Gingivitis: Forms and Clinical-Morphological Features
Gingival inflammation (gingivitis) often acts as a pre-stage to more severe lesions. Depending on the etiology and pathogenesis, several specific forms are distinguished:
- Acute necrotizing ulcerative gingivitis (Vincent's disease). It develops in immunocompromised individuals. The causative agent is a symbiosis of Fusobacterium fusiforme and Treponema vincentii. The process begins with necrosis of the interdental papillae and is accompanied by a putrid odor. A formidable complication is noma (gangrenous stomatitis), which affects the deep tissues of the face.
- Plasmacytic gingivitis. Characterized by diffuse gingival enlargement. Morphologically, it is defined by an inflammatory infiltrate of plasma cells, as well as spongiosis and intraepithelial microabscesses.
- Granulomatous gingivitis. Represents a reaction to foreign bodies (e.g., dental materials, gold or nickel particles). It manifests as small red spots in the interdental papillae area.
- Desquamative gingivitis. Characterized by enhanced shedding of the surface epithelium, vesicle formation, and erosions. Often a local manifestation of systemic autoimmune pathologies (lupus erythematosus, lichen planus, pemphigus).
- Chronic hyperplastic gingivitis. Frequently associated with mouth breathing (in bronchial asthma or nasal pathologies).
Periodontitis: Pathogenesis and Severity Grades
Periodontitis is characterized by chronic immune productive inflammation involving all periodontal tissues. The pathogenetic chain begins with marginal gingivitis, followed by the formation of dental plaque and calculus. Deepening of the gingival sulcus leads to the formation of a pathological periodontal pocket lined with granulation tissue and stratified squamous epithelium. Osteoclastic resorption of the alveolar bone occurs (lacunar, horizontal, and vertical).
The severity of the process is assessed based on clinical and radiological data:
- Initial stage: pocket depth up to 2.5 mm, bone loss up to 1/4 of the tooth root length.
- Mild grade: pocket 2.5–3.5 mm, bone loss up to 1/3 of the root, incomplete tooth mobility.
- Moderate grade: pocket 3.5–5 mm, bone loss up to 1/2 of the root, grade 1 mobility and tremas appear.
- Severe grade: pocket greater than 5 mm, bone loss exceeding 1/2 of the root. Grade 2–3 mobility is observed, with possible complete loss of the ligamentous apparatus and tooth loss.
Aggressive periodontitis is distinguished separately, 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 prior history of gingivitis. It is based on bone tissue dystrophy accompanied by smooth bone resorption and vascular wall hyalinosis. In early stages, periodontal pockets are absent, the gingiva is pale and firm. As it progresses, tooth roots become exposed, hyperesthesia develops, and fan-shaped tooth displacement occurs (mobility appears only at the severe stage).
Desmodontosis (idiopathic progressive periodontolysis) is a rare form occurring predominantly in children. It features rapid bone tissue 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 overgrowth of fibrous connective tissue. It can be both idiopathic and hereditary (in Laband and Murray-Puretic-Drescher syndromes).
Briefly: answers to topical questions
Which types of dental deposits participate in the pathogenesis of periodontitis?
- Subgingival dental plaque contributes to the development of periodontitis.
- Subgingival calculus belongs to dental deposits participating in the pathological process of periodontal diseases; it forms as a result of dental plaque calcification by gingival fluid and serum salts and is located beneath the gingival margin on the tooth root surface.
Which cells predominate in the inflammatory infiltrate in chronic periodontitis?
The sources do not specify which cells predominate in the inflammatory infiltrate in chronic periodontitis. It is noted that the infiltrate contains macrophages, lymphocytes, and plasma cells; neutrophilic leukocytes are also described in the granulation tissue of the periodontal pocket.
Distinguishing periodontitis from periodontosis is simple: "Periodontitis is Infection and pockets, Periodontosis is Recession of the gums and root exposure without inflammation."
Class and exam questions
What is the main difference between periodontitis and periodontosis?
Periodontitis begins with gingival inflammation and is always accompanied by periodontal pocket formation. Periodontosis is a primarily dystrophic bone process proceeding without preceding gingivitis, where pathological pockets are initially absent.
Which microorganisms cause Vincent's disease?
This is an opportunistic infection caused by a symbiosis of Plaut-Vincent's bacilli (Fusobacterium fusiforme) and Vincent's spirochetes (Treponema vincentii). Both microorganisms are permanent residents of the oral cavity.
What is noma and when does it occur?
Noma, or gangrenous stomatitis, is a formidable complication of acute necrotizing ulcerative gingivitis. The process affects the lips, cheeks, and deep facial tissues, taking the form of black gangrene, and can lead to death from sepsis or pneumonia.
What else to study on this topic
- Histological structure and cellular composition of the periodontal pocket wall.
- Mechanisms of osteoclastic and smooth bone tissue resorption.
- Hereditary and systemic diseases associated with desmodontosis.
- Morphological changes in the dental pulp and cementum in periodontitis.
- Genetic markers of aggressive periodontitis.
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