Marginal gingivitis is chiefly caused by local irritating factors, such as calcareous deposits on the teeth, food impaction, rough or overhanging filling margins and other dental restorations, misalignment of teeth, open contacts or other morphologic faults causing improper function, and hygienic neglect. These factors are, of course, complicated by such conditions as allergies, mouth breathing, medications, tobacco smoking, and hormonal changes. As with periodontal disease, individuals may be genetically predisposed to the development of this condition. Marginal gingivitis is the first stage in a complex periodontal syndrome that is further characterized by pocket formation and inflammation of the investing tissues (periodontitis) and, finally, by periodontal abscesses (see Plate 2-36). Clinically, the gingiva is conspicuous for a shiny pink, red, or even cyanotic surface, edema, and a strong bleeding tendency of the margins and papillae of the gum. In the initial stages of the condition, there is a deepening of the sulcus between the tooth and the gingiva; this is followed by a band of erythema, indicative of the inflamed gingiva, which can be along one or, most often, multiple teeth, resulting in edema of the inter- dental papillae that easily induces bleeding.
Hypertrophic gingivitis describes a frequent variation of the marginal type of inflammation, depending upon the individual response and the chronicity. An increase in size of the papillae is more noticeable than that of the free margin of gum and is especially related to accretions of calculus on the teeth. Hormonal alterations, as in menstruation, pregnancy, and menopause, will increase the degree of hypertrophy. Diffuse, idiopathic fibromatosis of the gingiva, which is free of inflammation, is normal in color, and presents a uniform proliferation of the gingiva in a firm, bulging mass throughout the jaw, is another form of hypertrophic gingivitis; it is similar to the gingival hyperplasia resulting from use of phenytoin.
Although the most common form of gingivitis, plaque-induced gingivitis, is limited to gingivitis associated with dental plaque and is distinct from other presentations of gingivitis, the bacterial plaque initiates the host response. The plaque accumulates in the interdentition gaps, the gingival grooves, and plaque traps that harbor plaque. The bacteria in the plaque activate lipopolysaccharides or lipoteichoic acid, which promotes the inflammatory response causing gingival hyperplasia. As the disease progresses, the bacterial situation becomes more complex, with an increase in numbers and types of bacteria present.
Necrotizing ulcerative gingivitis, or fusospirochetal gingivitis, commonly known as trench mouth, is a noncontagious opportunistic infection caused by bacte- ria indigenous to the mouth in a host with reduced tissue resistance. Predisposing factors include tobacco smoking, viral respiratory illnesses, poor nutritional status, psychological stress, and immunocompromised states such as HIV/AIDS. Chemoradiation therapy may also be a predisposing factor. Local causes include all conditions promoting growth of anaerobic organisms, such as gum flaps over third molar teeth, crowded and malpositioned teeth, inadequate contact areas, food impaction areas, and poor oral hygiene.
The flora of necrotizing ulcerating stomatitis typically includes one or more types of spirochetes and a fusiform bacillus. Ulceration and pseudomembrane formation are the specific lesions seen in this condition.
The acute form presents with a sudden onset of oral pain and constitutional symptoms of elevated temperature and malaise; it is more often seen in children or immunocompromised individuals. Submandibular lymphadenopathy is variable. Severe pain, a strong characteristic, malodourous breath, and gingival bleeding are marked; objectively, these signs are related to flat, punched-out, grayish ulcers, which erode the tips of the papillary gingivae and spread to the margins, which are covered by a thin diphtheritic-like membrane. On slight pressure, bleeding may occur from all affected areas. In severe cases the lesions spread to the tongue, palate, pharynx, and tonsils; profuse salivation, a thickly coated tongue, and bleeding are seen.
Chronic necrotizing gingivitis is a milder form of this disease; it exists from the outset or is a slowed down phase of the acute form. Subjective symptoms are much reduced. The first awareness is of bleeding when brushing the teeth. Careful retraction of the papillae may be necessary to reveal the typical necrosis. Pain is usually absent. The typical odor develops later because destruction proceeds slowly. The response to therapy is far slower in long-established cases, and recurrence is a constant hazard. As the architecture of the gingiva is altered, anaerobic areas are created and food retention is abetted, so that therapy against the infection alone is of only momentary value; it must be directed to a restoration of the proper gingival form.