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6. Gingivitis. Classification. Clinic, diagnosis, treatment and prophylaxis of catarrhal, hypertrophic and ulcerative-necrotic gingivitis. Localized periodontitis. Clinic, diagnosis, treatment and prevention.

The characteristics of gingival diseases in general have been described by Mariotti (1999) and are presented in Table 1. Although most, if not all, pathological conditions of the gingiva are affected to greater or lesser extents by bacterial activity, this section concentrates on:

(1) Those inflammatory conditions whose etiology is solely attributable to bacteria within dental plaque, excluding gingival inflammation associated with active destructive periodontitis.

(2) Those gingival conditions which, although primarily plaque induced, are modified by systemic disease or medication.

Table 1. Characteristics common to all gingival diseases.

From Mariotti (1999)

 

Typical bacterial gingivitis is usually a painless condition, even when the gums are bleeding. They become bright red and swell up. They are less firm than usual and may even be movable. They are likely to bleed during brushing and perhaps eating. Sometimes they bleed at night.

Herpetic gingivostomatitis also turns the gums bright red, but it can be easily distinguished because it’s usually quite painful. There are dozens of tiny white or yellow sores visible in the gums and inner cheeks.

The tartar that can be seen at the gum line may be the tip of the iceberg. It generally spreads between the teeth and gums, forcing the two apart and living in the newly created pocket. There, the bacteria release chemicals that can eat away at the bones that hold the roots of the teeth. These same chemicals cause bad breath. Eventually the teeth are no longer firmly fixed in position; they get loose and either fall out or have to be pulled out. This advanced form of gingivitis is called periodontitis. Surprisingly, it often causes no pain and the patient becomes aware of the disease due to bleeding gums or loose teeth.

Trench mouth, also known as Vincent’s infection, is a particularly severe form of gingivitis caused by a combination of two bacteria. Your dentist may refer to it by its other name, acute necrotizing ulcerative gingivitis (or ANUG). This disease causes a rapid onset of swelling, bleeding, severe pain, and terrible bad breath. The gums are grey in colour, and are often misshapen. The papillae (the pointed part of the gum between the teeth) often become flat and have an area of dead tissue. The disease is usually found to affect those in times of severe stress (e.g., students during exam sessions) and smokers. Its name dates back to the First World War when it often developed among soldiers in the trenches.

 

Gingivitis is easily diagnosed by the appearance of the gums. The appearance of the inflammation will help your doctor or dentist distinguish a bacterial infection from the herpes virus. Scrapings could yield information on the species of bacteria involved, but it’s rarely relevant to treatment, so it’s not generally done.

Occasionally, gingivitis is the first sign of some other disease such as diabetes or leukemia. A doctor may want to give someone with gingivitis a more thorough examination if there is severe gum disease for no apparent reason.

Gum disease has been linked to various health concerns such as premature birth, lung disease, heart disease, stroke, and heart attack. For clinical descriptive purposes, the gingiva may be divided into three zones

1. Marginal gingiva: The tissue at the junction of a tooth. Thus, for example, an inflammation confined only to this area may be termed a marginal gingivitis.

2. Papillary gingiva: The tissue in the interproximal area. Inflammation confined to this area may be termed papillary gingivitis.

3. Attached gingiva: The remaining gingival tissue extending from the marginal/papillary areas to the mucogingival junction. Changes throughout the vertical extent of the attached gingiva can be termed diffuse

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Characteristics of plaque-induced gingivitis.

 

 

 

 

 

 

 

 

 

 

 

Fig. Generalized hypertrophic gingivitis.

 

 

The use of the terms localized and generalized provides a useful descriptor of location for gingival changes within the mouth. For example, a subject may be characterized as having an area of diffuse gingivitis localized to the lower incisor area that is superimposed on a generalized marginal and papillary gingivitis. Exposure of the gingival tissues to dental plaque results in inflammation within the tissues which manifests as clinical signs of gingivitis. Table 7-3 describes typical alterations from health to disease commonly seen clinically. There are changes in color, size, shape, consistency and tendency for bleeding from the gingival sulcus. Patients may complain of bleeding on brushing and halitosis.

 

Pain is generally not a feature of dental plaque induced gingivitis although tenderness when brushing may be a complaint. Raised sulcus temperature has also been shown to be a feature of plaque induced gingival inflammation (Haffajee et al. 1992, Wolff et al. 1997, Loe et al. 1965, Muhlemann & Son 1971, Poison & Goodson 1985, Engelberger et al. 1983). The primary etiological factor, dental plaque, may be encouraged to accumulate by local factors facilitating its retention in marginal and papillary areas. Calculus, vertical or horizontal marginal deficiencies in restorations and rough surfaces on teeth or restorations are examples of such factors (Mariotti 1999). The reversibility of the condition is worth particular note. Loe et al. (1965) demonstrated a causal effect of dental bacterial plaque on the development of gingivitis.

