Parulis (epulides) and granulomas
The terms “epulis”, “parulis” and “gingival lump” are collective terms used in clinical practice to denote polypoid gingival lesions of unclear etiology. In most cases, these are reactive and inflammatory processes arising in response to chronic trauma (poorly fitting crowns, overhanging fillings, roots of decayed teeth).
Main types of epulides:
- Peripheral giant cell (reparative) granuloma. Develops in the soft tissues of the gingiva without primary bone involvement. When large, it may cause partial resorption of the alveolar process (a saucer-shaped depression on radiographs). Microscopically, it consists of fibrous tissue, myofibroblasts, mononuclear histiocytes, and multinucleated osteoclast-like cells. Sinusoidal blood flow, hemorrhages, and hemosiderin deposits are characteristic. Requires radical excision due to a tendency for recurrence.
- Angiomatous epulis. More common in children, adolescents, and pregnant women. This is a soft, bluish lesion with high bleeding tendency, histologically resembling capillary hemangioma.
- Fibromatous epulis. A firm, painless, pink overgrowth. Arises as an outcome of chronic productive inflammation when granulation tissue transforms into mature connective tissue.
Pyogenic granuloma and bacillary angiomatosis are clinically similar to epulides but are classified separately in modern nomenclature. Pyogenic granuloma has a lobular structure (a central vessel surrounded by capillaries and fibromyxoid tissue). Bacillary angiomatosis is caused by bacteria of the genus Bartonella and is typical for HIV-infected patients.
Pathologies of the lips and tongue
This group of mucosal diseases includes specific inflammatory processes of the lips (cheilitis) and tongue (glossitis).
Forms of cheilitis:
- Exfoliative: affects only the vermilion border of the lips, manifesting as chronic epithelial desquamation.
- Glandular: associated with congenital heterotopias and hypertrophy of minor salivary glands with subsequent infection.
- Contact (allergic): delayed-type hypersensitivity (DTH) reaction to allergens.
- Meteorological: inflammation caused by climatic factors (wind, UV radiation, cold).
- Precancerous forms: abrasive pre-cancerous cheilitis of Manganotti and actinic cheilitis.
Forms of glossitis:
- Desquamative (“geographic tongue”): alternation of areas of epithelial desquamation and areas of regeneration, creating a specific changing pattern on the tongue.
- Rhomboid: a chronic process of unclear etiology. Manifests as a lack of papillae and papillomatosis in a strictly demarcated rhomboid area anterior to the circumvallate papillae.
Stomatitis
Stomatitis represents a heterogeneous group of inflammatory, infectious, and allergic diseases of the oral mucosa. Opportunistic infections caused by opportunistic flora account for a significant proportion.
- Candidal stomatitis. Caused by Candida fungi in the setting of immunodeficiency, diabetes mellitus, antibiotic therapy, or poor hygiene. The acute pseudomembranous form (thrush) is characterized by soft white plaques, beneath which the erythematous mucosa is exposed.
- Herpetic stomatitis. Caused by herpes simplex virus type 1 (HSV-1). Manifests as painful vesicles and ulcers. The virus can persist in a latent form in the trigeminal ganglion, reactivating under stress or ultraviolet exposure. A pathognomonic sign is multinucleated giant cells with eosinophilic intranuclear inclusion bodies.
- Recurrent aphthous stomatitis. A chronic disease characterized by the formation of painful ulcers (aphthae) with an erythematous halo on the movable mucosa. The pathogenesis is associated with delayed-type hypersensitivity reactions.
- Medication-induced stomatitis. Develops via various hypersensitivity mechanisms: anaphylactic (Type I immediate hypersensitivity), fixed drug eruptions (Type III hypersensitivity with vasculitis), and contact (Type IV delayed-type hypersensitivity).
Precancerous lesions
It's important to distinguish precancerous lesions from preneoplastic diseases. The key criterion for precancer is histological detection of moderate or severe epithelial dysplasia. Current terminology uses the concepts of squamous intraepithelial neoplasia (SIN / SIN) and squamous intraepithelial lesions (SIL / SIL).
Leukoplakia and keratoses are clinical terms for white (or yellow-brown in smokers) plaques. The term "keratosis" is used when localized to the vermilion border of the lips, hard palate, gingiva, and dorsum of the tongue; "leukoplakia" is used for other areas. Microscopy reveals basal and spinous layer hyperplasia, acanthosis, and parakeratosis.
Briefly: answers to topical questions
What are the types of odontogenic jaw cysts?
Odontogenic jaw cysts are divided into developmental and inflammatory cysts. The following types are distinguished:
- Radicular cyst — a periapical cyst of inflammatory origin; includes apical, lateral, and residual radicular cysts.
- Paradental cyst — inflammatory collateral, mandibular, infected buccal cyst.
- Follicular cyst — a tooth-containing cyst.
- Odontogenic keratocyst — primordial cyst.
- Eruption cyst.
- Lateral periodontal cyst.
- Gingival cyst of infants and gingival cyst of adults.
- Glandular odontogenic cyst — sialo-odontogenic cyst.
- Subperiosteal cyst.
What is the pathogenesis and microscopic structure of the wall of a radicular jaw cyst?
The pathogenesis of a radicular cyst is associated with chronic inflammation and includes stages of fibrous capsule formation around the granuloma, its epithelialization, fluid secretion, and transformation of the cystogranuloma into a cyst. Microscopically, the cyst wall has a layered structure:
- Fibrous capsule — the outer connective tissue layer adjacent to the bone, sometimes containing calcifications.
- Granulation tissue — the middle layer with diffuse inflammatory infiltration and cholesterol crystals.
- Epithelial lining — the inner layer, represented by stratified squamous non-keratinizing epithelium.
During periods of inflammation exacerbation, the epithelium actively proliferates, forming characteristic reticulated extensions into the wall thickness.
What non-odontogenic (fissural) jaw cysts are distinguished in maxillofacial pathology?
In maxillofacial pathology, the following non-odontogenic or fissural cysts are distinguished, the development of which is associated with impaired facial embryogenesis:
- Nasopalatine duct cyst — incisive canal cyst; develops from epithelial remnants in the nasopalatine canal and is localized between the central maxillary teeth.
- Nasolabial cyst — nasoalveolar cyst; localized on the anterior wall of the maxilla in the projection of the roots of the lateral incisor and canine.
- Globulomaxillary cyst — globular-maxillary cyst; localized in the upper jaw between the lateral incisor and canine. In modern classification, it may be regarded not as a separate nosology, but as a keratocystic odontogenic tumor, lateral periodontal cyst, or radicular cyst.
What else to study on this topic
- Pathogenesis of sinusoidal blood vessel formation in reparative granuloma
- Histological picture of hyperkeratosis and acanthosis in leukoplakia
- Differential diagnosis of fixed drug eruptions
- Mechanisms of HSV-1 reactivation from the trigeminal ganglion
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