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Painful ulcers on gingiva, tongue, and buccal mucosa

A 29-year-old man with no prior history of mouth sores abruptly developed many 1- to 1.5-mm blisters on the gingiva (FIGURE 1A),tongue (FIGURE 1B), and buccal mucosa ­(FIGURE 1C), which evolved into small erosions accompanied by a low-grade fever 5 days prior to presentation. The patient had no history of any dermatologic conditions or systemic illnesses and was taking no medication.

Irregular ulcerations with a yellowish membrane and erythematous halo on the gingiva (A), lesions on the ventral surface of the tongue (B), and multiple grouped ulcerations on the buccal mucosa (C).
IMAGES COURTESY OF ROBERT T. BRODELL, MD

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Acute primary herpetic gingivostomatitis

Herpes simplex virus (HSV) is the causative agent for acute primary herpetic gingivostomatitis.1 HSV-1 is primarily responsible for oral mucosal infections, while HSV-2 is implicated in most genital and cutaneous lower body lesions.1 Herpetic gingivostomatitis often presents as a sudden vesiculoulcerative eruption anywhere in the mouth, including the perioral skin, vermillion border, gingiva, tongue, or buccal mucosa.2 Associated symptoms include malaise, headache, fever, and cervical lymphadenopathy; however, most ­occurrences are subclinical or asymptomatic.2

A diagnosis that’s more common in children. Primary HSV occurs in people who have not previously been exposed to the virus. While it is an infection that classically presents in childhood, it is not limited to this group. Manifestations often are more severe in adults.1

Utilize PCR for the diagnosis of herpetic gingivostomatitis because of its sensitivity, specificity, and rapid turnaround time.

Following an incubation period of a few days to 3 weeks, the primary infection typically lasts 10 to 14 days.1,2 Recurrence is highly variable and generally less severe than primary infection, with grouped vesicles often recurring in the same spot with each recurrence on the vermillion border of the lip. Triggers for reactivation include immunosuppression, pregnancy, fever, UV radiation, or trauma.1,2

Differential includes other conditions with mucosal lesions

Acute herpetic gingivostomatitis must be distinguished from other disease processes that cause ulcerative mucosal lesions.

Aphthous stomatitis (canker sores) is the most common ulcerative disease of the oral mucosa.3 It presents as painful, punched-out, shallow ulcers with a yellowish gray pseudomembranous center and surrounding erythema.3 No definitive etiology has been established; however, aphthae often occur after trauma.

Continue to: Herpangina...

 

 

Herpangina is caused by coxsackie A virus and primarily is seen in infants and children younger than 5.4 The papulovesicular lesions primarily affect the posterior oral cavity, including the soft palate, anterior tonsillar pillars, and uvula.4

Allergic contact dermatitis is precipitated by contact with an allergen and presents with pain or pruritus. Lesions are erythematous with vesicles, erosions, ulcers, or hyperkeratosis that gradually resolve after withdrawal of the causative allergen.5

Pemphigus vulgaris. Oral ulcerations of the buccal mucosa and gingiva are the first manifestation of pemphigus vulgaris in the majority of patients, with skin blisters occurring months to years later over areas exposed to frictional stress.6 Skin sloughs may be seen in response to frictional stress (Nikolsky sign).6

 

The new Dx gold standard is PCR

Acute herpetic gingivostomatitis usually is diagnosed by history and hallmark clinical signs and symptoms.1 In this case, our patient presented with a sudden eruption of painful blisters on multiple areas of the oral mucosa associated with fever. The diagnosis can be confirmed by viral culture, serology with anti-HSV IgM and IgG, Tzanck preparation, immunofluorescence, and polymerase chain reaction (PCR).1 Viral culture has been the gold standard for mucosal HSV diagnosis; however, PCR is emerging as the new gold standard because of its unrivaled sensitivity, specificity, and rapid turnaround time.7,8 Specimens for PCR are submitted using a swab of infected cells placed in the same viral transport ­medium used for HSV cultures.

Our patient’s culture was positive for HSV-1.

