of this pilot study was to establish patients’ willingness to complete a pre-encounter questionnaire that defines their FBSE preferences as well as to identify the anatomical areas that are of most concern.

This study was approved by the University of Kansas institutional review board as nonhuman subjects research. A pre-encounter questionnaire that included information about the benefits of FBSEs was administered to 34 patients, allowing them to identify anatomic locations that they wanted to exclude from the FBSE.

Following the patient visit (in which the identified anatomical locations were excluded), patients were given a brief exit survey that asked about (1) their preference for a pre-encounter FBSE questionnaire and (2) the impact of the questionnaire on their anxiety level throughout the encounter. Preference for asking was surveyed using a 10-point scale (10=strong preference for the pre-encounter survey; 1=strong preference against the pre-encounter survey). Change in anxiety was surveyed using a 10-point scale (10=strong reduction in anxiety after the pre-encounter survey; 1=strong increase in anxiety after the pre-encounter survey). Statistical analysis was performed using 2-tailed unpaired t tests, with P<.05 considered statistically significant.

Twenty female and 14 male patients were enrolled (mean age, 53 years)(Table). The most commonly excluded anatomical location on the pre-encounter survey was the genitals, followed by the buttocks, breasts/chest, legs, feet, and abdomen (Table); 10 (71%) male and 13 (65%) female respondents did not exclude any component of the FBSE.

The small sample size was a limitation of this study. Future studies can assess with greater precision the clear benefits of a pre-encounter survey as well as the benefits or drawbacks of a survey compared to other modalities that are aimed at reducing patient anxiety about the FBSE, such as having the physician directly ask the patient about areas to avoid during the examination.

A pre-encounter survey about the FBSE can serve as an efficient means of determining patient preference and reducing self-reported anxiety about the visit.

To the Editor:

A thorough full-body skin examination (FBSE) is an integral component of a dermatologic encounter and helps identify potentially malignant and high-risk lesions, particularly in areas that are difficult for the patient to visualize.¹ Despite these benefits, many patients experience discomfort and anxiety about this examination because it involves sensitive anatomical areas. The true psychological impact of an FBSE is not clearly understood; however, research into improving patient comfort in these circumstances can have a broad positive impact.² The purpose of this pilot study was to establish patients’ willingness to complete a pre-encounter questionnaire that defines their FBSE preferences as well as to identify the anatomical areas that are of most concern.

This study was approved by the University of Kansas institutional review board as nonhuman subjects research. A pre-encounter questionnaire that included information about the benefits of FBSEs was administered to 34 patients, allowing them to identify anatomic locations that they wanted to exclude from the FBSE.

Following the patient visit (in which the identified anatomical locations were excluded), patients were given a brief exit survey that asked about (1) their preference for a pre-encounter FBSE questionnaire and (2) the impact of the questionnaire on their anxiety level throughout the encounter. Preference for asking was surveyed using a 10-point scale (10=strong preference for the pre-encounter survey; 1=strong preference against the pre-encounter survey). Change in anxiety was surveyed using a 10-point scale (10=strong reduction in anxiety after the pre-encounter survey; 1=strong increase in anxiety after the pre-encounter survey). Statistical analysis was performed using 2-tailed unpaired t tests, with P<.05 considered statistically significant.

Twenty female and 14 male patients were enrolled (mean age, 53 years)(Table). The most commonly excluded anatomical location on the pre-encounter survey was the genitals, followed by the buttocks, breasts/chest, legs, feet, and abdomen (Table); 10 (71%) male and 13 (65%) female respondents did not exclude any component of the FBSE.

The small sample size was a limitation of this study. Future studies can assess with greater precision the clear benefits of a pre-encounter survey as well as the benefits or drawbacks of a survey compared to other modalities that are aimed at reducing patient anxiety about the FBSE, such as having the physician directly ask the patient about areas to avoid during the examination.

A pre-encounter survey about the FBSE can serve as an efficient means of determining patient preference and reducing self-reported anxiety about the visit.

To the Editor:

A thorough full-body skin examination (FBSE) is an integral component of a dermatologic encounter and helps identify potentially malignant and high-risk lesions, particularly in areas that are difficult for the patient to visualize.¹ Despite these benefits, many patients experience discomfort and anxiety about this examination because it involves sensitive anatomical areas. The true psychological impact of an FBSE is not clearly understood; however, research into improving patient comfort in these circumstances can have a broad positive impact.² The purpose of this pilot study was to establish patients’ willingness to complete a pre-encounter questionnaire that defines their FBSE preferences as well as to identify the anatomical areas that are of most concern.

This study was approved by the University of Kansas institutional review board as nonhuman subjects research. A pre-encounter questionnaire that included information about the benefits of FBSEs was administered to 34 patients, allowing them to identify anatomic locations that they wanted to exclude from the FBSE.

