Oral Cavity Lichen Planus And Stomatitis Pathology Notes

Oral Cavity

Oral Cavity Lichen Planus

• Lichen planus is usually a self-limited disease that involves both skin and mucosa.
• It most commonly resolves spontaneously 1 to 2 years after onset. Resolution often leaves postinflammatory hyperpigmentation of the area involved.
• Oral lesions may persist for years. Squamous cell carcinoma may develop in chronic mucosal and para mucosal lesions of lichen planus.

Read And Learn More: Pathology for Dental Students Notes

Pathogenesis of Lichen Planus:

The pathogenesis of lichen planus is not known. It appears that expression of altered antigens in basal epidermal cells or the dermo-epidermal junction elicits a cell-mediated cytotoxic (CD8+) T-cell response.

Morphology of Lichen Planus

• Gross of Morphology:
  • Sites:
    • Skin mainly of extremities (wrists and elbows)
    • Glans penis in males, and
    • Oral mucosa
• Skin lesions: They consist of itchy, violaceous, flat-topped papules that may coalesce focally to form plaques. These papules may be highlighted by white dots or lines called
  Wickham striae. Lesions are usually multiple and symmetrically distributed.
• Oral lesions: In the majority (70%) of patients, oral lesions are present as white, reticulated, or net-like areas involving the mucosa.

Microscopy of Lichen Planus:

• Dense, continuous infiltrate of lymphocytes along the dermo-epidermal junction (interface dermatitis) producing on an angulated zigzag contour (sawtooth).
• The lymphocytes are intimately associated with the basal layer of the epidermis, which shows degeneration, and necrosis of the dermo-epidermal interface.
• Anucleate, necrotic basal cells may be found among the inflammatory cells in the papillary dermis and are referred to as colloid or Civatte bodies.

Oral Cavity Stomatitis

Write a short note on Canker sores/aphthous ulcers.

• Stomatitis is the inflammation of the mucus membrane of the mouth.
• It can occur in several diseases.

Aphthous Ulcers (Canker Sores):

Aphthous ulcers are common, often recurrent, exceedingly painful, superficial oral mucosal ulcerations.

Etiology of Stomatitis: Unknown, but may be precipitated by emotional factors, stress, nutritional deficiency,

• Hormonal imbalance etc. Aphthous ulcers may also be associated with immunologic disorders such as celiac disease, inflammatory bowel disease, and Behçet disease.
• They are most common in the first 2 decades of life.
• The lesions appear as single or multiple, shallow, hyperemic ulcers covered by a thin exudate and rimmed by a narrow zone of erythema.
• Initially, the inflammatory infiltrate is mononuclear, but secondary bacterial infection may result in a neutrophilic infiltrate.
• It usually resolves spontaneously in 7 to 10 days. Sometimes it may persist for weeks (for example , in Immunocompromised patients).

Precancerous Lesions Of Oral Cavity

Write a short note on premalignant lesions of the oral cavity.

Leukoplakia and Erythroplakia. Or Write a short note on the definition and morphology of leukoplakia.

1. Leukoplakia:

Definition of Leukoplakia: It is defined as a white patch or plaque, not less than 5 mm in diameter, that cannot be removed (scraped off by rubbing and cannot be classified as any other diagnosable
disease.

If any white patches in the oral cavity can be given a specific diagnosis, it is not leukoplakia.

• Sites: May be seen anywhere in the oral cavity. The most common sites are the buccal mucosa, floor of the mouth, ventral surface of the tongue, palate, and gingiva.
• Number: It may be single or multiple.
• Appearance: White patches or plaques having sharply defined borders. The surface may be smooth or wrinkled.

2. Erythroplakia:

• Less common and appears as a red, velvety area within the oral cavity.
• It remains level with or slightly depressed about the surrounding mucosa.
• Microscopically, the epithelium is atypical and has an increased risk of malignant transformation than leukoplakia.
• Intermediate forms, which have the characteristics of both leukoplakia and erythroplakia, are termed speckled leukoerythroplakia.

Features of Leukoplakia and Erythroplakia:

Age and Gender:

List the differences between erythroplakia and leukoplakia.

• Both leukoplakia and erythroplakia may be found in adults of any age, but they are usually seen between 40 to 70 years.
• Male to female ratio is 2: 1

Etiology:

Write a short note on the etiology and morphology of leukoplakia.

• Both have multifactorial origins.
• Associated with the use of tobacco (cigarettes, pipes, cigars, and chewing tobacco).

