Ulcerative Lesions
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Table of Contents
- Actinomycosis
- Acute Necrotizing Ulcerative Gingivitis (ANUG, Vincent’s disease, trench-mouth)
- Aphthous Stomatitis (aphthous ulcers, canker sore)
- Behçet’s Disease (BS, silk-road disease)
- Crohn’s Disease
- Histoplasmosis
- Lupus Erythematosus
- Squamous Cell Carcinoma (epidermoid carcinoma)
- Syphilis
- Tuberculosis
ACTINOMYCOSIS
Actinomycosis is a rare infection caused by filamentous anaerobic gram-positive bacteria of the Actinomycetaceae family, mainly the israelii species. The disease leads to suppurative and granulomatous soft tissue lesions. Risk factors for actinomycosis include immunosuppression, osteoradionecrosis, leukemia, and mucosal damage. The common clinical presentation includes:
- Pain, paresthesia, low-grade fever, and persistent swelling.
- Discharge with drainage fluid containing yellow sulfur granules (bacterial colonies).
- Hard, chronic enlargement of the jaw.
- Bone lesions may be destructive with accompanying rarefaction and/or sclerosis.
- Mandible is the most common site.
Diagnosis can be challenging because of nonspecific presenting signs (pain, edema) and nonspecific imaging findings (necrotic/cystic areas surrounded by fibrosis). Diagnosis is based on the lesion history, clinical presentation and cytological findings, which may include:
- Peripheral club-like structures in bacterial colonies.
- Positive bacterial culture.
Your differential diagnosis should include:
- Another infection (fungal, staphylococcal, streptococcal).
- Malignant neoplasm.
Treatment options include:
- Surgical debridement.
- Antibiotics (penicillin).
ANUG
Acute Necrotizing Ulcerative Gingivitis (ANUG, Vincent’s disease, trench-mouth) is a relatively rare non-communicable microbial disease caused by Fusobacterium nucleatum, Borrelia vincentii, and other bacterial species including Prevotella. If left untreated, ANUG can progress to cause rapid tissue destruction and/or necrotizing ulcerative periodontitis (NUP). Risk factors for ANUG include an impaired host immune response, poor oral hygiene, nutritional deficiencies, intense smoking, and psychological stress. The common clinical presentation includes:
- Edematous and blunted (“punched-out”) interdental papillae with crateriform necrosis.
- Pain, regional lymphadenopathy, fetor oris (bad breath), fever, and malaise.
- Ulcerated areas are covered with a grayish pseudomembrane.
- Gingiva bleeds easily.
Diagnosis is usually based on the lesion history and clinical presentation only. Your differential diagnosis should include:
- Leukemia or other Immunosuppression-related condition.
- Other infections (herpetic gingivostomatitis).
- Vesiculobullous diseases (mucous membrane pemphigoid, erosive/bullous lichen planus, pemphigus vulgaris, paraneoplastic pemphigus).
Treatment options include:
- Identification and elimination of predisposing factor(s).
- Local debridement and ultrasonic scaling.
- Instructions related to oral hygiene (at home care).
- Topical chlorhexidine or povidone-iodine.
- Systemic antibiotics (tetracycline, metronidazole).
APHTHOUS STOMATITIS
Aphthous Stomatitis (aphthous ulcers, canker sore) is a common not contagious condition that affects around 20% of the population. It results in the formation of recurrent painful ulcers on non-keratinized oral mucosa. The cause is idiopathic and multifactorial, likely involving the activation of a cell-mediated immune response. Risk factors for aphthous ulcers include increased stress/anxiety, hormonal changes, dietary changes, and trauma. The common clinical presentation includes:
- Recurrent painful ulcers commonly restricted to non-keratinized oral/pharyngeal mucosa.
- Well-circumscribed ulcers with yellow fibrinous base and erythematous halo.
- Usually 1-4 episodes a year.
There are three common clinical forms:
- Minor variant – the most common subtype that leads to multiple small (<1cm) oval/round ulcers which heal after a week or two.
- Major variant – also called Sutton’s ulcers, they are generally larger (>1cm) solitary ulcers that may persist for many weeks and often heal with scarring.
- Herpetiform variant – the least common subtype that often leads to large (10-100) groups of small (1-2mm) superficial ulcers that heal within a week or two. The ulceration is not linked with the herpes simplex virus.
Diagnosis is usually based on the lesion history and clinical presentation only. Your differential diagnosis should include:
- Traumatic ulceration.
- Chancre.
- Herpes simplex stomatitis.
- Cyclic neutropenia.
Treatment options include:
- Identification and elimination of predisposing factor(s).
- Palliative care.
- Tetracycline-based oral rinse.
- Topical corticosteroid therapy.
- Intralesional corticosteroid injections.
- Short-duration systemic corticosteroids.
