Risk Factors for Periodontitis
Over the past 15 years, research has demonstrated a direct relationship between the use of tobacco and periodontal disease.1 This research has improved clinicians' understanding of how tobacco interacts with periodontal structures, particularly with regard to tissue destruction, ie, the action of the bacteria on the tissue and host response against this bacteria. MacGregor's studies noted that smokers demonstrate a greater accumulation of calculus and consequently, higher bacterial concentration.2 The saliva of smokers, which has an increased flux and pH, provides a suitable environment for calculus formation due to its increased concentration of Ca2. At present, microbiological studies have not been able to demonstrate a difference in the subgingival bacteria between smoking and nonsmoking patients.3
The nonsurgical treatment of pathogenic bacteria is identical in smoking and nonsmoking patients. According to Wolff et al, the bacteria observed in healthy sites is capable of inducing structural damage in periodontal sites of lower resistance. Consequently, tobacco has a greater effect on the host site rather than the microbiology. Tobacco affects three elements of the periodontium: the fibroblasts,4 the bone cells, and the vascularization. Although tobacco has numerous byproducts, nicotine is most often the focus of clinical research. Nicotine absorbed by inhalation or by diffusion through the oral membrane causes varying systemic effects. According to McGuire et al, nicotine and its metabolites (cotinine) are present in the saliva, in the gingival fluid, and on the root surfaces.5 Raulin et al describe an inhibition of the adhesion and proliferation of the fibroblasts, and a reduced production of fibronectin and collagen-1, an augmentation of collagenase activity.6
Smoking also has a detrimental effect on vascularization. Although gingival fluid has been observed to increase upon smoking, it decreases over extended time periods as a result of the vasoactive effects of nicotine and increased diffusion of epinephrine and norepinephrine.7 Histometric studies have noted the vasoconstriction of the periodontal capillaries and buccal mucosa, combined with the vascular effects associated with high levels of carboxyhemoglobin from carbon monoxide, result in a hypoxy and ischemic necrosis that is typical of acute necrosis gingivitis. The consequences of these effects are limited, however, and often contradictory.8
While numerous studies have proven that the use of tobacco produces an inflammatory or immune host response in the periodontal system, it also increases the possibility of developing a pulmonary edema. Researchers have also focused on the bacterial effects of phagocytosis and chemotaxis, which appear to be decreased by tobacco and the related reduction of oxygen in smoking patients.
Periodontitis is a chronic inflammatory disease whose progression is dependent on the response of the affected host body. Since the gingiva is in a constant balance between pathological wounding by bacterial plaque and wound healing, any metabolic disturbance (eg, diabetes) in the host compromises tissue repair and healing and accelerates the progression of periodontitis.9 Current research, however, has not established significant differences in the clinical parameters between diabetic and nondiabetic patients. A 3-year longitudinal study of diabetes mellitus patients determined that the duration of the diabetic condition and a patient's metabolic control may effect the onset of periodontitis.10
Oral Hygiene and Dental Factors
The role of bacterial plaque as an etiological factor in the development of chronic inflammatory periodontal disease has been well documented. While various antimicrobial agents have demonstrated the ability to chemically control plaque growth and reduce gingival inflammation, study has indicated that the primary means of controlling supragingival plaque is through mechanical action.11 Several toothbrush designs enable the successful removal of plaque at buccal, lingual, and occlusal surfaces, although interproximal surfaces must be cleaned with interdental brushes, floss, irrigating devices, or wooden sticks in order to facilitate plaque removal in patients suffering from moderate to severe periodontitis.12 Plaque retention and its associated bacterial presence can also be affected by dental factors such as malposition with irregular alignment, missing teeth, incomplete eruption, defective restoration, tooth surface irregularities, and untreated decay.12
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Periodontal disease is affected by complex genetic factors as well; these influences vary significantly in each patient. Variations in subgingival flora and response to bacterial invasion have also been observed in clinical study. Genetically controlled substances such as interleukin-1, which is secreted by macrophages that are stimulated by antigens, also vary in each patient. Since interleukin-1 attaches to osteoblasts and fibroblasts to produce collagenase that causes bone resorption, this genetic factor must also be addressed in relation to periodontal disease.
Influence of Diet, Stress, and Aging
Investigators have examined the role of diet and determined that it, too, has the potential to increase the risk of periodontal disease. The consumption of cariogenic or soft food that may predispose a patient to tooth loss or occlusal deficiencies can cause the proliferation of bacteria in the oral environment. It is evident that high levels of stress can reduce the host's immune defense. Geriatric patients are also at increased risk for periodontal disease due to involved complications (eg, heart disease, diabetes, hypertension, arthritis) in these patients. Recent studies indicate that even if periodontal disease is not a direct consequence, aging is certain to aggravate these symptoms.
The infectious etiology of periodontal disease has been clearly established, and this knowledge should be used in the prevention, diagnosis, and treatment of the condition. The precision of the clinical diagnosis, however, may be inadequate unless it is supplemented by the use of advanced diagnostic devices. For example, analysis of the flora enables the clinician to distinguish between the clinical presentations of two forms of the disease (eg, chronic gingivitis and periodontitis) that may exhibit similar symptoms.
