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Periodontitis is a chronic inflammatory disease of the gums resulting from an opportunistic infection of endogenous plaque biofilm. It usually manifests as a worsening of gingivitis and then, if untreated, with loosening and loss of teeth. Other symptoms are rare except in patients with HIV infection or in whom abscesses develop, in which case pain and swelling are common. Diagnosis is based on inspection, periodontal probing, and x-rays. Treatment involves dental cleaning that extends under the gums and a vigorous home hygiene program. Advanced cases may require antibiotics and surgery.
Periodontitis usually develops when gingivitis, usually with abundant plaque and calculus beneath the gingival margin, has not been adequately treated. In periodontitis, the deep pockets can harbor anaerobic organisms that do more damage than those usually present in simple gingivitis. The organisms trigger chronic release of inflammatory mediators, including cytokines, prostaglandins, and enzymes from neutrophils and monocytes. The resulting inflammation affects the periodontal ligament, gingiva, cementum, and alveolar bone. The gingiva progressively loses its attachment to the teeth, bone loss begins, and periodontal pockets deepen. With progressive bone loss, teeth may loosen, and gingiva recedes. Tooth migration is common in later stages, and tooth loss can occur.
The classifications described here are based on the American Academy of Periodontology's (AAP) classification system for periodontal diseases and conditions (1999):
Other AAP designations are abscesses of the peridontium, periodontitis associated with endodontic lesions, and developmental or acquired deformities and conditions. In developmental or acquired deformities and conditions, faulty occlusion, causing an excessive functional load on teeth, plus the requisite plaque and gingivitis may contribute to progression of a particular type of periodontitis characterized by angular bony defects.
Chronic periodontitis is the most common type of periodontitis. It occurs most often in adults > 35 yr, but adolescents and even children with primary dentition can be affected. It is characterized by its slow rate of progression, with periods of exacerbation and remission, and also by a correlation between the extent of destruction and the presence of local factors such as plaque.
About 85% of the population is affected to a mild degree, but the most advanced cases are seen in < 5% of the population. Because of its slow progression, the patient's age at presentation is not always indicative of when the disease started. Patients with significant disease tend to be > 35 yr, and tooth loss typically starts in a patient's 40s.
Based on the extent of disease, chronic periodontitis is classified further as
Aggressive periodontitis is much less common than chronic periodontitis. It usually occurs in children (sometimes before age 3 yr) or young adults but also occurs in older adults. It is characterized by its familial aggregation and rapid progression of bone loss and even tooth loss. The extent of destruction usually is disproportionate to the extent of plaque or calculus. By definition, patients have no systemic illness, whereas in periodontitis as a manifestation of systemic disease, patients do have a systemic illness. Neutrophil and macrophage/monocyte function may be abnormal.
Localized aggressive periodontitis (formerly called localized juvenile periodontitis), occurs mostly in healthy adolescents. Patients often have significant colonization of Aggregatibacter actinomycetemcomitans (formerly Actinobacillus actinomycetemcomitans), and a strong antibody response to infecting bacteria often occurs. Typically, the signs of inflammation are minor. The disease is detected by periodontal probing or x-rays, which show localized, deep (vertical) bone loss. Disease involves at least two of the 1st molars and incisors and no more than two other teeth. Bone loss progresses faster than in chronic periodontitis, often at a rate of 3 to 4 μm/day; it is unclear whether localized aggressive periodontitis can be self-arresting.
Generalized aggressive periodontitis (formerly called rapidly progressive periodontitis) occurs mostly in patients aged 20 to 35. It is often associated with A. actinomycetemcomitans , Porphyromonas gingivalis , Eikenella corrodens , and many gram-negative bacilli, but cause and effect are not clear. A weak antibody response to infecting bacteria often occurs. All teeth may be affected, which must include ≥ 3 that are not 1st molars or incisors.