Continue to: Prompt use of antivirals is key

 

 

Prompt use of antivirals is key

Treatment of acute HSV gingivostomatitis involves symptomatic management with topical anesthetics, oral analgesics, and normal saline rinses.1 Acyclovir is an established therapy; however, it has poor bioavailability and gastrointestinal absorption.1 Valacyclovir has improved bioavailability and is well tolerated.1 For primary herpes gingivostomatitis, we favor 1 g twice daily for 7 days.1 Our patient responded well to this valacyclovir regimen and healed completely in 1 week.

CORRESPONDENCE
Robert T. Brodell, MD, 2500 N State St, Jackson, MS 39216; rbrodell@umc.edu

References

1. Ajar AH, Chauvin PJ. Acute herpetic gingivostomatitis in adults: a review of 13 cases, including diagnosis and management. J Can Dent Assoc. 2002;68:247-251.

2. George AK, Anil S. Acute herpetic gingivostomatitis associated with herpes simplex virus 2: report of a case. J Int Oral Health. 2014;6:99-102.

3. Akintoye SO, Greenburg MS. Recurrent aphthous stomatitis. Dent Clin N Am. 2014;58:281-297.

4. Scott LA, Stone MS. Viral exanthems. Dermatol Online J. 2003;9:4.

5. Feller L, Wood NH, Khammissa RA, et al. Review: allergic contact stomatitis. Oral Surg Oral Med Oral Pathol Oral Radiol. 2017;123:559-565.

6. Bascones-Martinez A, Munoz-Corcuera M, Bascones-Ilundain C, et al. Oral manifestations of pemphigus vulgaris: clinical presentation, differential diagnosis and management. J Clin Exp Dermatol Res. 2010;1:112.

7. LeGoff J, Péré H, Bélec L. Diagnosis of genital herpes simplex virus infection in the clinical laboratory. Virol J. 2014;11:83.

8. Centers for Disease Control and Prevention. Genital HSV infections. www.cdc.gov/std/tg2015/herpes.htm. ­Updated June 4, 2015. Accessed September 26, 2019.

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Author and Disclosure Information

University of Mississippi School of Medicine, University of Mississippi Medical Center, Jackson (Dr. Fitzpatrick); Department of Dermatology, Department of Pathology, University of Mississippi Medical Center, Jackson (Dr. Brodell); University of Rochester School of Medicine and Dentistry, New York (Dr. Brodell).
rbrodell@umc.edu

DEPARTMENT EDITOR
Richard P. Usatine, MD

University of Texas Health at San Antonio

Dr. Brodell has received consultant fees from Intraderm Pharmaceuticals and has performed clinical trials for Genentech, Novartis, Glaxo-Smith- Kline, Corrona Registry, and Janssen Biotech, Inc. Dr. Fitzpatrick reported no potential conflict of interest relevant to this article.

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The Journal of Family Practice - 68(8)
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465-467
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Author and Disclosure Information

University of Mississippi School of Medicine, University of Mississippi Medical Center, Jackson (Dr. Fitzpatrick); Department of Dermatology, Department of Pathology, University of Mississippi Medical Center, Jackson (Dr. Brodell); University of Rochester School of Medicine and Dentistry, New York (Dr. Brodell).
rbrodell@umc.edu

DEPARTMENT EDITOR
Richard P. Usatine, MD

University of Texas Health at San Antonio

Dr. Brodell has received consultant fees from Intraderm Pharmaceuticals and has performed clinical trials for Genentech, Novartis, Glaxo-Smith- Kline, Corrona Registry, and Janssen Biotech, Inc. Dr. Fitzpatrick reported no potential conflict of interest relevant to this article.

Author and Disclosure Information

University of Mississippi School of Medicine, University of Mississippi Medical Center, Jackson (Dr. Fitzpatrick); Department of Dermatology, Department of Pathology, University of Mississippi Medical Center, Jackson (Dr. Brodell); University of Rochester School of Medicine and Dentistry, New York (Dr. Brodell).
rbrodell@umc.edu

DEPARTMENT EDITOR
Richard P. Usatine, MD

University of Texas Health at San Antonio

Dr. Brodell has received consultant fees from Intraderm Pharmaceuticals and has performed clinical trials for Genentech, Novartis, Glaxo-Smith- Kline, Corrona Registry, and Janssen Biotech, Inc. Dr. Fitzpatrick reported no potential conflict of interest relevant to this article.

