Chapter 199 Periodontal Disease
Periodontal disease is an inclusive term used to describe an inflammatory condition of the gingiva (gingivitis) or periodontium (periodontitis) or both. Periodontal disease usually involves a disease process that typically progresses from gingivitis to periodontitis.1,2 It may be a manifestation of a more systemic condition such as diabetes mellitus, collagen diseases, leukemia or other disorders of leukocyte function, anemia, or vitamin deficiency states.1 Periodontal disease may also contribute to systemic disease. For example, periodontal disease has been linked to atherosclerosis via an increased level of serum C-reactive protein, a marker for inflammation and a strong risk factor for coronary artery disease.3
Because alveolar bone loss may be noninflammatory, our definition of periodontal disease excludes the processes causing only the loss of teeth (the majority of which are due to osteoporosis or endocrine imbalances).1 These conditions reflect systemic disease, with local factors playing only a minor role; therefore the focus should be on treating the underlying condition rather than the “periodontal disease.” In this context, noninflammatory alveolar bone loss should be viewed as a separate entity, since it involves a different etiology (see Chapter 194).
The focus of this chapter is the use of nutrition and lifestyle improvement as an adjunctive therapy to aid in the control and prevention of the causes of inflammatory periodontal disease. This is a good example of a condition that is probably best treated with combined expertise (i.e., a dentist or periodontist and a nutritionally minded physician). Although oral hygiene is of great importance in treating and preventing periodontal disease, it is insufficient in many cases. The host defense must be normalized if development and progression of the disease are to be controlled.1,4 To a large extent, the nutritional status of the individual determines the status of host defense factors.
The prevalence of periodontal disease increases directly with age. The rate of periodontal disease is approximately 15% at age 10, 38% at age 20, 46% at age 35, and 54% at age 50. As a group, men have a higher prevalence and severity of periodontal disease than women. Periodontal disease is inversely related to increasing levels of education and income. Rural inhabitants have a higher level of severity and prevalence than their urban counterparts.1
Understanding the underlying pathophysiology of any disease process leads to a more effective treatment plan. In periodontal disease this involves understanding the normal host protective factors in the periodontium. Page and Schroeder4 concluded: “Clearly bacteria are essential agents, but their presence is in itself insufficient; host factors must be involved if the disease is to develop and progress.”
The gingival sulcus, a V-shaped crevice that surrounds each tooth, is bounded by the surface of the tooth on one side and the epithelium lining the free margin of the gingiva on the other. The anatomy of the gingival sulcus is ideal for bacterial growth, because it is resistant to the washing and cleansing action of saliva. Furthermore, the gingival fluid (sulcular fluid) provides a rich nutrient source for microorganisms. The clinical determination of the depth of the gingival sulcus is an important diagnostic parameter. Patients with periodontal disease should be monitored; biannual visits to the dentist should be sufficient in most cases.
