An inflammatory lesion caused by bacteria affecting the tissues housing the roots of the teeth. The disease, sometimes called pyorrhea, increases in prevalence and severity with increasing age, and it is the principal cause of tooth loss in adult humans throughout the world. When only the gum tissue or gingiva is affected, the disease is called gingivitis, but when the process extends into the deeper structures it is known as periodontitis. The diseased tissues appear abnormally red and slightly swollen, and they tend to bleed, sometimes profusely, when the teeth are brushed. In some cases the gums may become thickened and scarred, and they may recede, exposing the root surface. As the disease advances, the attachment of the gum to the tooth is lost, creating a periodontal pocket, a large portion of the gum is destroyed, and the bone surrounding the roots is resorbed. The teeth become loose, abscesses form, and extraction is required.
Both gingivitis and periodontitis are caused by bacteria that form plaques on the surfaces of the teeth at the gingival sulcus or pocket. These plaques may contain 250 or more separate microbial species. Plaques of any microbial composition can cause gingivitis, but specific bacteria appear to be necessary for induction of periodontitis. Among the bacteria involved in periodontitis are various species of Porphyromonas, Bacteroides, Actinobacillus, Eikenella, Fusobacterium, Wolinella, and other less well-characterized species. Spirochetes are present in active lesions, but their role remains unclear. The bacteria extend apically along the interface between the tooth root and the gingival tissue and causes periodontal pockets to form.
The principal features of the pathogenesis of periodontitis have been described. The lesions begin as an acute inflammatory response followed by a dense accumulation of lymphoid cells. There is a net loss of collagen in the area nearest the junctional epithelium and periodontal pocket, with scarring and fibrosis of the connective tissues at more distant sites. The junctional epithelium is converted into an ulcerated pocket epithelium, the alveolar bone housing the tooth roots is resorbed, and the periodontal ligament is destroyed. Products released by infiltrating leukocytes, including prostaglandins, interleukins and collagenase, and other hydrolytic enzymes, are involved in tissue destruction.
Bacterial colonization and extension activate several host defense mechanisms. The most effective of these is the accumulation of functional neutrophilic granulocytes between the surface of the plaque and the gingival tissue. These cells tend to counter and limit microbial extension. The bacteria appear to invade the periodontal connective tissues, where they induce immunopathologic and other destructive inflammatory reactions in the host, and these lead, in major part, to the observed tissue destruction. Periodontal destruction is episodic, with periods of exacerbation characterized by highly acute inflammation, followed by periods of quiescence.
Although bacteria are essential for induction of the disease, predisposing factors are also important, though their elucidation is not complete. Individuals who manifest functionally abnormal neutrophilic granulocytes or monocytes are unusually susceptible to the severe early onset forms of periodontitis. The leukocyte abnormality appears to be genetically transmitted. The early-onset forms have been designated as prepubertal, juvenile, and rapidly progressive periodontitis; adult periodontitis has a later onset and does not seem to be related to leukocyte abnormalities. Some persons with acquired immune deficiency syndrome (AIDS) manifest a highly destructive, unique form of periodontitis. Other predisposing conditions include unusually stressful situations and periods of hormone imbalance occurring at puberty, during pregnancy, and in some women taking birth control drugs.
Good daily oral hygiene practices, including vigorous brushing of the exposed surfaces of the teeth and use of dental floss, interproximal brushes, and other devices to clean between the teeth, constitute the most effective measures to prevent periodontal disease. Basic ingredients of treatment of existing disease include bringing the infection under control and establishing conditions which preclude reinfection. All of the microbial deposits must be removed from the crown and root surfaces. In individuals with severe forms of periodontitis, these procedures may be supplemented by use of antibiotics either systematically or directly into the pocket. These procedures usually lead to reduction of the inflammation and to some shrinkage in the gums, but the periodontal pockets remain. Based on the traditional view that treated pockets may become reinfected and the disease may continue to spread, surgical treatment may be performed with the aim of reducing pocket depth and restoring normal tissue contours. Alternatively, regenerative procedures use various grafting materials, including freeze-dried decalcified bone or bone substitutes and guided tissue regeneration. To perform guided tissue regeneration, flaps are opened in the gingival tissue and the root surfaces are thoroughly cleaned; a porous membrane is placed around the tooth, covering the bone defect with or without placing grafts, and flaps covering the membranes are sutured into place. The membrane permits the wound site to become populated with cells having the capacity to generate new bone, cementum, and periodontal attachment. See also Tooth disorders.
