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PubMed1980

Interrelationship of inflammation and tooth mobility (trauma) in pathogenesis of periodontal disease.

A series of studies has investigated interactions between periodontal trauma and marginal periodontitis in relation to the initiation, progression and treatment of periodontal disease. Lesions of trauma in the periodontal ligament consequent to either single or jiggling displacing forces result in morphologic alterations in the ligament and alveolar bone. These changes do not initiate the loss of connective tissue attachment characteristic of marginal periodontitis. Studies conducted in squirrel monkeys and beagle dogs in which jiggling forces have been produced subjacent to an established marginal periodontitis reported increased loss of alveolar bone, but the accelerated loss of attachment which occurred in the dog model did not occur in the monkey model. To clarify the relative importance of inflammation and tooth mobility in the treatment of advanced periodontal disease, periodontal response was evaluated after removing traumatic and/or inflammatory components. Elimination of trauma in the presence of existing marginal inflammation did not reduce tooth mobility or increase bone volume. Osseous regeneration and decreased tooth mobility occurred after resolving both components, however, similar findings occurred after resolving inflammation in the presence of continued tooth mobility. Resolution of marginal inflammation is of prime importance in the management of periodontal disease. After resolution of inflammation, bone regeneration may occur around mobile teeth and, furthermore, any residual tooth mobility does not result in increased loss of connective tissue attachment.

Animals↗
PubMed2000

A practical approach to the diagnosis and treatment of periodontal disease.

BACKGROUND: Both nonsurgical and surgical periodontal therapies are important in the control of most forms of periodontal disease. Sometimes, nonsurgical therapy is adequate to control the disease in mild cases and to slow progression and maintain periodontal stability in more advanced cases. Other times, both therapies may be indicated to obtain satisfactory results. The author presents treatment guidelines and recommendations for periodontal therapy. METHODS: The author searched the dental literature for information pertaining to periodontal therapy. RESULTS: The author found evidence-based data to support the effectiveness of nonsurgical and surgical periodontal therapy in controlling periodontal disease. Nonsurgical periodontal therapy requires time, effort, and good diagnostic and clinical skills to obtain satisfactory results. The results are determined by evaluating the patient's periodontal disease after active therapy, at which time additional surgical or nonsurgical treatment may be recommended. Evaluation should continue throughout the lifelong supportive phase of periodontal therapy. CONCLUSION: Clinicians should continue to develop and enhance their diagnostic skills, assess factors that affect diagnosis and prognosis, formulate a comprehensive treatment plan, render appropriate treatment, evaluate the outcome and determine when periodontal care is indicated. CLINICAL IMPLICATION: Failure to comply with monitoring the patient's periodontal status may lead to uncontrolled disease and eventually premature tooth loss. Premature tooth loss can be prevented through patient education and application of evidence-based nonsurgical and surgical therapy.

Clinical Protocols↗
PubMed2005

Lipoprotein-associated phospholipase A2 and plasma lipids in patients with destructive periodontal disease.

OBJECTIVES: Periodontitis is believed to be an independent risk factor of cardiovascular disease (CVD) and to be associated with a moderate systemic inflammatory reaction and hyperlipidaemia. Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is an enzyme that has been shown to be a risk factor of CVD and that is involved in the degradation of the phospholipid mediator platelet-activating factor (PAF), a potent mediator of inflammation. MATERIAL AND METHODS: In the present study, we measured concentrations of plasma lipids and plasma activity of Lp-PLA(2) in 32 patients (mean age 43+/-11 years) with moderate-to-severe periodontitis before and 3 months after local treatment. RESULTS: Periodontal therapy resulted in a significant reduction of local inflammation and tissue destruction as reflected in reduced pocket depths and reduced bleeding indices. Pre- and post-treatment plasma lipid levels were (median and range, mmol/l): total cholesterol (C) 5.01 (3.94-7.15) and 4.91 (3.32-8.01); low-density lipoprotein-cholesterol (LDL-C) 3.14 (2.40-4.84) and 2.96 (1.39-5.04); HDL-C 1.27 (0.73-2.17) and 1.25 (0.74-2.55); triglycerides 1.37 (0.48-5.11) and 1.14 (0.38-792). Using the Wilcoxon's rank test, neither parameter showed a significant change. In contrast to the lacking response of plasma lipids, we observed a significant reduction in the activity of Lp-PLA(2). Local treatment lowered the enzyme activity by about 10% from 3.61+/-0.99 to 3.29+/-0.94 micromol/ml/h (mean+/-SD; p<0.001). The pre-treatment values of Lp-PLA(2) and LDL-C significantly correlated with clinical parameters of inflammation and periodontal destruction. CONCLUSION: This study indicates that treatment of periodontitis significantly reduces the serum activity of Lp-PLA(2), which is believed to be an independent cardiovascular risk factor.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2006

[Correlation between periodontal disease and coronary atherosclerotic heart disease].