Behçet’s Disease
Behçet’s Disease (BS, silk-road disease) is an incurable multisystem autoimmune disorder of unknown etiology that leads to inflammation of the blood vessels. BS can affect the skin, mucosa, joints, eyes, vessels, nervous and gastrointestinal system. Mucocutaneous lesions are a hallmark of BS. Risk factors for BS include fatigue/stress, histamine-rich food (fermented foods, alcohol, aged cheeses, eggplant, avocado, citrus foods, dried fruit, legumes, and processed meats), and smoking. The common clinical presentation includes:
- Painful oral ulceration mainly localized on the lips, gingiva, cheeks and tongue.
- Ulcerations disappear in 3-4 days without scarring.
- May include ocular lesions and cutaneous ulcers or acne-like papulopustular lesions.
- Superficial venous thrombosis and deep vein thrombosis (DVT) are the most frequent vascular manifestations
Diagnosis is usually based on the lesion history and clinical presentation only. Your differential diagnosis should include:
- Erythema multiforme.
- Reiter’s syndrome.
- Crohn’s disease.
- Mucous membrane pemphigoid.
- Erosive lichen planus
Treatment options include:
- Systemic corticosteroids.
- Immunosuppressive medications (interferon, TNFα inhibitors, Azathioprine, cyclosporine, chlorambucil, methotrexate).
- Thalidomide.
- Dapsone (antibiotic) and colchicine (anti-inflammatory).
CROHN'S DISEASE
Crohn’s Disease is a subtype of inflammatory bowel disease (IBD) that causes chronic relapsing transmural inflammation of any section of the gastrointestinal tract, leading to abdominal pain, diarrhea, obstruction, weight loss and/or perianal lesions. The cause of Crohn’s disease is unknown and the condition is progressive and destructive. The common clinical presentation includes:
- Oral granulomas (submucosal nodules).
- Polypoid masses with fissures and ulceration along the buccal/labial sulcus.
- Aphthous-like oral ulcers.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include non-caseating epithelioid granulomas within submucosa. Your differential diagnosis should include
- Fungal or mycobacterial infections.
- Tertiary syphilis and other treponemal infections.
- Major aphthous ulcers
Treatment options include:
- Palliative management of intestinal symptoms.
- Non-steroidal anti-inflammatory drugs and/or systemic corticosteroids.
- Intralesional corticosteroid injections.
HISTOPLASMOSIS
Histoplasmosis is a fungal infection caused by Histoplasma capsulatum which is endemic to the Ohio and Mississippi River valleys. Transmission is via spore inhalation, leading to pulmonary lesions with possible dissemination to secondary sites. Most infections are subclinical and self-limiting in immunocompetent patients. Organ involvement due to disseminated histoplasmosis can be fatal if untreated. The common clinical presentation includes:
- Chronic ulcerations with necrosis.
- Elevated nodular margins around ulcers that may resemble squamous cell carcinoma.
- A cobblestone appearance on the tongue
Diagnosis is based on the lesion history, clinical presentation and serological findings or culture analysis. Your differential diagnosis should include:
- Tuberculosis.
- Squamous cell carcinoma or other malignancy.
- Other deep fungal infections (coccidioidomycosis, cryptococcosis, and blastomycosis).
- Chronic traumatic ulcer.
- Tertiary syphilis.
- Crohn’s disease.
Treatment options include various antifungal agents (Amphotericin B, ketoconazole, fluconazole, itraconazole). The condition may be self limiting and the prognosis is generally good.
LUPUS ERYTHEMATOSUS
Lupus Erythematosus is an incurable multisystem autoimmune disease most common in women over 40 years of age. It is characterized by abnormal autoantibody production and immune complex deposition. Symptoms are variable, and may include joint pain, fever, hair loss, mouth ulcers, lymphadenopathy, lethargy, and a red rash on the face (butterfly rash). Risk factors include exposure to sunlight, smoking, vitamin D deficiency, and certain infections. There are three forms/variations; discoid lupus erythematosus, subacute cutaneous lupus erythematosus, and systemic lupus erythematosus. Oral lesions are seen in about 40% of patients with systemic lupus erythematosus. The common clinical presentation includes:
- Lichenoid, keratotic, and erosive mucosal lesions.
- Labial vermilion with crusted, exfoliative, erythematous, and keratotic appearance.
- Butterfly rash.
Diagnosis is based on the lesion history, clinical presentation, direct immunofluorescent examination and microscopic findings, which may include:
- Deposits of immunoglobulins and complement proteins.
- Vacuolar interface dermatitis.
Your differential diagnosis should include:
- Lichen planus.
- Candidiasis.
- Lichen planus or lichenoid reaction.
- Leukoplakia.
Treatment options include:
- Systemic corticosteroids and other immunosuppressive agents.