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A 29-year-old man with no prior history of mouth sores abruptly developed many 1- to 1.5-mm blisters on the gingiva (FIGURE 1A),tongue (FIGURE 1B), and buccal mucosa ­(FIGURE 1C), which evolved into small erosions accompanied by a low-grade fever 5 days prior to presentation. The patient had no history of any dermatologic conditions or systemic illnesses and was taking no medication.

Irregular ulcerations with a yellowish membrane and erythematous halo on the gingiva (A), lesions on the ventral surface of the tongue (B), and multiple grouped ulcerations on the buccal mucosa (C).
IMAGES COURTESY OF ROBERT T. BRODELL, MD

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Acute primary herpetic gingivostomatitis

Herpes simplex virus (HSV) is the causative agent for acute primary herpetic gingivostomatitis.1 HSV-1 is primarily responsible for oral mucosal infections, while HSV-2 is implicated in most genital and cutaneous lower body lesions.1 Herpetic gingivostomatitis often presents as a sudden vesiculoulcerative eruption anywhere in the mouth, including the perioral skin, vermillion border, gingiva, tongue, or buccal mucosa.2 Associated symptoms include malaise, headache, fever, and cervical lymphadenopathy; however, most ­occurrences are subclinical or asymptomatic.2

A diagnosis that’s more common in children. Primary HSV occurs in people who have not previously been exposed to the virus. While it is an infection that classically presents in childhood, it is not limited to this group. Manifestations often are more severe in adults.1

Utilize PCR for the diagnosis of herpetic gingivostomatitis because of its sensitivity, specificity, and rapid turnaround time.

Following an incubation period of a few days to 3 weeks, the primary infection typically lasts 10 to 14 days.1,2 Recurrence is highly variable and generally less severe than primary infection, with grouped vesicles often recurring in the same spot with each recurrence on the vermillion border of the lip. Triggers for reactivation include immunosuppression, pregnancy, fever, UV radiation, or trauma.1,2

Differential includes other conditions with mucosal lesions

Acute herpetic gingivostomatitis must be distinguished from other disease processes that cause ulcerative mucosal lesions.

Aphthous stomatitis (canker sores) is the most common ulcerative disease of the oral mucosa.3 It presents as painful, punched-out, shallow ulcers with a yellowish gray pseudomembranous center and surrounding erythema.3 No definitive etiology has been established; however, aphthae often occur after trauma.

Continue to: Herpangina...

 

 

Herpangina is caused by coxsackie A virus and primarily is seen in infants and children younger than 5.4 The papulovesicular lesions primarily affect the posterior oral cavity, including the soft palate, anterior tonsillar pillars, and uvula.4

Allergic contact dermatitis is precipitated by contact with an allergen and presents with pain or pruritus. Lesions are erythematous with vesicles, erosions, ulcers, or hyperkeratosis that gradually resolve after withdrawal of the causative allergen.5

Pemphigus vulgaris. Oral ulcerations of the buccal mucosa and gingiva are the first manifestation of pemphigus vulgaris in the majority of patients, with skin blisters occurring months to years later over areas exposed to frictional stress.6 Skin sloughs may be seen in response to frictional stress (Nikolsky sign).6

 

The new Dx gold standard is PCR

Acute herpetic gingivostomatitis usually is diagnosed by history and hallmark clinical signs and symptoms.1 In this case, our patient presented with a sudden eruption of painful blisters on multiple areas of the oral mucosa associated with fever. The diagnosis can be confirmed by viral culture, serology with anti-HSV IgM and IgG, Tzanck preparation, immunofluorescence, and polymerase chain reaction (PCR).1 Viral culture has been the gold standard for mucosal HSV diagnosis; however, PCR is emerging as the new gold standard because of its unrivaled sensitivity, specificity, and rapid turnaround time.7,8 Specimens for PCR are submitted using a swab of infected cells placed in the same viral transport ­medium used for HSV cultures.

