Gingivitis is inflammation of the gingival tissues in the absence of clinical attachment lost. It may be characterized by edema, erythema, increased gingival temperature, and occasionally pain. As the inflammation and loss of connective tissue is confined to the soft tissues, teeth are not in jeopardy of being lost.
Gingivitis is ordinarily reversible with appropriate therapy. Periodontitis is inflammation that affects and destroys the attachment apparatus. The histology is marked by apical migration of the junctional epithelium from the cementoenamel junction, loss of connective tissue attachment, loss of periodontal ligament, and destruction of bone.
Increased probing depths may occur or the gingivitis may recede as attachment is lost. Continuation of this loss of attachment will eventually lead to the loss of the tooth. The progress of periodontitis may be arrested with proper therapy. In certain situations, lost attachment apparatus may be surgically regenerated.
Gingival disease modified by systemic factors:
Puberty-associated gingivitis, menstrual cycle-associated gingivitis, and pregnancy-associated gingivitis. These conditions are all associated with changes in steroid hormone levels, primarily progesterone and estrogen. Gingivitis have been associated with increased levels of Prevotella intermedia in the inflamed sites.
In puberty-associated gingivitis, the gingivitis inflammation may be exaggerated even with apparently minimal amounts of plaque. Menstrual cycle-associated gingivitis may appear in a very mild form. Increased gingival crevicular fluid flow has been seen in a majority of subjects during ovulation.
Pregnancy-associated gingivitis has perhaps the most radical changes, with the possible appearance of a pyogenic granuloma. It is an extreme response to gingivitis inflammation, characterized as a painless protuberance of the gingiva that bleeds readily at slight provocation.
Gingivitis modified by medications. There are three major drugs that can induce an overgrowth of gingival tissues. Phenytoin is used as an antiseizure medication, nifedipine and several of the other calcium channel blockers are antihypertensive/antiarrhythmic drugs, and cyclosporine A is an immunosuppressant.
Overgrowth appears to be related to the level of plaque accumulation. Approximately 50% of phenytoin patients are susceptible to this overgrowth. It has been estimated that 20% of patients on calcium- channel blockers, and 20% to 30% of patients on cyclosporine A are susceptible to drug-induced gingivitis overgrowth.
Nonplaque-induced gingival lesions. Many of these lesions are relatively rare with the exception of the herpes- virus and Candida infections. Herpesvirus infections must be cautiously treated due to their contagious nature while the lesions are shedding virus.
Treatment of gingivitis must be deferred when the patient presents with a weeping lesion. Candida infections may be problematic if there is no apparent cause (recent antibiotic use, illness) for the infection. Candida infections have a high association with human immunodeficiency virus (HIV) infection, so a thorough patient work-up may be necessary in the face of an unexplainable Candida infection.
Gingivitis manifestations of systemic conditions. Mucocutaneous disorders: These disorders include the dermatologic/autoimmune diseases of lichen planus, pemphigoid, pemphigus vulgaris, erythema multiforme, lupus erythematosus, and drug-induced disorders.
These disorders at one time were classified as desquamative gingivitis, a descriptive term signifying desquamation or falling away of the surface epithelium of the gingiva. These gingivitis disorders are actually auto- immune in nature with no clear etiology. It is critical that a definitive diagnosis be obtained, for while they all may have a similar appearance, pemphigus has a higher morbidity, while the mucocutaneous disorders are difficult to manage for patient comfort.
Gingivitis manifestations of systemic conditions: Linear gingival erythema.
This lesion is characterized by a bright erythematous margin of the free gingiva. It is associated with immunosuppression, particularly HIV infection. The erythema does not resolve with the removal of plaque.
Gingivitis manifestations of systemic conditions: Allergies. Allergic reactions may take on a variety of forms from mild erythema and edema to severe inflammation to an apparent lichenoid appearance. The challenge is to be sure that the inflammation is not plaque related.
A diagnosis of plasma cell gingivitis may be made by biopsy. The allergen must then be identified and, if possible, eliminated from the oral cavity. Allergens include amalgam, base metals used in fixed prosthodontics, flavoring agents in dentifrices and chewing gum, chili peppers, and other foodstuffs. It may be difficult to identify the offending agent. Changes must be made one at a time, often a time-consuming process, in order to identify the allergen.
What Are Some of the Distinguishing Characteristics of the New Classifications of Gingivitis?
Gingivitis associated with dental plaque only. As the name implies, bacterial plaque must be present to initiate the gingival inflammation. This inflammation may be characterized by changes in gingival color, contour, and possibly consistency; slight elevation of intrasulcular temperature; bleeding on gentle probing; an increase in gingival crevicular fluid flow (now as an exudate); and the inflammation is confined to the soft tissues. Local factors may include restoration overhangs, open contacts, and other plaque traps and impediments to good oral hygiene.
How Is a Periodontal Case Type Formulated Using the American Academy of Periodontology Case Type System?
The case type refers to the level of disease severity, not the specific diagnosis. Case type may be applied to each type of gingivitis and periodontitis.
Case Type 1: Gingivitis, the gingivitis Inflammation confined to the soft gingival tissues only. All gingivitis, irrespective of the level of inflammation, is considered to be in this category.
Case Type 2: Mild Periodontitis. This category signifies the beginning of attachment loss, up to approximately 20% of the attachment apparatus on the root. There may be some pocketing and initial mobility. Furcation involvement, when present, is confined to a Class I involvement.
Case Type 3: Moderate Periodontitis. This category signifies further loss of the attachment apparatus, up to approximately 40% to 45%. There is increased bone loss, pocket depth, mobility, and furcation involvement. Furcas may have Class II involvement.
Case Type 4: Severe Periodontitis. There is severe attachment loss, deep gingivitis pocketing, and mobility, pathology migration of teeth, and Class II and possibly Class III furcation involvement.