OBJECTIVE: To investigate the correlation between coronary atherosclerotic heart disease (CAD) and periodontal disease (PD). METHOD: Forty-five patients with CAD (CAD group) and 40 patients without CAD (control group) were compared with their pathological changes of periodontal tissues and inflammatory markers [high sensitive C reactive protein (hsCRP), interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha)]. RESULTS: Univariate analysis showed that the prevalence of PD was 84.44% in CAD group and 22.50% in control group (P < 0.01). The levels of hsCRP, IL-1beta, and TNF-alpha were (5.75 +/- 1.26) mg/L, (10.32 +/- 2.96) ng/L, and (9.17 +/- 2.14) ng/L in CAD group and (1.13 +/- 0.73) mg/ L, (2.87 +/- 1.45) ng/L, and (5.84 +/- 1.96) ng/L in control group (P < 0.01). Gingival index and plaque index were statistically different between two both groups (P < 0.01). Logistic regression analysis showed that in addition to pulse pressure and low density lipoprotein cholesterol, periodontal disease index was a higher risk factor of CAD. Its relative risk was 1.217 (95% CI was 1.120-1.805, P < 0.05). CONCLUSION: PD can cause CAD. The improvement of public oral health plays an important role in the prevention and treatment of CAD.

Adult↗
PubMed1981

Actinobacillus endocarditis associated with periodontal disease.

Actinobacillus actinomycetemcomitans, an organism associated with rapidly destructive periodontal disease (periodontitis), is a rare cause of endocarditis in children. This report presents a case of A. actinomycetemcomitans endocarditis in a 6-year-old child with rapidly destructive periodontal disease. A leukotoxic antigen was documented in the strain of A. actinomycetemcomitans isolated from the patient's blood.

Actinobacillus Infections↗
PubMed1975

[Somatologic morbidity study-- Berlin 1972. 2. Incidence of periodontal diseases, condition of oral hygiene].

Using the Periodontal Disease Index and the Oral Hygiene Index, the authors determined the periodontal and oral hygiene conditions of 3853 individuals (18 to 100 years of age) selected at random from the Berlin population 67% of these individuals presented with periodontal disease; 10% were threatened by periodontal disease. The symptom "tooth loosening" was stated in 18%. The mean PDI was 2.93. The mean plaque incidence (index according to Quingley and Hein) amounted to 1.4 in subjects without periodontal disease, and to 2.2 in periodontally diseased individuals. The means supragingival calculus -- subgingival calculus ratio (index according to King) in these groups was 0.53 and 0.85, respectively.

Adolescent↗
PubMed1986

Periodontal disease. Etiology and pathogenesis.

Periodontal disease is the number-one cause of the early loss of teeth in dogs and cats. Some of the factors in the adult animal that play a major role in the development of periodontal diseases are discussed in this article, including overcrowding, malocclusions, diet, developmental defects, and metabolic and systemic disease.

Animals↗
PubMed1984

New concepts of destructive periodontal disease.

The most common forms of destructive periodontal disease have been thought to slowly and continuously progress until treatment or tooth loss. Recently, data have become available which are inconsistent with this "continuous disease" hypothesis. Data from longitudinal monitoring of periodontal attachment levels and alveolar bone in humans and in animals suggest that periodontal disease progresses by recurrent acute episodes. In addition, rates of attachment loss have been measured in individual sites which are faster than those consistent with the continuous disease hypothesis or slower than those expected from estimates of prior loss rates. To account for these observations, a model of destructive periodontal disease is described in which bursts of activity occur for short periods of time in individual sites. These bursts appear to occur randomly at periodontal sites throughout the mouth. Some sites demonstrate a brief active burst of destructive periodontal disease (which could take a few days to a few months) before going into a period of remission. Other sites appear to be free of destructive periodontal disease throughout the individual's life. The sites which demonstrate destructive periodontal activity may show no further activity or could be subject to one or more bursts of activity at later time periods. Comparison of monitored loss rates for a year with mean loss rates prior to monitoring suggested that there may be relatively short periods in an individual's life in which many sites undergo periodontal destruction followed by periods of extended remission. An extension of the random disease model is also suggested in which bursts of destructive periodontal disease activity occur with higher frequency during certain periods of an individual's life.