Following the patient visit (in which the identified anatomical locations were excluded), patients were given a brief exit survey that asked about (1) their preference for a pre-encounter FBSE questionnaire and (2) the impact of the questionnaire on their anxiety level throughout the encounter. Preference for asking was surveyed using a 10-point scale (10=strong preference for the pre-encounter survey; 1=strong preference against the pre-encounter survey). Change in anxiety was surveyed using a 10-point scale (10=strong reduction in anxiety after the pre-encounter survey; 1=strong increase in anxiety after the pre-encounter survey). Statistical analysis was performed using 2-tailed unpaired t tests, with P<.05 considered statistically significant.

Twenty female and 14 male patients were enrolled (mean age, 53 years)(Table). The most commonly excluded anatomical location on the pre-encounter survey was the genitals, followed by the buttocks, breasts/chest, legs, feet, and abdomen (Table); 10 (71%) male and 13 (65%) female respondents did not exclude any component of the FBSE.

The small sample size was a limitation of this study. Future studies can assess with greater precision the clear benefits of a pre-encounter survey as well as the benefits or drawbacks of a survey compared to other modalities that are aimed at reducing patient anxiety about the FBSE, such as having the physician directly ask the patient about areas to avoid during the examination.

A pre-encounter survey about the FBSE can serve as an efficient means of determining patient preference and reducing self-reported anxiety about the visit.

The Diagnosis: Epidermolysis Bullosa Acquisita 

Epidermolysis bullosa acquisita (EBA) is a rare autoimmune blistering disorder characterized by tense bullae, skin fragility, atrophic scarring, and milia formation.¹ Blisters occur on a noninflammatory base in the classic variant and are trauma induced, hence the predilection for the extensor surfaces.² Mucosal involvement also has been described.¹ The characteristic findings in EBA are IgG autoantibodies directed at the N-terminal collagenous domain of type VII collagen, which composes the anchoring fibrils in the basement membrane zone.¹ Differentiating EBA from other subepidermal bullous diseases, especially bullous pemphigoid (BP), can be difficult, necessitating specialized tests.  

Biopsy of the perilesional skin can help identify the location of the blister formation. Our patient's biopsy showed a subepidermal blister with granulocytes. The differential diagnosis of a subepidermal blister includes BP, herpes gestationis, cicatricial pemphigoid, EBA, bullous systemic lupus erythematosus, dermatitis herpetiformis, linear IgA disease, and porphyria cutanea tarda. 

Direct immunofluorescence (DIF) was performed on the biopsy from our patient, which showed linear/particulate IgG, C3, and IgA deposits in the basement membrane zone, narrowing the differential diagnosis to BP or EBA. To differentiate EBA from BP, DIF of perilesional skin using a salt-split preparation was performed. This test distinguishes the location of the immunoreactants at the basement membrane zone. The antibody complexes in BP are found on the epidermal side of the split, while the antibody complexes in EBA are found on the dermal side of the split. Indirect immunofluorescence on salt-split skin also has been used to distinguish EBA from BP but is only conclusive if there are circulating autoantibodies to the basement membrane zone in the serum, which occurs in approximately 50% of patients with EBA and 15% of patients with BP.³ The immune complexes in our patient were found to be on the dermal side of the split after DIF on salt-split skin, confirming the diagnosis of EBA (Figure).  

Differentiating EBA from BP has great value, as the diagnosis affects treatment options. Bullous pemphigoid is fairly easy to treat, with most patients responding to prednisone.³ Epidermolysis bullosa acquisita usually is resistant to therapy. The disease course is chronic with  exacerbations and remissions. Dapsone often is used to control the disease, though this therapy for EBA is not currently approved by the US Food and Drug Administration. The recommended initial dose of dapsone is 50 mg daily and should be increased by 50 mg each week until remission, usually 100 to 250 mg.⁴ We prescribed dapsone for our patient upon clinical suspicion of EBA before the DIF on salt-split skin was completed. A trial of prednisone may be warranted for EBA if there is no response to dapsone or colchicine, but the response is unpredictable. Cyclosporine usually results in a quick response and may be considered if there is clinically severe disease and other treatment alternatives have failed.⁴ 

The Diagnosis: Epidermolysis Bullosa Acquisita 

Epidermolysis bullosa acquisita (EBA) is a rare autoimmune blistering disorder characterized by tense bullae, skin fragility, atrophic scarring, and milia formation.¹ Blisters occur on a noninflammatory base in the classic variant and are trauma induced, hence the predilection for the extensor surfaces.² Mucosal involvement also has been described.¹ The characteristic findings in EBA are IgG autoantibodies directed at the N-terminal collagenous domain of type VII collagen, which composes the anchoring fibrils in the basement membrane zone.¹ Differentiating EBA from other subepidermal bullous diseases, especially bullous pemphigoid (BP), can be difficult, necessitating specialized tests.  