Our patient’s culture was positive for HSV-1.

Continue to: Prompt use of antivirals is key

 

 

Prompt use of antivirals is key

Treatment of acute HSV gingivostomatitis involves symptomatic management with topical anesthetics, oral analgesics, and normal saline rinses.1 Acyclovir is an established therapy; however, it has poor bioavailability and gastrointestinal absorption.1 Valacyclovir has improved bioavailability and is well tolerated.1 For primary herpes gingivostomatitis, we favor 1 g twice daily for 7 days.1 Our patient responded well to this valacyclovir regimen and healed completely in 1 week.

CORRESPONDENCE
Robert T. Brodell, MD, 2500 N State St, Jackson, MS 39216; rbrodell@umc.edu

A 29-year-old man with no prior history of mouth sores abruptly developed many 1- to 1.5-mm blisters on the gingiva (FIGURE 1A),tongue (FIGURE 1B), and buccal mucosa ­(FIGURE 1C), which evolved into small erosions accompanied by a low-grade fever 5 days prior to presentation. The patient had no history of any dermatologic conditions or systemic illnesses and was taking no medication.

Irregular ulcerations with a yellowish membrane and erythematous halo on the gingiva (A), lesions on the ventral surface of the tongue (B), and multiple grouped ulcerations on the buccal mucosa (C).
IMAGES COURTESY OF ROBERT T. BRODELL, MD

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Acute primary herpetic gingivostomatitis

Herpes simplex virus (HSV) is the causative agent for acute primary herpetic gingivostomatitis.1 HSV-1 is primarily responsible for oral mucosal infections, while HSV-2 is implicated in most genital and cutaneous lower body lesions.1 Herpetic gingivostomatitis often presents as a sudden vesiculoulcerative eruption anywhere in the mouth, including the perioral skin, vermillion border, gingiva, tongue, or buccal mucosa.2 Associated symptoms include malaise, headache, fever, and cervical lymphadenopathy; however, most ­occurrences are subclinical or asymptomatic.2

A diagnosis that’s more common in children. Primary HSV occurs in people who have not previously been exposed to the virus. While it is an infection that classically presents in childhood, it is not limited to this group. Manifestations often are more severe in adults.1

Utilize PCR for the diagnosis of herpetic gingivostomatitis because of its sensitivity, specificity, and rapid turnaround time.

Following an incubation period of a few days to 3 weeks, the primary infection typically lasts 10 to 14 days.1,2 Recurrence is highly variable and generally less severe than primary infection, with grouped vesicles often recurring in the same spot with each recurrence on the vermillion border of the lip. Triggers for reactivation include immunosuppression, pregnancy, fever, UV radiation, or trauma.1,2

Differential includes other conditions with mucosal lesions

Acute herpetic gingivostomatitis must be distinguished from other disease processes that cause ulcerative mucosal lesions.

Aphthous stomatitis (canker sores) is the most common ulcerative disease of the oral mucosa.3 It presents as painful, punched-out, shallow ulcers with a yellowish gray pseudomembranous center and surrounding erythema.3 No definitive etiology has been established; however, aphthae often occur after trauma.

Continue to: Herpangina...

 

 

Herpangina is caused by coxsackie A virus and primarily is seen in infants and children younger than 5.4 The papulovesicular lesions primarily affect the posterior oral cavity, including the soft palate, anterior tonsillar pillars, and uvula.4

Allergic contact dermatitis is precipitated by contact with an allergen and presents with pain or pruritus. Lesions are erythematous with vesicles, erosions, ulcers, or hyperkeratosis that gradually resolve after withdrawal of the causative allergen.5

Pemphigus vulgaris. Oral ulcerations of the buccal mucosa and gingiva are the first manifestation of pemphigus vulgaris in the majority of patients, with skin blisters occurring months to years later over areas exposed to frictional stress.6 Skin sloughs may be seen in response to frictional stress (Nikolsky sign).6

 

The new Dx gold standard is PCR

Acute herpetic gingivostomatitis usually is diagnosed by history and hallmark clinical signs and symptoms.1 In this case, our patient presented with a sudden eruption of painful blisters on multiple areas of the oral mucosa associated with fever. The diagnosis can be confirmed by viral culture, serology with anti-HSV IgM and IgG, Tzanck preparation, immunofluorescence, and polymerase chain reaction (PCR).1 Viral culture has been the gold standard for mucosal HSV diagnosis; however, PCR is emerging as the new gold standard because of its unrivaled sensitivity, specificity, and rapid turnaround time.7,8 Specimens for PCR are submitted using a swab of infected cells placed in the same viral transport ­medium used for HSV cultures.