Microscopy of Leukoplakia and Erythroplakia:

• Leukoplakia:
  • Surface stratified squamous epithelium shows a spectrum of changes ranging from hyperkeratosis and acanthosis to lesions with variable degree of dysplastic changes (including carcinoma in situ).
  • The subepithelial region shows inflammatory infiltration of lymphocytes and macrophages, the intensity of which is proportional to the degree of dysplasia.
• Erythroplakia:
  • Epithelium shows erosions with dysplasia, carcinoma in situ, or frank carcinoma.
  • The subepithelial region shows intense inflammatory reaction and vascular dilatation, which is responsible for the reddish clinical appearance.

Oral Cavity Hairy Leukoplakia

• Hairy leukoplakia is a distinctive oral lesion and is seen in immunocompromised patients.
• About 80% of patients with hairy leukoplakia are infected with the human immunodeficiency virus (HIV) and the remaining 20% are seen in patients who are immunocompromised for other reasons (for example, Cancer therapy or transplant immunosuppression).
• Etiology: It is due to Epstein–Barr virus (EBV) infection.
• Site: Located mostly on the lateral edges/border of the tongue.

Morphology of Hair Leukoplakia:

• Gross: White, confluent patches of fluffy (“hairy”) thickenings, which cannot be scraped off.
• Microscopy: It shows hyperparakeratosis and acanthosis with “balloon cells” in the upper spinous layer of the epithelium.

Oral Cavity Squamous Cell Carcinoma

In India, oral cavity cancer is the most common malignant tumor.

Etiology of Squamous cell carcinoma:

Write a short note on the etiology of squamous cell carcinoma of the oral cavity.

Squamous cell carcinoma (SCC) of the oral cavity is a multifactorial disease usually seen in middle-aged men.

Risk Factors Squamous cell carcinoma:

1. Tobacco products and smoking:

Any irritating smoked product increases the risk of tumors of the oral cavity. Nicotine in tobacco and other tobacco leaf components causes cancer.

Carcinogens in tobacco can act as initiators, as well as promoters. Risk increases with the amount and duration of tobacco use. Tobacco may be used either for smoking or as
smokeless tobacco.

• Smoking: It may be in the form of cigarette, beedi, cigar, pipe smoking, or reverse smoking (smoking a cheroot with the burning end inside the mouth is practiced in certain regions of India). Regular marijuana use has also been associated with oropharyngeal cancer.
• Smokeless tobacco:
  • It is in the form of a betel quid/pan that contains several ingredients such as areca nut, slaked lime, and tobacco, which are wrapped in a betel leaf.
  • It is commonly used in India and Southeast Asia and is associated with a marked increase in oral cancer.
  • Betel quid appears to be the major carcinogen. However, it may also be related to slaked lime and the areca nut.
  • Other methods of tobacco consumption include snuff dipping and tobacco chewing.
  • Oral cancers are found on the buccal and gingival surfaces in the sites where tobacco products are held in contact with the mucosa for long periods.

2. Alcohol consumption of Squamous cell carcinoma:

It is another important etiologic factor and acts synergistically with tobacco as either a cocarcinogen (increasing the risk) or a promoter (decreasing the lag time). The risk of oral SCC is magnified in individuals who smoke as well as consume alcohol.

3. Other risk factors of Squamous cell carcinoma:

• Radiation exposure and solar actinic radiation (sunlight).
• Welding, metal refining, diesel exhaust, wood stove, and asbestos exposure.
• Chronic irritation of the mucosa: It may be due to ill-fitting dentures, jagged teeth, or chronic infections.
• Vitamin A deficiency and immunosuppression.
• Poor nutrition.

Role of Oncogenic HPV Virus Infection:

High-risk HPV types 16 and 18 and, less commonly low-risk HPV types 6 and 11 have been found in oral carcinomas.

Inherited Genomic Instability:

A family history of head and neck cancer is a risk factor and is thought to be due to inherited genomic instability.

Pathogenesis of Squamous cell carcinoma:

Write a short note on the etiology and morphology of oral cancer.

The development of squamous cell carcinoma is a multi-step process. It involves sequential activation of oncogenes and inactivation of tumor suppressor genes in a clonal population of
cells.

• Inactivation of the p16 gene (about 80% of the cases) → stratified squamous epithelium undergoes hyperplasia/hyperkeratosis.
• Mutation of the p53 tumor suppressor gene is associated with the progression of hyperplasia/ hyperkeratosis to dysplasia.
• Amplification and overexpression of the cyclin D1 gene constitutively activate cell cycle progression.

