Gingivitis is an inflammatory condition of the gingival tissue or the gums most commonly due to a bacterial infection. It is inflammation of the gingiva with the attachment of the connective tissue to the tooth remaining at the original level, that is, without attachment loss. The condition is restricted to the soft-tissue area of the gingival epithelium and connective tissue. Among all the periodontal diseases, gingivitis is considered to be the commonest. There are various forms of gingivitis based on clinical appearance, duration of infection, severity, and etiology. However, the chronic form of gingivitis that is caused by plaque is considered to be the most common variant. Gingivitis is characterized by swelling and redness in the affected area, along with bleeding upon probing. It is associated with an inflammatory reaction upon the pro-inflammatory cytokines, which are known to be responsible for causing a balance between humoral and cell-mediated immune responses.
Based on the etiology, gingivitis can be classified into five types.
Plaque Induced Gingivitis
This is the most common cause of gingivitis. Plaque is a thin film that forms on the tooth surface due to poor oral hygiene. If not regularly removed, it can harden up and form calculus. As plaque harbors a large number of bacteria, inflammation can occur in the gingival due to the bacteria. The infection usually begins when the immune system of the body gets reduced due to some local or systemic conditions. Also, some local factors can contribute to the formation of plaque, such as crowding of teeth due to which plaque removal becomes difficult. Malaligned teeth often require orthodontic correction, which adds on to the difficulty in cleansing. A dental prosthesis that does not have an adequate fit or is not properly finished can act as a nidus for plaque accumulation. In children, tooth eruption is also frequently associated with gingivitis as plaque accumulation tends to increase in the area where primary teeth are exfoliating, and permanent teeth are erupting as oral hygiene may be difficult to be maintained in these areas. This is referred to as eruption gingivitis. The systemic conditions which can cause gingivitis include blood dyscrasias such as leukemia. It may lead to diffuse gingival swelling.
This form of gingivitis occurs due to the presence of any other infection in the oral cavity, such as dental caries. A hypersensitive reaction to an allergen can trigger the infiltration of plasma cells in the gingiva and causing plasma cell gingivitis. The allergen can be chewing gum, certain components of toothpaste, cinnamon, mint, red pepper, etc. Infectious gingivitis can also occur as a reaction to some low-grade injury to the local tissues such as fractured teeth, overhanging restorations, overextended flanges of the denture, and faulty fixed dental prosthesis with poor pontic design (saddle pontic) or over contoured margins.
This may occur due to deficiency of vitamin C. It has been found that modern lifestyle with the intake of an increased amount of refined carbohydrates and an increased ratio of omega-6 to omega-3 fatty acids can promote the inflammatory process. The mechanism by which carbohydrates with a high glycemic index promotes inflammatory process is through activation of NFkB and oxidative stress.
This form of gingivitis occurs during pregnancy, puberty, or steroid therapy. It has been documented in the literature that in pregnancy, there is an increase in the level of circulating female sex hormones that are responsible for causing pregnancy gingivitis. In puberty, gingival inflammation occurs even without the presence of plaque. This is referred to as puberty gingivitis. It has been found that in the cytoplasm of the cells of the gingiva, receptors for both estrogens and testosterone that have a high affinity for these hormones are present. The receptors for estrogen are specifically present in the basal and spinous layers of the epithelium. In the connective tissue, such receptors are found in the fibroblasts and endothelial cells of small vessels. Therefore, the gingiva is an easy target organ for these steroid hormones resulting in gingivitis. It has been observed that during adolescence, gingivitis appears earlier in girls (eleven to thirteen years) than in boys (thirteen to fourteen years).
Various drugs used for the systemic conditions can cause gingivitis as a side effect such as phenytoin (used for epileptic seizures), calcium channel blockers (used for angina, high blood pressure), anticoagulants and fibrinolytic agents, oral contraceptive agents, protease inhibitors, vitamin A and analogs. The mechanism behind this gingival inflammation is thought to be the ability of the metabolites of these drugs to induce the proliferation of fibroblasts. An imbalance between the synthesis and the degradation of the extracellular matrix leads to the accumulation of immature proteins in the extracellular matrix, particularly collagen. This, in turn, results in gingivitis.
Apart from this, various risk factors can contribute to gingivitis. These include the personal habits of the patient (smoking and tobacco chewing), systemic conditions (diabetes), genetic factors (hereditary gingival fibromatosis), and local conditions (dry mouth, crowded teeth).
Gingivitis is the commonest periodontal disease that is found to be more prevalent in males as compared to females as it has been found that females tend to follow better oral care regimes and thus in maintaining oral hygiene. It is commonly seen in children and adults. Studies have found gingivitis to be more prevalent in people with low socioeconomic status as people with high socioeconomic status tend to show a more positive attitude towards the maintenance of oral hygiene. Also, they have better access to health care options. There have been studies that found gingivitis to be more prevalent in pregnant women as compared to non-pregnant women. Also, the severe form of gingivitis has been found to be predominant in pregnant women.
Inadequate oral hygiene leads to bacterial plaque accumulation which, if not removed, triggers an acute inflammatory response within less than a week. This is the initial stage of gingivitis characterized by an increase in gingival crevicular fluid and number of neutrophils. The collagen fibers start destroying along with the deposition of fibrin. At one week, gingivitis proceeds to an early stage with the transition from neutrophilic to lymphocytic infiltration predominantly. Further progression into the chronic stage leads to an established lesion with predominantly plasma cells and B lymphocytes. As it progresses, pocket formation occurs, resulting in separation of gingiva from the tooth. The persistent inflammation leads to the breakdown of the periodontal ligament and resorption of the adjacent alveolar bone, which may ultimately result in tooth loss.