Our patient’s culture was positive for HSV-1.

Continue to: Prompt use of antivirals is key

 

 

Prompt use of antivirals is key

Treatment of acute HSV gingivostomatitis involves symptomatic management with topical anesthetics, oral analgesics, and normal saline rinses.1 Acyclovir is an established therapy; however, it has poor bioavailability and gastrointestinal absorption.1 Valacyclovir has improved bioavailability and is well tolerated.1 For primary herpes gingivostomatitis, we favor 1 g twice daily for 7 days.1 Our patient responded well to this valacyclovir regimen and healed completely in 1 week.

CORRESPONDENCE
Robert T. Brodell, MD, 2500 N State St, Jackson, MS 39216; rbrodell@umc.edu

References

1. Ajar AH, Chauvin PJ. Acute herpetic gingivostomatitis in adults: a review of 13 cases, including diagnosis and management. J Can Dent Assoc. 2002;68:247-251.

2. George AK, Anil S. Acute herpetic gingivostomatitis associated with herpes simplex virus 2: report of a case. J Int Oral Health. 2014;6:99-102.

3. Akintoye SO, Greenburg MS. Recurrent aphthous stomatitis. Dent Clin N Am. 2014;58:281-297.

4. Scott LA, Stone MS. Viral exanthems. Dermatol Online J. 2003;9:4.

5. Feller L, Wood NH, Khammissa RA, et al. Review: allergic contact stomatitis. Oral Surg Oral Med Oral Pathol Oral Radiol. 2017;123:559-565.

6. Bascones-Martinez A, Munoz-Corcuera M, Bascones-Ilundain C, et al. Oral manifestations of pemphigus vulgaris: clinical presentation, differential diagnosis and management. J Clin Exp Dermatol Res. 2010;1:112.

7. LeGoff J, Péré H, Bélec L. Diagnosis of genital herpes simplex virus infection in the clinical laboratory. Virol J. 2014;11:83.

8. Centers for Disease Control and Prevention. Genital HSV infections. www.cdc.gov/std/tg2015/herpes.htm. ­Updated June 4, 2015. Accessed September 26, 2019.

References

1. Ajar AH, Chauvin PJ. Acute herpetic gingivostomatitis in adults: a review of 13 cases, including diagnosis and management. J Can Dent Assoc. 2002;68:247-251.

2. George AK, Anil S. Acute herpetic gingivostomatitis associated with herpes simplex virus 2: report of a case. J Int Oral Health. 2014;6:99-102.

3. Akintoye SO, Greenburg MS. Recurrent aphthous stomatitis. Dent Clin N Am. 2014;58:281-297.

4. Scott LA, Stone MS. Viral exanthems. Dermatol Online J. 2003;9:4.

5. Feller L, Wood NH, Khammissa RA, et al. Review: allergic contact stomatitis. Oral Surg Oral Med Oral Pathol Oral Radiol. 2017;123:559-565.

6. Bascones-Martinez A, Munoz-Corcuera M, Bascones-Ilundain C, et al. Oral manifestations of pemphigus vulgaris: clinical presentation, differential diagnosis and management. J Clin Exp Dermatol Res. 2010;1:112.

7. LeGoff J, Péré H, Bélec L. Diagnosis of genital herpes simplex virus infection in the clinical laboratory. Virol J. 2014;11:83.

8. Centers for Disease Control and Prevention. Genital HSV infections. www.cdc.gov/std/tg2015/herpes.htm. ­Updated June 4, 2015. Accessed September 26, 2019.

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