Morphology of Squamous cell carcinoma:

• Site: Anywhere in the oral cavity. Common sites are the lower lip, the ventral surface of the tongue, the floor of the mouth, the buccal mucosa, the soft palate, and the gingiva.
• Gross:
  • Early stages: It appears either as raised, firm, pearly plaques or as irregular, roughened, or verrucous areas of mucosal thickening. May be superimposed on a leukoplakia or erythroplakia.
  • Later: It may appear as ulcerated and protruding gray-white masses with irregular and indurated (rolled) borders.
• Microscopy: Squamous cell carcinomas range from well-differentiated keratinizing neoplasms to poorly differentiated/anaplastic tumors. However, the histological grading does not correlate with behavior.

Spread of Squamous cell carcinoma:

• Local: The tissue involved depends on the primary site.
• Lymph node: The involved site of the lymph node depends on the location of the primary tumor. The more anterior the tumor, more is spread to the cervical nodes. Carcinomas of the base of the tongue and oropharynx metastasize to the deep retropharyngeal lymph nodes.
• Blood spread: It spreads to the lungs, liver, and bones.

Verrucous of Squamous cell carcinoma:

Verrucous carcinoma (Ackerman tumor) is a variant of well-differentiated squamous cell carcinoma.

• Site: Most common in the buccal mucosa and lower gingiva.
• Age and gender: Most are elderly males.
• Etiology: Tobacco, especially chewing or snuff dipping, and HPV infection.

Morphology of Squamous cell carcinoma

• Gross: Large, fungating, soft papillary growth.
• Microscopy: The surface epithelium shows hyperkeratosis, acanthosis, and benign-appearing papillomatosis. Rete pegs are swollen and voluminous and extend into the deeper tissues.
• Spread: May infiltrate the soft tissues of the cheek, mandible, or maxilla, and invade perineurial spaces. Regional lymph node metastases are exceedingly rare, and distant metastases have not been reported.

Oral Cavity Odontogenic Cysts

• The majority of odontogenic cysts are derived from remnants of odontogenic epithelium present within the jaws.
• Epithelial-lined cysts are quite common in the jaws.

Dentigerous (Follicular) Cyst:

Definition of Odontogenic Cysts: It is a cyst that originates around the crown of an unerupted tooth and is thought to be due to the accumulation of flid between the developing tooth and the dental follicle.

• Radiography: These are unilocular lesions most often associated with impacted third molar (wisdom) teeth.
• Microscopy: They are lined by a thin layer of stratified squamous epithelium. Dense chronic inflammatory cell infiltrate is seen in the connective tissue stroma.
• Treatment: Complete removal of the cyst is curative.

Odontogenic Keratocyst (OKC):

• Also called a keratocystic odontogenic tumor.
• It must be differentiated from other odontogenic cysts because of its aggressive behavior.
• Can be seen at any age but are most often between ages 10 and 40.
• It occurs most commonly in males within the posterior mandible.
• The majority are solitary.
• Radiography: Well-defied unilocular or multilocular radiolucencies.
• Microscopy: The cyst is lined by a thin layer of keratinized stratified squamous epithelium with a prominent basal cell layer. It has a corrugated epithelial surface.
• OKCs are locally aggressive and recurrence rates are high.

Odontogenic Tumors

• Odontogenic tumors constitute a group of lesions having diverse histologic appearances and clinical behavior. Some are true neoplasms (both benign and malignant), while others are likely to be hamartomas.
• Odontogenic tumors are derived from odontogenic epithelium, ectomesenchyme, or both. Ameloblastoma is the most common and clinically significant tumor.

Ameloblastoma of Odontogenic Tumors:

Write a short note on the pathology of ameloblastoma.

Write a short note on ameloblastoma.

• Most common slow-growing, benign but locally invasive epithelial odontogenic tumor. It has an indolent course in most cases.

• Age: Most often seen during the 3rd to 5th decades of life.
• Sites: Commonly arise in the molar ramus and the maxilla.
• Origin: Arises from the odontogenic epithelium and shows no ectomesenchymal differentiation.
• Radiology: Shows multilocular destruction of the involved bone.
• Gross: It is grey-white, commonly cystic, and replaces and expands the involved bone.
• Microscopy: It can show various patterns:
  • Follicular pattern: It is the most common pattern. The tumor shows follicles of varying sizes and shapes separated by fibrous tissue. The follicles appear similar to the enamel organ and consist of a central area of stellate cells resembling the stellate reticulum. The central area may show cystic changes. The peripheral layer of these follicles is cuboidal to columnar and appears to have a palisading arrangement.
  • Plexiform pattern: The tumor cells form irregular plexiform masses or networks of strands. The stroma is scanty and may show microcyst formation.
  • Acanthomatous pattern: Islands of tumor cells show squamous metaplasia.
  • Basal cell pattern: Appears similar to basal cell carcinoma of the skin.
  • Granular cell pattern: Tumor cells have acidophilic granular cytoplasm.
• Treatment: Wide surgical resection to prevent recurrences.