Prepubertal periodontitis, an uncommon type of aggressive periodontitis (and not recognized in the 1999 AAP classification), can result from one of the genetic disorders listed below (see Periodontitis as a manifestation of systemic disease) but also may have its own mutation. It affects deciduous teeth, usually shortly after eruption. Generalized acute proliferative gingivitis and rapid alveolar bone destruction are its hallmarks. Patients also have frequent bouts of otitis media and are usually diagnosed by age 4 yr. In some patients, the disease resolves before the permanent teeth erupt.
Periodontitis as a manifestation of systemic disease is considered in patients who have inflammation disproportionate to plaque or other local factors and who also have a systemic disease. However, distinguishing whether a disease is causing periodontitis or contributing to plaque-induced periodontitis is often difficult.
Systemic diseases associated with hematologic disease that can manifest as periodontitis include
Systemic diseases associated with genetic disorders that can manifest as periodontitis include
Familial, and cyclic neutropenia
Leukocyte adhesion deficiency syndromes
Glycogen storage disease
Infantile genetic agranulocytosis
Ehlers-Danlos syndrome (types IV and VIII)
Necrotizing ulcerative periodontitis is a particularly virulent, rapidly progressing disease. It is often called HIV-associated periodontitis because HIV is a common cause. Clinically, it resembles acute necrotizing ulcerative gingivitis combined with generalized aggressive periodontitis. Patients may lose 9 to 12 mm of attachment in as little as 6 mo.
Pain is usually absent unless an acute infection forms in one or more periodontal pockets or if HIV-associated periodontitis is present. Impaction of food in the pockets can cause pain at meals. Abundant plaque along with redness, swelling, and exudate are characteristic. Gums may be tender and bleed easily, and breath may be foul. As teeth loosen, particularly when only one third of the root is in the bone, chewing becomes painful.
Inspection of the teeth and gingiva combined with probing of the pockets and measurement of their depth are usually sufficient for diagnosis. Pockets deeper than 4 mm indicate periodontitis.
Dental x-rays reveal alveolar bone loss adjacent to the periodontal pockets.
Treatment of modifiable risk factors such as poor oral hygiene, diabetes, and smoking improves outcomes.
For all forms of periodontitis, the first phase of treatment consists of thorough scaling (professional cleaning with hand or ultrasonic instruments) and root planing (removal of diseased or toxin-affected cementum and dentin followed by smoothing of the root) to remove plaque and calculus deposits. Thorough home oral hygiene is necessary and includes careful brushing, flossing, and use of a rubber tip to help clean. It may include chlorhexidine swabs or rinses. A therapist should help teach the patient how to do these procedures. The patient is reevaluated after 3 wk. If pockets are no deeper than 4 mm at this point, the only treatment needed is regular cleanings. Sometimes a flap of gum tissue is made to allow access for scaling and planing of deeper parts of the root.
If deeper pockets persist, systemic antibiotics can be used. A common regimen is amoxicillin 500 mg po tid for 10 days. In addition, a gel containing doxycycline or microspheres of minocycline can be placed into isolated recalcitrant pockets. These drugs are resorbed in 2 wk.
Another approach is to surgically eliminate the pocket and recontour the bone (pocket reduction/elimination surgery) so that the patient can clean the depth of the normal crevice (sulcus) between the tooth and gingiva. In certain patients, regenerative surgery and bone grafting are done to encourage alveolar bone growth. Splinting of loose teeth and selective reshaping of tooth surfaces to eliminate traumatic occlusion may be necessary. Extractions are often necessary in advanced disease. Contributing systemic factors should be controlled before initiating periodontal therapy.
Ninety percent of patients with necrotizing ulcerative periodontitis due to HIV (HIV-associated periodontitis) respond to combined treatment with scaling and planing, irrigation of the sulcus with povidone-iodine (which the dentist applies with a syringe), regular use of chlorhexidine mouth rinses, and systemic antibiotics, usually metronidazole 250 mg po tid for 14 days.
Localized aggressive periodontitis requires periodontal surgery plus oral antibiotics (eg, amoxicillin 500 mg qid or metronidazole 250 mg tid for 14 days).
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