Adult↗
PubMed1983

Progression of periodontal disease in adult subjects in the absence of periodontal therapy.

Progression of periodontal disease in adult subjects in the absence of periodontal therapy was monitored in 2 populations. One group of 64 Swedish subjects (mean age 40.5 years at entry) with mild to moderate periodontal attachment loss was monitored for attachment level changes at baseline, 3 and 6 years. A second group of 36 Americans (mean age 34.3 years at entry) with advanced destructive periodontal disease was monitored for attachment level changes at baseline and 1 year. Of 4101 sites examined at baseline and at 3 years in the Swedish subjects, only 158 sites (3.9%) showed attachment loss of more than 2 mm. No measurable change was found in 1440 sites (35.1%). Of 4097 sites examined at 3 and 6 years, 67 sites (1.6%) showed attachment loss greater than 2 mm; 57.4% of sites showed no measurable change; and 19 sites (0.5%) showed a decrease in probeable attachment level of more than 2 mm. During the 6-year interval, 523 sites (11.6%) showed attachment loss of more than 2 mm; 20% of sites showed no measurable change and 11 sites (0.2%) showed more than 2 mm of attachment "gain". Approximately 50% of sites that showed no measurable change in the first 3-year period showed loss in the next 3 years. In contrast, of the sites which showed some level of attachment loss in the first period, approximately 2/3 showed no loss in the second monitoring period. Of 3210 sites monitored in the American subjects, 102 sites (3.2%) exhibited more than 2 mm of additional attachment loss; 26% of sites showed no measurable change and 138 sites (4.3%) showed a decrease in probeable attachment level of more than 2 mm. The association between attachment level changes and initial attachment level (baseline) was examined by regression analysis. The slopes of the regression lines for both populations were not consistent with a hypothesis that sites with more advanced attachment loss are more prone to additional destruction, in the absence of treatment, than sites with initially less attachment loss. In the American group, some sites with initially advanced attachment loss, exhibited a decrease in probing attachment level.

Adolescent↗
PubMed1990

[The clinical and etiological study on juvenile periodontal disease].

Seven juvenile periodontally diseased patients were evaluated for clinical, microbiologic and local or systemic host factors. Three patients showed the localized from of periodontitis clinically and radiographically and by deep periodontal pockets associated with the molars and incisors. Four were in the generalized froms, in which in most cases all teeth were affected. The results in both diseased froms on the predominant cultivable subgingival microflora, the composition of which was not different from that in adult periodontitis, consisted of significantly increased proportions of Gram-negative anaerobic rods, Bacteroides sp. and B. gingivalis, Haemophilus sp. and H. actinomycetemcomitans were detected in 1/3 of the localized and 2/4 of the generalized periodontitis. They were of no value in distinguishing activity that enhanced disease in the generalized from. Elevated serum IgG responses were noted with B. gingivalis. No markedly functional abnormalities of neutrophils from peripheral blood have been demonstrated, however it might function with systemic factors, like an insulin-dependent diabetes. Morphologic characteristics of the oral and periodontal tissue in localized periodontitis were that the pattern of destruction was confined to specific teeth groups characterized by extensive the bucco-lingual width ratio of the dental crown to alveolar bone width. These observations indicate that the generalized form of juvenile periodontitis lesions were associated not only with the presence of subgingival bacteria, but also with conditions such as local morphologic and systemic or constitutional factors, individual variation in relation to destructive and protective aspects of the defense mechanisms.

Adolescent↗
PubMed2006

Periodontal disease and atherosclerosis from the viewpoint of the relationship between community periodontal index of treatment needs and brachial-ankle pulse wave velocity.

BACKGROUND: It has been suggested that periodontal disease may be an independent risk factor for the development of atherosclerosis. However, the relationship between periodontal disease and atherosclerosis has not been fully elucidated. This study aimed to assess the effects of periodontal disease on atherosclerosis. METHODS: The study design was a cross-sectional study. Subjects were 291 healthy male workers in Japan. We used the Community Periodontal Index of Treatment Needs (CPITN) score, average probing depth and gingival bleeding index (rate of bleeding gums) to assess the severity of periodontal disease. We also used the Brachial-Ankle Pulse Wave Velocity (baPWV) as the index for the development of atherosclerosis. RESULTS: The unadjusted odds ratio (OR) of atherosclerosis in relation to the CPITN score was 1.41 [95% CI: 1.16-1.73]. However, after adjustment for age, systolic blood pressure and smoking, the CPITN score had no relationship with atherosclerosis (adjusted OR: 0.91 [0.68-1.20]). CONCLUSION: Our results show no relationship between mild periodontal disease and atherosclerosis after appropriate adjustments.