 

 

GINGIVITIS ASSOCIATED WITH

LOCAL CONTRIBUTING FACTORS

 

 

 

Tooth abnormalities such as enamel pearls and cemental tears

 

There are several factors related to tooth anatomy suchas enamel projections and enamel pearls that modify or predispose to plaque induced gingival disease (Blieden 1999). Enamel pearls are ectopic deposits of enamel and various shapes, usually associated with furcation areas on molars (Moskow &Canut 1990). Enamel pearls are found in 1.1-5.7% of molar teeth and the maxillary second molars are most commonly involved (Loh 1980)regime. Increasing levels of inflammation developed in association with increasing plaque formation.

Abatement of these inflammatory levels to baseline levels followed the re-introduction of effective plaque control measures.

 

HISTOPATHOLOGIC FEATURES OF GINGIVITIS

Upon exposure to the organisms within dental plaque, changes occur in the gingival vascular complex, the cellular content of the connective tissue and in the junctional epithelium. These underlying alterations are largely responsible for the clinical changes described above (Egelberg 1966).Vascular changes include substantial increases in the number of patent vessels. Dilation of the vessels is also a feature. Alterations in permeability of the vessel walls and in the hydrostatic pressure within these vessels give rise to fluid and cellular exchange between blood and gingival connective tissue. Edema and color changes to a more red or reddish blue are consequences of these underlying changes. The junctional epithelium shows infiltration with migrating leucocytes and up to 70% of the volume of the affected region of the junctional epithelium may be made up of bacteria and their products as well as cellular, fluid and molecular products of the inflammatory lesion in the underlying connective tissue. This disrupted junctional epithelium, together with the increased number of patent vessels in the plexus of vessels contiguous to the junctional epithelium, is responsible for the tendency for inflamed gingiva to bleed on gentle stimulation. There is an increase in sulcular fluid flow and a concomitant increase in the number of leukocytes found in the gingival fluid (Payne et al. 1975, Page & Schroeder 1976, Greenstein et al. 1981).

 

 

HISTOPATHOLOGIC FEATURES OF GINGIVITIS

Upon exposure to the organisms within dental plaque, changes occur in the gingival vascular complex, the cellular content of the connective tissue and in the junctional epithelium. These underlying alterations are largely responsible for the clinical changes described above (Egelberg 1966).

Vascular changes include substantial increases in the number of patent vessels. Dilation of the vessels is also a feature. Alterations in permeability of the vessel walls and in the hydrostatic pressure within these vessels give rise to fluid and cellular exchange between blood and gingival connective tissue. Edema and color changes to a more red or reddish blue are consequences of these underlying changes. The junctional epithelium shows infiltration with migrating leucocytes and up to 70% of the volume of the affected region of the junctional epithelium may be made up of bacteria and their products as well as cellular, fluid and molecular products of the inflammatory lesion in the underlying connective tissue. This disrupted junctional epithelium, together with the increased number of patent vessels in the plexus of vessels contiguous to the junctional epithelium, is responsible for the tendency for inflamed gingiva to bleed on gentle stimulation. There is an increase in sulcular fluid flow and a concomitant increase in the number of leukocytes found in the gingival fluid (Payne et al. 1975, Page & Schroeder 1976, Greenstein et al. 1981).

GINGIVITIS ASSOCIATED WITH LOCAL CONTRIBUTING FACTORS

Tooth abnormalities such as enamel pearls and cemental tears

 There are several factors related to tooth anatomy such as enamel projections and enamel pearls that modify or predispose to plaque induced gingival disease (Blieden 1999). Enamel pearls are ectopic deposits of enamel and various shapes, usually associated with furcation areas on molars (Moskow &Canut 1990). Enamel pearls are found in 1.1-5.7% of molar teeth and the maxillary second molars are most commonly involved (Loh 1980).

Dental restorations

Subgingival margin discrepancies of restorations and violation of the biologic width can affect the health of the adjacent gingival tissues (Bjorn et al. 1969, Garguiloet al. 1961). Subgingival margins of restorations can cause greater inflammation when compared with subgingival restorative margins (Nevins & Skurow 1984). The severity of the marginal discrepancy, the amount of time it is present and the ability of the patient to maintain the area free of plaque are important factors in determining the extent of damage to the periodontium. Root fractures Root fractures are often associated with inflammation of the gingivae because of the enhanced plaque accumulation in the fracture line (Meister et al. 1980).