In most instances, gingivitis may go unnoticed by the patient as the disease may exist and progress without any symptoms. If asymptomatic, the patient may give a history of bleeding from the gingiva while brushing, flossing, and sometimes eating particularly hard food (apples) along with bad breath that does not resolve even after brushing.
The gingival swelling can be graded into four types.
Physical examination of the oral cavity by the dentist may reveal the presence of inflamed, tender, and swollen gingiva that may bleed on probing depending on the stage of gingivitis.
As gingivitis is a soft tissue disease, radiographic evaluation is not helpful. Lab investigations are also routinely not required.
The prime objective of treating gingivitis is to reduce inflammation. This is achieved by using different instruments to remove dental plaque deposits. Gingivitis, in its initial stages, can be easily managed if the patient starts following oral hygiene protocol, which includes regular tooth brushing with the correct technique involved along with flossing. If the condition persists, then it may be due to other etiological factors for which the patient should consult the dentist. If it is drug-induced, the doctor can change the medication to resolve the condition. If it is due to nutritional deficiency, supplements can be prescribed. In the majority of the cases, it is plaque-induced, and therefore the dentist should remove the plaque and/calculus if present by scaling and root planing procedures. Medications in the form of antiseptic mouthwash that contains chlorhexidine can also be used by the patient to disinfect the mouth. Antiseptic and antibiotic chips are also available, which release the medication (chlorhexidine and minocycline) constantly. These can be inserted into the pockets after scaling and root planing. In severe cases, patients can also be prescribed antibiotics. Other causes, such as faulty prosthesis should be identified by the dentist and should be replaced.
There are studies on the effect of medicinal or herbal plants on the management of gingivitis. The mechanism of action of these plants on gingivitis is due to their anti-inflammatory property. Such medicinal plants include pomegranate, tea, and chamomile. The flavonoids and tannins present in these plants are potent anti-inflammatory and astringent phytochemicals. Therefore, they can resolve both gingival bleeding and inflammation. Some studies proved that there is a synergistic effect when the herbal plants are prescribed along with conventional mechanical procedures of plaque removal, such as scaling.
Gingivitis should be differentiated from periodontitis as clinically, and both may present with the same features, such as gingival bleeding on probing. They can be differentiated histologically and radiographically.
The condition gingivitis undergoes through four different stages before progressing to periodontitis if not treated. The different stages of gingivitis were first explained by Page and Schroeder in 1976.
Initial lesion: It is the first stage of gingivitis characterized by the response of resident leukocytes and endothelial cells to the plaque (a bacterial biofilm). This stage is devoid of any clinical signs of inflammation. However, in the histological sections, the changes are evident. The local blood vessels dilate in response to the neuropeptides, which are produced by the cytokines as a result of the metabolic products of bacteria. Then the neutrophils start migrating towards the inflammatory site.
Early lesion: This stage is characterized by an increase in the number of neutrophils. In this stage, the clinical signs of gingivitis, such as redness and bleeding from gingival, start appearing. There is an increase in the gingival crevicular fluid. Histologically, there is a proliferation of the epithelium to form rete pegs. The complement proteins are activated.
Established lesion: This stage is marked by a shift from an innate immune response to an acquired immune response. There is increased collagenolytic activity in this stage along with an increase in the number of macrophages, plasma cells, T and B lymphocytes. Clinically, changes in the color and contour of the gingival can easily be seen along with gingival bleeding. It is categorized under moderate to severe stage of gingivitis.
Advanced lesion: This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible. The inflammatory changes and the bacterial infection starts affecting the supporting tissues of the teeth and the surrounding structures such as gingival, periodontal ligament, and alveolar bone resulting in their destruction and, eventually, tooth loss.
Gingivitis, if identified and treated, can easily be resolved as the condition is reversible in its early stages. However, chronic gingivitis, if left untreated, can progress to periodontitis and can ultimately result in bone destruction, causing tooth loss.
The most common complication or sequelae of chronic gingivitis, if not treated, is the progression of the inflammation towards the underlying tissue and bone, resulting in periodontitis. The ultimate consequence of such an event is tooth loss. Gingivitis always precedes periodontitis. However, gingivitis does not always progress to periodontitis. Chronic gingivitis can progress to acute necrotizing ulcerative gingivitis, also known as trench mouth if not treated and when the patient neglects oral hygiene completely or when the immune system of the patient is compromised. The condition is commonly seen in developing countries where the living conditions are poor. It is categorized under a severe form of gingivitis associated with pain, gingival bleeding, and ulceration. It is characterized by marked gingival edema, spontaneous bleeding, or bleeding in response to minimal local trauma. It may be associated with localized pain, altered taste (metallic taste mostly), and halitosis.
The patient should be educated on the importance of maintaining good oral hygiene, which can prevent the formation of plaque and, thus, gingivitis. Patients should be taught the correct brushing technique, frequency of brushing (twice daily) along with the use of floss. Also, the importance of a balanced diet and regular dental visits every six months should be emphasized. Mouthwash and gel containing antiseptic and anti-inflammatory properties can also be advised to the patient.
To improve the treatment outcome of gingivitis, an interprofessional approach is required to identify the causes of gingivitis and to intervene at an early stage before its progression to periodontitis. Also, a thorough knowledge of the epidemiological pattern is required for planning the public-health services as plaque-induced gingivitis can be seen at any age of the dentate population. The complication of gingivitis i.e., periodontitis, is not just limited to tooth loss, but it has an effect on general systemic health too. Thus, both the dentists and the physicians must be aware of the adverse effects of periodontitis on the systemic health of the patient.
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