Bacterial plaque has long been considered the etiologic agent in most forms of periodontal disease.1 However, an appreciation of host defense factors has now developed.1,4 Bacteria are known to produce and secrete numerous compounds that are quite detrimental to the status of the host’s defense mechanisms. These compounds include the following1:
Polymorphonuclear neutrophils (PMNs) constitute a first line of defense against microbial overgrowth. Defects in PMN functions are “catastrophic” to the periodontium.1,4 PMN functions are depressed in the geriatric population as a whole and in patients with diabetes, Crohn’s disease, Chédiak-Higashi syndrome, Down syndrome, and juvenile periodontitis.1,4 These patients are at extremely high risk for developing rapidly progressing periodontal disease, as are people with transient neutropenia. Transient defects in PMN function may be responsible for the periods of quiescence and exacerbation noted in periodontal disease. In addition to serving a vital role in protecting against periodontal disease, PMNs also play a major role in tissue destruction. PMNs release numerous free radicals, collagenases, hyaluronidases, inflammatory mediators, and an osteoclast stimulator.1,4
These leukocytes are found in increased numbers in periodontal disease. They serve to phagocytize bacteria and debris and are the primary source of prostaglandins in the diseased gingiva, releasing large quantities of enzymes believed to play a major role in collagen destruction.1,4
The major role lymphocytes play in periodontal disease involves lymphokine production. Their role in periodontal disease is overshadowed by the roles of the other immune system components discussed, but lymphokines are involved in promoting PMN and monocyte chemotaxis, fibroblast destruction, and osteoclast activation.1,4
The complement system is composed of at least 22 proteins and accounts for more than 10% of the total serum globulin. On activation, complement components act in a cascade fashion. Complement can be activated via the classic or alternative pathway. The complement system plays a critical role in immunologic and nonspecific resistance to infection and in the pathogenesis of tissue injury. The products of complement activation regulate a number of events, including the release of mediators from mast cells; promotion of smooth muscle contraction; chemotaxis of PMNs, monocytes, and eosinophils; and phagocytosis by immune adherence.5 The net effect is an increase in gingival permeability, resulting in the increased penetration of bacteria and bacterial by-products and, in essence, the initiation of a positive feedback cycle.1,4
Other effects of complement activation include solubilization of immune complexes, cell membrane lysis, neutralization of viruses, and the killing of bacteria.5 In periodontal disease, activation of complement via the alternative pathway within the periodontal pocket is possibly the major factor in tissue destruction.
Mast cell degranulation is also a major factor in periodontal disease. Degranulation results in the release of inflammatory mediators (i.e., histamine, prostaglandins, leukotrienes, kinins, serotonin, heparin, and serine proteases).1 Mast cell degranulation can be initiated by IgE complexes, complement components, mechanical trauma, endotoxins, and free radicals. The finding of increased IgE concentrations in the gingivae of patients with periodontal disease suggests that allergic reactions may be a factor in the progression of the disease in some patients.6
Faulty dental restorations and prostheses are common causes of gingival inflammation and periodontal destruction.1 Overhanging margins provide an ideal location for the accumulation of plaque and the multiplication of bacteria. If the restoration is a silver amalgam filling, there may be even more involvement due to decreased activities of antioxidant enzymes. Mercury accumulation results in a depletion of the free radical–scavenging enzymes glutathione peroxidase, superoxide dismutase, and catalase.7 The proteoglycans and glycosaminoglycans of the collagen matrix are particularly sensitive to free radical damage.8
Tobacco smoking is associated with increased susceptibility to severe periodontal disease and tooth loss.1,9,10 (In fact, tobacco smoking is associated with increased susceptibility to virtually every major chronic disease.) Many of the harmful effects of tobacco smoking result from free radical damage, particularly to epithelial cells. Furthermore, smoking greatly reduces the levels of ascorbic acid, thereby potentiating its damaging effects.11 Carotenes and flavonoids have been shown to greatly reduce some of the toxic effects of smoking.12,13
In addition to cigarette smoking, there is a dose-dependent association between alcohol consumption and periodontal disease.14 Presumably the combination of smoking and drinking alcohol produces an even greater negative effect on periodontal health.
The collagen matrix of the periodontal membrane serves as periosteum to the alveolar bone and enables the dissipation of the tremendous amount of pressure exerted during mastication.15 The status of the collagen matrix of the periodontium, specifically the extracellular proteoglycans of the gingival epithelium, determines the rate of diffusion and the permeability of inflammatory mediators, bacteria and their by-products, and destructive enzymes from the oral cavity.16,17 Owing to the high rate of protein turnover in periodontal collagen, the integrity of the collagen matrix in this area is extremely vulnerable to atrophy when the necessary cofactors for collagen synthesis (e.g., protein; vitamins C, B6 and A; zinc; copper) are absent or deficient.15
The collagen of the periodontium is particularly rich in glycosaminoglycans.15–18 Heparin sulfate, dermatan sulfate, and chondroitin sulfate proteoglycan 4 are the major glycosaminoglycans present. Stabilization of collagen is the major treatment goal (see later).