Adult↗
PubMed2000

Plasma lipid and blood glucose levels in patients with destructive periodontal disease.

Hyperlipidaemia and hyperglycaemia are major risk factors for cardiovascular disease. In recent years, some evidence has been presented that periodontal disease is associated with an increased risk of cardiovascular disease. To further elucidate this association, we have studied standard blood chemistry variables known as risk markers for cardiovascular disease in periodontally diseased and healthy subjects. We have measured levels of plasma lipids and fasting blood glucose in 39 subjects with moderate periodontal disease (age 50-60 years) and compared the results with those obtained in 40 age- and sex-matched controls. Both groups were systemically healthy according to their medical history. Total cholesterol, low density lipoprotein cholesterol and triglycerides were significantly higher in periodontally diseased subjects by about 8% (p<0.03), 13% (p<0.003) and 39% (p<0.001), respectively, when compared to controls. Although subjects with diabetes were excluded from the study, we found significantly higher blood glucose levels in the patient than in the control group (85 +/- 25 versus 73 +/- 17 mg/dl; p<0.02). There was also a significantly higher frequency of pathological plasma lipid profiles in the patient than in the control group. The results indicate that hyperlipaemia and pre-diabetes may be associated with periodontal disease in systemically healthy subjects. These data do not allow us to decide, whether periodontal disease causes an increase in hyperlipaemia and in a prediabetic state or whether periodontal disease and cardiovascular disease share hyperlipidaemia and the prediabetic state as common risk factors.

Aged↗
PubMed1998

Position paper of The American Academy of Periodontology: periodontal disease as a potential risk factor for systemic diseases.

This paper on periodontal disease as a potential risk factor for systemic diseases was prepared by the Research, Science and Therapy Committee of The American Academy of Periodontology. It is intended to provide information regarding the role of periodontal disease in systemic diseases, including bacteremia, infective endocarditis, cardiovascular disease and atherosclerosis, prosthetic device infection, diabetes mellitus, respiratory diseases, and adverse pregnancy outcomes.

Arteriosclerosis↗
PubMed1998

Periodontal disease and diet in domestic pets.

Periodontal disease is the most common oral condition seen in domestic pets. In addition to the discomfort caused in the affected animal, there is strong circumstantial evidence to show that a focus of infection in the mouth may cause disease of distant organs. Consequently, prevention of periodontal disease is of paramount importance for the general health and well-being of pets. The presence of plaque on the tooth surfaces is the primary cause of periodontal disease. However, the mechanisms by which disease develops are by no means fully understood. Dietary texture does have an effect on the accumulation of dental deposits and consequently on disease development and progression. Daily toothbrushing remains the single most effective means of removing plaque, thus preventing periodontal disease. On the basis of current knowledge, the best way to maintain healthy periodontal tissues in our pets is frequent toothbrushing. The use of a dental hygiene chew and/or a diet designed to reduce dental deposits can be useful adjunctive measures and should be recommended.

Animals↗
PubMed1996

The impact of new technologies to diagnose and treat periodontal disease. A look to the future.