- Topical corticosteroid agents for intraoral lesions.
- Low-dose hydroxychloroquine.
- Intralesional corticosteroid injections.
SQUAMOUS CELL CARCINOMA
Squamous Cell Carcinoma (epidermoid carcinoma) is the most common head and neck malignancy. The tongue is the most common subsite and is associated with higher mortality when compared to other affected areas. Risk factors include tobacco-derived carcinogens, excessive alcohol consumption, and possibly exposure to human papillomavirus (HPV 16 and 18). The common clinical presentation includes:
- Early lesion – white or red-white macule (leukoplakia, erythroplakia).
- Mature lesion – ulceration, induration, elevated margins.
- Advanced lesion – may impede function/movement or erode adjacent bone.
- Most likely found on the lateral surface of the tongue, floor of the mouth, and lower lip vermilion.
- Trismus or cervical lymphadenopathy may indicate metastases.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- Invasive islands and cords of epithelial cells.
- Nuclear pleomorphism with large nuclei (increased nuclear to-cytoplasmic ratio).
- Dyskeratosis.
- Architectural disorganization of proliferating cells.
Your differential diagnosis should include:
- Chronic traumatic ulcer.
- Primary syphilis.
- Actinic keratosis.
- Keratoacanthoma.
- Wart.
- Another neoplasm (basal cell carcinoma or melanoma).
Treatment options include:
- Surgical excision.
- Combined surgery and radiation therapy.
- Chemotherapy.
SYPHILIS
Syphilis is a sexually transmitted infection caused by the helically coiled spirochaete bacterium Treponema pallidum. It may also be transmitted from a mother to her child during pregnancy or at birth, resulting in congenital syphilis. There are four stages of infection (primary, secondary, tertiary and latent) and symptoms may vary accordingly. The common clinical presentation includes:
Primary syphilis (highly infectious):
- A firm nodule or papule.
- Painless labial ulceration that appears firm (indurated).
- Intraoral chancre (ulcer covered by a pseudomembrane).
- Regional cervical lymphadenopathy.
- Spontaneous resolution.
Secondary syphilis (highly infectious):
- Develops 6 weeks to 6 months after initial untreated lesion.
- Reddish brown macular cutaneous rash peri-orally.
- Irregular serpiginous ulcers/erosions covered by mucoid exudate.
- Lymphadenopathy.
- Spontaneous resolution.
Tertiary syphilis:
- Develops 3 to 10 years after initial untreated lesion.
- Atrophic glossitis with leukoplakia-like features.
- Painless gumma (often large, destructive, solitary granulomatous ulcer) commonly seen on the midline of the tongue or palate.
Congenital syphilis:
- Presents with the Hutchinson’s triad: interstitial keratitis, malformed teeth (Hutchinson incisors and mulberry molars), and eighth nerve deafness.
Diagnosis is based on the lesion history, clinical presentation, serological and direct fluorescent antibody studies, and microscopic findings which may include:
- Positive result using dark field microscopy of serous fluid from a chancre.
- Abundant spirochetes embedded within a mixed cellular inflammatory infiltrate.
Since the condition exists in many variations, your differential diagnosis should include:
- Viral infections (measles, rubella, mononucleosis).
- Deep fungal infection.
- Kawasaki disease.
- Traumatic ulcer
- Squamous cell carcinoma.
- Leukoplakia.
- Midline granuloma.
- Condyloma acuminata.
- Genital warts.
- Herpes simplex, herpes zoster.
Treatment options include:
- Parenteral penicillin or ceftriaxone.
- Oral tetracycline or doxycycline.
TUBERCULOSIS
Tuberculosis is an infectious disease usually caused by the Gram-positive highly aerobic bacteria Mycobacterium tuberculosis. Though it generally affects the lungs, other parts of the body (including the oral cavity) may be involved. If not treated, tuberculosis has a 50% mortality rate. The common clinical presentation includes:
- Chronic, non healing indurated ulcer with raised rolled borders.
- Chronic cough with blood-containing mucus, fever, night sweats, and weight loss.
- Intrabony lesions are lytic and sequestrate appearing (radiographically) similar to osteomyelitis.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- Centrally necrotic granulomas with peripheral multinucleated Langhans’ giant cells.
- Positive Fite or Ziehl-Neelsen tissue staining of microorganisms.
Your differential diagnosis should include:
- Squamous cell carcinoma.
- Syphilis.
- Deep fungal infection
- Traumatic ulcer.
- Lymphoma.
Treatment of TB uses antibiotics to kill the bacteria. Effective TB treatment is difficult due to the structure of the mycobacterial cell wall and the possible presence of multidrug-resistant organisms. Treatment usually involves systemic chemotherapy (isoniazid, rifampin, pyrazinamide, ethambutol, streptomycin).
