Gingivitis: Forms, Clinical, and Morphological Features
Gingival inflammation (gingivitis) often acts as a precursor to more severe periodontal lesions. Depending on etiology and pathogenesis, several specific forms are distinguished:
- Acute necrotizing ulcerative gingivitis (Vincent's disease). Develops in immunocompromised individuals. The causative agents are a symbiosis of Fusobacterium fusiforme and Treponema vincentii. The process begins with necrosis of the interdental papillae and is accompanied by a fetid odor. A severe complication is noma (gangrenous stomatitis), which destroys deep facial tissues.
- Plasmacytic gingivitis. Characterized by diffuse gingival enlargement. Morphologically, it features an inflammatory infiltrate composed of plasma cells, along with spongiosis and intraepithelial microabscesses.
- Granulomatous gingivitis. Represents a hypersensitivity reaction to foreign bodies (e.g., dental materials, gold, or nickel particles). Manifests as small red spots in the interdental papillae zone.
- Desquamative gingivitis. Characterized by accelerated shedding of the surface epithelium, vesicle formation, and erosions. Often a local manifestation of systemic autoimmune disorders (lupus erythematosus, lichen planus, pemphigus).
- Chronic hyperplastic gingivitis. Frequently associated with mouth breathing (in asthma or nasal pathologies).
Periodontitis: Pathogenesis and Severity Stages
Periodontitis is characterized by chronic, immune-mediated, productive inflammation involving all periodontal tissues. The pathogenetic chain begins with marginal gingivitis, followed by dental plaque and calculus formation. Deepening of the gingival sulcus leads to the formation of a pathological periodontal pocket, lined with granulation tissue and stratified squamous epithelium. Osteoclastic bone resorption of the dental alveolus (lacunar, horizontal, and vertical) occurs.
The severity of the process is assessed using clinical and radiographic data:
- Initial stage: pocket depth up to 2.5 mm, bone loss up to 1/4 of the root length.
- Mild stage: pocket depth 2.5–3.5 mm, bone loss up to 1/3 of the root, incomplete tooth mobility.
- Moderate stage: pocket depth 3.5–5 mm, bone loss up to 1/2 of the root, grade 1 mobility and diastemats/tremas appear.
- Severe stage: pocket depth greater than 5 mm, bone loss exceeding 1/2 of the root length. Grade 2–3 mobility is observed, with potential complete loss of the ligamentous apparatus and tooth loss.
Aggressive periodontitis is distinguished separately; it is associated with immune system defects, genetic markers (HLA-DRB1), and a hyperergic response to Porphyromonas gingivalis.
Dystrophic and Idiopathic Periodontal Lesions
In addition to inflammatory diseases, primarily dystrophic processes can develop in the periodontium.
Periodontosis is a generalized disease with no history of preceding gingivitis. It is based on bone tissue dystrophy accompanied by smooth bone resorption and vascular wall hyalinization. In early stages, periodontal pockets are absent; the gingiva is pale and firm. As it progresses, tooth roots become exposed, hypersensitivity develops, and fan-shaped tooth migration occurs (mobility appears only in the late stage).
Desmodontosis (idiopathic progressive periodontolysis) is a rare form occurring primarily in children. It is characterized by rapid bone lysis without an osteoclastic reaction. The causative agent is often Actinobacillus actinomycetemcomitans. The disease frequently accompanies severe systemic syndromes (histiocytosis, Gaucher disease, Down syndrome, diabetes mellitus).
Gingival fibromatosis (elephantiasis of the gums) is a slowly progressive proliferation of fibrous connective tissue. It can be idiopathic or hereditary (associated with Laband and Murray–Puretic–Drescher syndromes).