Biopsy of the perilesional skin can help identify the location of the blister formation. Our patient's biopsy showed a subepidermal blister with granulocytes. The differential diagnosis of a subepidermal blister includes BP, herpes gestationis, cicatricial pemphigoid, EBA, bullous systemic lupus erythematosus, dermatitis herpetiformis, linear IgA disease, and porphyria cutanea tarda. 

Direct immunofluorescence (DIF) was performed on the biopsy from our patient, which showed linear/particulate IgG, C3, and IgA deposits in the basement membrane zone, narrowing the differential diagnosis to BP or EBA. To differentiate EBA from BP, DIF of perilesional skin using a salt-split preparation was performed. This test distinguishes the location of the immunoreactants at the basement membrane zone. The antibody complexes in BP are found on the epidermal side of the split, while the antibody complexes in EBA are found on the dermal side of the split. Indirect immunofluorescence on salt-split skin also has been used to distinguish EBA from BP but is only conclusive if there are circulating autoantibodies to the basement membrane zone in the serum, which occurs in approximately 50% of patients with EBA and 15% of patients with BP.³ The immune complexes in our patient were found to be on the dermal side of the split after DIF on salt-split skin, confirming the diagnosis of EBA (Figure).  

Differentiating EBA from BP has great value, as the diagnosis affects treatment options. Bullous pemphigoid is fairly easy to treat, with most patients responding to prednisone.³ Epidermolysis bullosa acquisita usually is resistant to therapy. The disease course is chronic with  exacerbations and remissions. Dapsone often is used to control the disease, though this therapy for EBA is not currently approved by the US Food and Drug Administration. The recommended initial dose of dapsone is 50 mg daily and should be increased by 50 mg each week until remission, usually 100 to 250 mg.⁴ We prescribed dapsone for our patient upon clinical suspicion of EBA before the DIF on salt-split skin was completed. A trial of prednisone may be warranted for EBA if there is no response to dapsone or colchicine, but the response is unpredictable. Cyclosporine usually results in a quick response and may be considered if there is clinically severe disease and other treatment alternatives have failed.⁴ 

The Diagnosis: Epidermolysis Bullosa Acquisita 

Epidermolysis bullosa acquisita (EBA) is a rare autoimmune blistering disorder characterized by tense bullae, skin fragility, atrophic scarring, and milia formation.¹ Blisters occur on a noninflammatory base in the classic variant and are trauma induced, hence the predilection for the extensor surfaces.² Mucosal involvement also has been described.¹ The characteristic findings in EBA are IgG autoantibodies directed at the N-terminal collagenous domain of type VII collagen, which composes the anchoring fibrils in the basement membrane zone.¹ Differentiating EBA from other subepidermal bullous diseases, especially bullous pemphigoid (BP), can be difficult, necessitating specialized tests.  

Biopsy of the perilesional skin can help identify the location of the blister formation. Our patient's biopsy showed a subepidermal blister with granulocytes. The differential diagnosis of a subepidermal blister includes BP, herpes gestationis, cicatricial pemphigoid, EBA, bullous systemic lupus erythematosus, dermatitis herpetiformis, linear IgA disease, and porphyria cutanea tarda. 

Direct immunofluorescence (DIF) was performed on the biopsy from our patient, which showed linear/particulate IgG, C3, and IgA deposits in the basement membrane zone, narrowing the differential diagnosis to BP or EBA. To differentiate EBA from BP, DIF of perilesional skin using a salt-split preparation was performed. This test distinguishes the location of the immunoreactants at the basement membrane zone. The antibody complexes in BP are found on the epidermal side of the split, while the antibody complexes in EBA are found on the dermal side of the split. Indirect immunofluorescence on salt-split skin also has been used to distinguish EBA from BP but is only conclusive if there are circulating autoantibodies to the basement membrane zone in the serum, which occurs in approximately 50% of patients with EBA and 15% of patients with BP.³ The immune complexes in our patient were found to be on the dermal side of the split after DIF on salt-split skin, confirming the diagnosis of EBA (Figure).  

Differentiating EBA from BP has great value, as the diagnosis affects treatment options. Bullous pemphigoid is fairly easy to treat, with most patients responding to prednisone.³ Epidermolysis bullosa acquisita usually is resistant to therapy. The disease course is chronic with  exacerbations and remissions. Dapsone often is used to control the disease, though this therapy for EBA is not currently approved by the US Food and Drug Administration. The recommended initial dose of dapsone is 50 mg daily and should be increased by 50 mg each week until remission, usually 100 to 250 mg.⁴ We prescribed dapsone for our patient upon clinical suspicion of EBA before the DIF on salt-split skin was completed. A trial of prednisone may be warranted for EBA if there is no response to dapsone or colchicine, but the response is unpredictable. Cyclosporine usually results in a quick response and may be considered if there is clinically severe disease and other treatment alternatives have failed.⁴