Cervical root resorption

 Cervical root resorption may result in inflammation particularly when a communication is established with the gingival sulcus leading to enhanced plaque formation .

 

 

TREATMENT OF PLAQUE INDUCED GINGIVITIS

The treatment of plaque induced gingivitis is primarily self-administered plaque control. Although mechanical plaque control remains the mainstay for plaque control, chemical control of plaque is an effective option for those individuals who, because of physical or mental disability, cannot effectively apply mechanical means. However, the presence of plaque retaining factors, such as dental calculus or inadequate restorations, may result in either method being ineffective. Professional intervention is needed to eliminate these as an adjunct to self-administered plaque control. The important sequel of gingivitis is progression of the inflammatory process to involve the underlying connective tissue attachment and periodontal ligament which, in a proportion of susceptible individuals (currently thought to be approximately 10%), leads to major destruction of most of the supporting structures of the dentition . The data currently available would suggest that periodontitis can be successfully halted in the majority of individuals by elimination of the causative bacteria and their products, thereby reducing the levels of inflammation. The return of inflammation to sites treated for periodontitis is not uncommon in susceptible patients. The possibility exists that this recurrent inflammation may be confined to the gingival tissues and may not lead to further periodontal attachment loss. However, as there are currently no reliable methods to confirm such a phenomenon, the return of inflammation is viewed by clinicians as a recurrence of periodontitis and not as a gingival contained inflammation that is reversible with oral hygiene methods alone (Mariotti 1999, Sheiham 1997).

 

GINGIVAL DISEASES MODIFIED BY ENDOCRINE FACTORS

Pregnancy associated gingivitis

 

Pregnancy is associated with an exaggerated response of the gingiva to local irritants. The gingivae show levels of inflammation, often characterized by edema, color and contour change and propensity to bleed on with testosterone levels >_ 8.7 nmol/L). Mouth breathing, which often accompanies Angle’s classification 2 division 1 malocclusion, is considered by some to be an exacerbating factor in children and adolescents. A differentiation between the effects of mouth breathing and hormonal influences on gingival inflammation can therefore be difficult.

Menstrual cycle associated gingivitis

Although bright red hemorrhagic lesions have been described prior to the onset of menses, clinically detectable changes do not seem to be associated with the menstrual cycle. However, an increase in gingival fluid by 20% has been described in 75% of women during ovulation (Muhlemann 1948, Hugoson 1971). Treating and Preventing Gingivitis

Thorough flossing and brushing can prevent gingivitis. Tartar control toothpaste, though not scientifically evaluated, may also help with prevention.

Some types of antibacterial mouthwash may also be helpful. The most effective ones contain the ingredient chlorhexidine (e.g., Perichlor®, Denti-Care®). Most traditional mouthwashes contain high amounts of alcohol, which may cause alcohol burn. These mouthwashes can be very irritating to already inflamed gums. They also do not get rid of sulphur-containing compounds (bacteria toxins) that cause bad breath. Mouthwashes containing chlorhexidine or chlorine dioxide will control bacterial growth.

Electric toothbrushes are also more effective than manual toothbrushes in removing the plaque that causes gingivitis.

Studies have shown that brushing can prevent gingivitis in adults and children. Flossing appears not to help in children, though it’s a good habit for them to form. However, people with diseases that make gingivitis more likely (such as diabetes) shouldn’t rely on good oral hygiene alone to prevent it. Treating the disease itself is very important in preventing gingivitis.

Once plaque has turned to tartar, only a dentist can remove it. Dentists recommend having your teeth professionally cleaned every year or every 6 months. Plaque and tartar removal can also be the treatment for early gingivitis. Once the plaque and tartar are gone, the inflammation tends to subside quickly.

If the disease develops into periodontitis, periodontal deep cleaning or periodontal surgery may be needed. This involves opening up the gums to get at the infected area. Infected tissue is removed, and the root of the threatened tooth is scaled (the tartar is scraped off). Sometimes this can be done without actually cutting the gum (periodontal deep cleaning). Really severe disease might even require bone grafts.

Acute herpetic gingivostomatitis can’t be cured, but it goes away on its own after about 2 weeks. Pregnancy tumours can be removed by a dentist.

Trench mouth, or acute necrotizing ulcerative gingivitis (ANUG), can be treated with appropriate antibiotics and thorough tooth and gum cleaning by a dental professional. Early treatment by your dentist is recommended.

Postmenopausal women who have desquamative gingivitis may benefit from hormone replacement therapy.