Obvious erythema & edema. No stippling, bleeding on probing
Fiery redness, edematous & hyperplastic swelling, complete absence of stippling, bleeding on probing & spontaneous hemorrhage.
Mild gingivitis in anterior area : Mild erythema in maxilla. Slight edematous swelling & erythema. In mandible, slight edematous swelling & erythema. Papilla Bleeding Index : Grade 1 & 2 Stained plaque : Small plaque accumulations arounds the necks of the teeth & in interdental areas.
The two earliest symptoms of gingival inflammation preceding established gingivitis are:
increased gingival crevicular fluid production rate and
bleeding from the gingival sulcus on gentle probing
shown that bleeding on probing appears earlier than a change in color or other visual signs of inflammation.
Moderate gingivitis in anterior teeth :Erythema & enlargement of gingiva pronounced in mand than in maxilla. Papilla Bleeding Index : grade 3 & 4 Stained plaque : Moderate plaque accumulation in maxilla. Heavier plaque in mandible. Radiographically, no destruction of interdental bony septa.
The most common cause of abnormal gingival bleeding on probing is chronic inflammation. The bleeding is chronic or recurrent and is provoked by mechanical trauma (e.g., from toothbrushing, toothpicks, or food impaction) or by biting into solid foods such as apples.
In cases of moderate or advanced periodontitis, the presence of bleeding on probing is considered a sign of active tissue destruction.
Acute episodes of gingival bleeding are caused by injury or occur spontaneously in acute gingival disease.
Spontaneous bleeding or bleeding on slight provocation can occur in acute necrotizing ulcerative gingivitis. In this condition, engorged blood vessels in the inflamed connective tissue arc exposed by ulceration of the necrotic surface epithelium.
Gingival bleeding Associated with Systemic Changes
In some systemic disorders, gingival hemorrhage occurs spontaneously or after irritation and is excessive and difficult to control.
A hemostatic mechanism failure and result in abnormal bleeding (vitamin C deficiency or allergy such as Schonlein-Hchoch purpura) , platelet disorders (thrombocytopcnic purpura) , hypopro-thrombincmia (vitamin K deficiency) , other coagulation defects (hemophilia, leukemia, Christmas disease)
Both chronic and acute inflammation produce changes in the normal firm, resilient consistency of the gingiva.
As noted in the preceding discussion, in chronic gingivitis, both destructive (edematous) and reparative (fibrotic) changes coexist and the consistency of the gingiva is determined.
Changes in the Surface Texture of the Cingiva
Loss of surface stippling is tin early sign of gingivitis. In chronic inflammation the surface is either smooth and shiny or firm and nodular, depending on whether the dominant changes are exudative or fibrotic.
Interproximally, inflammation spreads to the loose connective tissue around the blood vessels, through the fibers, and then into the bone through vessel channels that perforate the crest of the interdental septum at the center of the crest toward the side of the crest or at the angle of the septum and it may enter the bone through more than one channel.
Less frequently, the inflammation spreads from the gingiva directly into the periodontal ligament and from there into the interdental septum.
Facially and lingually, inflammation from the gingiva spreads along the outer periosteal surface of the bone and penetrates into the marrow spaces through vessel channels in the outer cortex.
Characteristic clinical findings in patients with chroni periodontitis include supragingival and subgingiva plaque accumulation that is frequently associated with calculus formation, gingival inflammation, pocket formation, loss of periodontal attachment and loss of alveolar bone.
The gingiva ordinarily is slightly to moderately swollen and exhibits alterations in color ranging from pale red to magenta.
The rate of disease progression is usually slow but may be modified by systemic and/or environmental and behavioral factors.
Onset of chronic periodontitis can occur at any time, and the first signs may be detected during adolescence in the presence of chronic plaque and calculus accumulation.
Chronic periodontitis does not progress at an equal rate in all affected sites throughout the mouth. Some involved areas may remain static for long periods of time/ whereas others may progress more rapidly.
More rapidly progressive lesions occur most frequently in interproximal areas and are usually associated with areas of greater plaque accumulation and inaccessibility to plaque control measures
Periodontal destruction is frequently seen among family members and across different generations within a family, suggesting the possibility of a genetic basis to the susceptibility to periodontal disease.
Recurrent studies have demonstrated a familial aggregation of localized and generalized aggressive periodonlitis.