The last 25 years have brought unprecedented advances to our understanding of periodontal disease. Consider that in 1970 periodontitis was believed to effect most individuals over the age of 35 years, to progress steadily in an individual once initiated until teeth were lost, to be the primary cause of tooth loss in adults, to be caused by the bacterial mass accumulating on the tooth surface and subgingivally, and to involve the host in some fashion or another. In the 25 years since then, impressive research advances in the epidemiology of periodontal disease, the specific bacterial etiology of periodontal disease and the immunoinflammatory mediators of periodontal tissue destruction have greatly altered our view of periodontal disease. Thus, given these research advances in the understanding of periodontitis, what may the future hold for improved diagnosis and treatment of periodontal disease? Impressive research into new ways to diagnose the periodontal diseases is well underway. Investigators are seeking new ways to diagnose an individual's degree of risk for periodontal disease initiation, susceptibility to disease progression, level of disease "activity" and the likely response to treatment and recurrence of active disease. New diagnostic tests should greatly advance our ability to more accurately and specifically diagnose periodontal disease. The future also looks promising for new treatment strategies to slow or arrest periodontal disease progression. The bacterial specificity of periodontal disease etiology revealed since 1970 has logically led to the use of antibiotics in periodontitis treatment. In the late 1980s the concept of locally delivering antibiotics to the periodontal pocket was introduced, and subsequent clinical trials have indicated that it is possible to reduce pocket depth and inflammation with tetracycline locally delivered to the periodontal pocket. Likely, we have barely scratched the surface in studying the efficacy of locally delivery antimicrobial agents to alter the progression of periodontal disease. As new agents are developed and better delivery systems to the periodontal pocket are developed, the future should see a variety of antimicrobial agents available which can slow periodontal disease progression. The future also holds promise for slowing periodontal disease progression by blocking inflammatory pathways important in periodontal tissue destruction. Clinical trials of flubiprofen, naproxen and ketoprofen indicate that it is possible to slow periodontal disease progression with non-steroidal anti-inflammatory drugs which inhibit one destructive pathway. In addition, data from animal models indicate that chemically modified tetracycline as an inhibitor of collagenase can slow disease progression in animals. Again, we have likely only just begun to explore the wide range of molecular mediators of tissue destruction which may be targeted for blocking and thereby slow or arrest periodontal disease progression. Last, research into regenerating periodontal structures lost as a result of disease has had a noteworthy record of progress in the past 25 years. Techniques that utilize bone grafts, root treatments, tissue guiding membranes or polypeptide growth factors have ably indicated that it is possible to regenerate new attachment structures in humans. As investigators continue to unravel the mysteries of the embryonic development of the periodontium, the ability to predictably regenerate lost periodontal attachment structures holds great promise for the future.

Adult↗
PubMed1997

Treatment paradigms in periodontal disease.

The prevailing treatment paradigm in periodontal disease relies on debriding the tooth surfaces to keep the bacterial load below the level that triggers tissue loss. When debridement cannot be easily accomplished because of deep pocketing, access surgery is recommended. The debridement approach that involves access surgery is successful in 80% to 85% of patients. Patients who do not respond are often treated with systemic antibiotics. This paradigm, which is based on the nonspecific plaque hypothesis, is labor-intensive and relies on antibiotics only as a last resort. This nonspecific treatment paradigm is in contrast with the specific plaque hypothesis, which states that a limited number of bacterial species are specifically involved in most forms of periodontal disease. Some studies have significantly associated anaerobic bacteria with advanced forms of periodontal disease. These observations led us to hypothesize that most forms of periodontal disease are anaerobic infections, which can be treated by antimicrobials such as metronidazole or clindamycin. Three double-blind studies have shown that 1 to 2 weeks of unsupervised use of metronidazole-plus-debridement was significantly better than placebo-plus-debridement in reducing the need for periodontal surgery. These findings suggest that treatments based on the specific plaque hypothesis give clinicians and patients a choice regarding treatment options in periodontal disease.

Anti-Bacterial Agents↗
PubMed2004

Hypochlorous acid and taurine-N-monochloramine in periodontal diseases.

Chronic periodontitis is a multi-factorial disease involving anaerobic bacteria and the generation of an inflammatory response, including the production of metalloproteinases, pro-inflammatory cytokines, and eicosanoids. Hypochlorous acid (HOCl) and taurine-N-monochloramine (TauCl) are the end-products of the neutrophilic polymorphonuclear leukocyte (PMN) respiratory burst. They act synergistically to modulate the inflammatory response. In the extracellular environment, HOCl and TauCl may directly neutralize interleukin 6 (IL-6) and several metalloproteinases, while HOCl increases the capacity of alpha(2)-macroglobulin to bind Tumor Necrosis Factor-alpha, IL-2, and IL-6, and facilitates the release of various growth factors. TauCl inhibits the production of inflammatory mediators, prostaglandins, and nitric oxide. HOCl activates tyrosine kinase signaling cascades, generating an increase in the production of extracellular matrix components, growth factors, and inflammatory mediators. Thus, HOCl and TauCl appear to play a crucial role in the periodontal inflammatory process. Taken together, these findings may offer opportunities for the development of novel host-modulating therapies for the treatment of periodontitis.

Animals↗
PubMed1987

Malpractice and periodontal disease.

The treatment of periodontal disease is, at the present time, the focus of a large percentage of all dental malpractice cases. Consequently, dentists may find it helpful to be aware of the somewhat unique nature of litigation arising out of professional services provided with respect to periodontal disease. The operation of the statute of limitations in this context, whereby a dentist--at least in many states--can be sued several years after treatment of a patient terminates, makes caution, in terms of the maintenance of records and the purchase of insurance, an absolute essential.

Dental Records↗