While developments in bacterial testing may reduce the risk of complications following treatment, the means to use such evaluation are only in the preliminary phase. The tests presently available to consumers seek to detect, identify, and quantify the presence of bacteria in periodontal sites in a cost-effective, efficacious manner. To date, three categories of tests have been developed: enzymatic, immunological, and genetic. The first evaluates the enzymatic activity of bacteria; this system (BANA) determines the pseudotripsine hydrolytic activity of three primary bacterial strains and can be utilized in clinical practice. Immunological probes measure antiserum or monoclonal antibodies of the target bacteria, and immunofluorescence microscopic techniques and agglutination tests (ELISA) may be available for clinicians in the future. The genetic probe, a recent contribution to periodontal bacteriology, reacts to a portion of or the entire bacteria gene and has been conducted by research laboratories.
In order to determine a more efficacious manner of controlling periodontal disease, researchers have also attempted to isolate its path of transmission. Recent investigations have highlighted the possibility of disease transmission through the saliva and from parent to child as a result of pathogenesis.13 In addition, clinicians must observe strict asepsis protocols to ensure that the disease is not transmitted intraorally by bacteria that adheres to the periodontal probe itself.14
This brief overview of periodontal disease has discussed the clinical presentation of the condition as well as several factors that must be evaluated in its diagnosis and treatment. The objective of periodontal treatment should primarily consist of infection control and the prevention of recolonization. The diagnosis can now be established through clinical examination, radiographic analysis, and novel microbiological evaluation. The regeneration process - including complicated hard and soft tissue grafting procedures and implant therapy - cannot be considered until infection control is achieved. Since a 67% recurrence of the disease has been determined 5 years postoperatively, it should be acknowledged that the initial mechanical treatment must be supplemented with antibiotic therapy. In order to determine the appropriate antibiotic, the clinician must also identify the bacterial strain. Once this has occurred, infection control can be realized by mechanical treatment, surgery, antiseptics, or local delivery of antibiotics associated with anti-inflammatories.
Substantial research has already been conducted in an effort to develop new means of treating periodontal disease. Although longitudinal studies are necessary to evaluate the long-term prognosis of local drug application, initial reports on the utility of this modality are favorable. Local delivery systems have the potential to regulate periodontal disease, but controlled studies are required to determine the type of lesion and specific situations where this therapy would be most efficient.13 Since the host tissue, which is responsible for the initiation and progression of periodontal disease, has recently been identified as the cause of tissue breakdown, a new treatment concept that blocks the host response and controls the etiological bacteria has been developed. The first approach is to utilize nonsteroidal anti-inflammatory drugs in the course of therapy, and the second is to use the enzymatic effect of tetracycline antibiotics.15 Through the use of such advanced chemotherapeutic treatments, it is believed that the management of chronic periodontal disease may one day become a reality.
- Genco R. Current view of risk factors for periodontal diseases. J Periodontol 1996;67:1041-1049.
- MacGregor IDM, Edgar WM, Greenwood AR. Effects of cigarette smoking on the rate of plaque formation. J Clin Periodontol 1985;12:35-41.
- Brochut PF, Cimasoni G, Tabagisme, Parodonte I. Rev Mens Suisse Odonto-stomatol 1997;8:673-680.
- Hanes PJ, Schuster GS, Lubas S. Binding, uptake, and release of nicotine by human gingival fibroblasts. J Periodontol 1991;62:147-152.
- McGuire JR, McQuade MJ, Rossmann JA, et al. Cotinine in saliva and gingival crevicular fluid of smokers with periodontal disease. J Periodontol 1989;60:176-181.
- Raulin LA, McPherson JC, McQuade MJ, Hanson BS. The effect of nicotine on the attachment of human fibroblasts to glass and human root surfaces in vitro. J Periodontol 1988;59:318-325.
- MacLaughlin WS, Lovat GM, MacGregor ID, Kelly PJ. The immediate effects of smoking on gingival fluid flow. J Clin Periodontol 1993;20:448-451.
- Ketabi M, Hirsch RS. The effects of local anesthetic containing adrenaline on gingival blood flow in smokers and non-smokers. J Clin Periodontol 1997;24(12):888-892.
- Doxey DL, Cutler CW, Iacopino AM. Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model. J Periodontol 1998;69(2):113-119.
- Sbordone L, Ramaglia L, Barone A, et al. Periodontal status and subgingival microbiota of insulin-dependent juvenile diabetics: A 3-year longitudinal study. J Periodontol 1998;69(2):120-122.
- Christou V, Timmerman MF, Van der Velden U, Van der Weijden FA. Comparison of different approaches of interdental oral hygiene: Interdental brushes versus dental floss. J Periodontol 1998;69(7):759-764.
- Woodall IR. Comprehensive dental hygiene care.
- Greenstein G, Polson A. The role of local drug delivery in the management of periodontal diseases: A comprehensive review. J Periodontol 1998;69(5):507-520.
- Papaioannou W, Bollen C, Van Eldere J, Quirynen M. The adherence of periodontopathogens to periodontal probes. A possible factor in intraoral transmission. J Periodontol 1996;66:1164-1169.
- Golub LM, Lee HM, Greenwald RA, et al. A matrix metalloproteinase inhibitor reduces bone-type collagen degradation fragments and specific collagenases in gingival crevicular fluid during adult periodontitis. Inflamm Res 1997;46:310-319.