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Gum Disease (Periodontitis) Without routine cleanings our gums may become infected (gum disease). The ability for calculus and tarter to accumulate underneath our gums increases tremendously. When this occurs our gums start to bleed and the bone that supports our teeth starts to melt away. With the loss of bone and the structures that support our teeth the possibility of tooth loss increases. There is also an increased risk of a serious mouth infection that can cause great pain. If this occurs please call immediately, we can arrest the disease and prevent tooth loss.
Typically, periodontitis is first diagnosed when a patient is > 35 yr old. The etiology of periodontitis is similar to that of gingivitis, but in periodontitis, the presence of specific organisms in the plaque may be more important than the total amount of plaque. Faulty occlusion causing an excessive functional load on teeth may contribute to disease progression. Systemic diseases that predispose patients to periodontitis include diabetes mellitus (especially type I), Down syndrome, Papillon-Lefèvre syndrome, Crohn's disease, neutropenia, agranulocytosis, lazy leukocyte syndrome, hypogammaglobulinemia, Chédiak-Higashi syndrome, hypophosphatasia, and acrodynia. Symptoms and SignsPeriodontitis usually begins with gingivitis. Abundant calculus deposits beneath the gingival margin are characteristic. The gingivae progressively lose their attachment to the teeth, and bone loss begins so that the periodontal pockets deepen. Destruction of the supporting osseous tissue is evident radiographically. With progressive bone loss, teeth may loosen and gingivae recede. Tooth migration is common in later stages. Pain is usually absent unless an acute infection (eg, abscess formation in one or more periodontal pockets) supervenes. Impaction of food in the pockets can cause discomfort and pain at meals. Localized juvenile periodontitis (formerly
called periodontosis) is associated with Actinobacillus
actinomycetemcomitans. It occurs in otherwise seemingly healthy
adolescents. Typically, signs of inflammation are relatively minor. The
condition is detected with a periodontal probe or found on x-rays, which show
localized, deep (vertical) bone loss, commonly limited to the first molars and
the incisors.
Prepubertal periodontitis is an uncommon condition that affects deciduous teeth, often shortly after eruption. Affected patients are usually diagnosed by age 4 yr. Typically, a child has defective polymorphonuclear leukocytes and has had frequent bouts of otitis media. Generalized acute proliferative gingivitis and rapid alveolar bone destruction are its hallmarks. In some patients, the disease burns out before the permanent teeth erupt; in others, it appears to be a generalized version of localized juvenile periodontitis. Treatment regimens are under investigation. Rapidly progressive periodontitis is commonly associated with A. actinomycetemcomitans, Porphyromonas gingivalis, and many gram-negative asaccharolytic rods. It occurs in patients aged 20 to 35 yr. Some cases may be sequelae of undiagnosed localized juvenile periodontitis or prepubertal periodontitis, but others appear de novo. Most patients have some polymorphonuclear leukocyte dysfunction, often for chemotaxis. HIV-associated periodontitis is a particularly virulent, rapidly progressing form. Clinically, it resembles acute necrotizing ulcerative gingivitis imposed on rapidly progressive periodontitis. Patients may lose 9 to 12 mm of attachment in as little as 6 mo. Unlike most forms of periodontitis, the HIV-associated form is accompanied by pain, intense erythema, and spontaneous bleeding. About 10% of cases of HIV-associated periodontitis do not respond to conventional local therapy and systemic antibiotics. TreatmentFor all forms of periodontitis, the first phase of treatment consists of oral hygiene instruction, thorough scaling and root planing to remove calculus deposits, and reevaluation after 3 mo. For HIV-associated periodontitis, treatment also includes intrasulcular povidone irrigation, regular use of chlorhexidine mouth rinses, and systemic antibiotics; metronidazole 250 mg tid (usually for 14 days) is the drug of choice. For localized juvenile periodontitis, treatment invariably requires periodontal surgery plus antibiotics (eg, a tetracycline 250 mg qid or metronidazole 250 mg tid for 14 days). If pockets are no deeper than 3 to 4 mm after initial therapy, no further treatment is needed. If deeper pockets persist, systemic antibiotics to alter the presumably pathogenic flora can be tried. A common regimen is tetracycline 250 mg qid for 10 days. Some tetracyclines, by inhibiting collagenase, diminish bone destruction. They also concentrate in the gingival sulcus. In addition, fabric filaments containing tetracycline can be packed into recalcitrant pockets for 7 to 10 days. Another approach is to surgically eliminate the pocket and recontour the bone so that the patient can clean the depth of the sulcus. Regenerative surgical and biologic techniques may be attempted 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 unavoidable in advanced disease. If present, systemic factors should be controlled before initiating periodontal therapy.
Arestin is a minocycline based antibiotic placed directly at the site of the periodontal infection. This product is quickly becoming the mode of choice for the eradication of the causes of the disease. Ask our dental professional about this great product. It's the first FDA approved needle-free subgingival anesthetic agent providing patients an option in anesthesia for SRP procedures. More information links |
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Bone
loss progresses faster than in adult periodontitis, often at a rate of 3 to 4
µ/day. In many patients, chemotaxis of polymorphonuclear leukocytes is
defective.
