Loading...
(1/161) The antimicrobial treatment of periodontal disease: changing the treatment paradigm.

Over the last 100 years, methods of surgical periodontal treatment have enjoyed a history of success in improving oral health. The paradigm of care is based on the "non-specific plaque hypothesis"--that is, the overgrowth of bacterial plaques cause periodontal disease, and the suppression of this overgrowth reduces disease risk. The central feature of this approach to care is the removal of inflamed gingival tissue around the teeth to reduce periodontal pocket depth, thereby facilitating plaque removal by the dentist and by the patient at home. Over the last 30 years, with the recognition that periodontal disease(s) is caused by specific bacteria and that specific antimicrobial agents can reduce or eliminate the infection, a second paradigm has developed. This new paradigm, the "specific plaque hypothesis", focuses on reducing the specific bacteria that cause periodontal attachment loss. The contrast between the two paradigms can be succinctly stated as follows: The antimicrobial therapy reduces the cause, while the surgical therapy reduces the result of the periodontal infection. The specific plaque hypothesis has two important implications. First, with the increasing attention to evidence-based models for prevention, treatment, outcome assessment, and reimbursement of care, increasing attention and financial effort will be channeled into effective preventive and treatment methods. Second, the recent observations that periodontal infections increase the risk of specific systemic health problems, such as cardiovascular disease, argue for the prevention and elimination of these periodontal infections. This review highlights some of the evidence for the specific plaque hypothesis, and the questions that should be addressed if antimicrobial agents are to be used responsively and effectively.  (+info)

(2/161) Tooth loss in periodontal patients.

OBJECTIVE: To compare tooth loss between patients who received surgical therapy for chronic periodontitis and those who received nonsurgical therapy alone. METHODS: A retrospective chart study was conducted at Dalhousie University. All patients who had periodontal treatment and were active cases for at least 10 years were included (n = 335). The sample consisted of 120 males (35.8%) and 215 females (64.2%). Ages ranged from 16 to 77 (mean = 46.1 +/- 12.0 years). All patients received nonsurgical therapy; 44.8% received periodontal surgery as well. Variables recorded were demographics, initial attachment loss, treatment type, recall frequency, patient compliance and history of extracted teeth. Independent t-tests or chi-squared tests were used to compare these for surgical and nonsurgical patients. ANOVA was used to test for interactions between initial attachment loss, age, gender, compliance and type of therapy a patient received as reasons for tooth loss. RESULTS: 521 teeth were lost in 69 patients (20.6% of sample). Of teeth lost, 61.8% were due to periodontal disease; 24.8% to caries; 13.2% to other reasons. Patients initially diagnosed with early attachment loss lost an average of 0.37 (+/- 1.33) teeth. Patients diagnosed with moderate attachment loss lost an average of 1.50 (+/- 2.54) teeth and those diagnosed with advanced attachment loss lost an average of 3.11 (+/- 3.01) teeth. Those who received surgical therapy lost more teeth (mean = 1.31 +/- 2.36) than those who received nonsurgical treatment (mean = 0.68 +/- 1.87; p = 0.001). However, initial attachment loss was the only factor that could predict tooth loss. The type of therapy (surgical or nonsurgical) was not statistically significant. CONCLUSIONS: Most periodontal patients (79.4%) who received treatment at this dental school clinic did not lose any teeth due to periodontal disease over at least 10 years. Although patients who had surgical therapy lost more teeth than those who had nonsurgical therapy alone, this was not an important predictor of tooth loss.  (+info)

(3/161) C-telopeptide pyridinoline cross-links (ICTP) and periodontal pathogens associated with endosseous oral implants.

Detection of periodontal or peri-implant sites exhibiting progressing disease or those at risk of deterioration has proven difficult. Pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP), a marker specific for bone degradation found in gingival crevicular fluid (GCF), has been associated with both bone and attachment loss in periodontitis and may be useful for predicting disease activity. The aim of this cross-sectional study was to examine the relationship between ICTP levels and subgingival species around implants and teeth from 20 partially and 2 fully edentulous patients. GCF and plaque samples were collected from the mesiobuccal site of each implant and tooth. Radioimmunoassay techniques were utilized to determine GCF ICTP levels. Plaque samples were analyzed utilizing checkerboard DNA-DNA hybridization. Traditional clinical parameters were assessed. Seventy-one implants and 370 teeth from 22 subjects were examined. ICTP levels and subgingival plaque composition were not significantly different between implants and teeth. Implant sites colonized by Prevotella intermedia, Capnocytophaga gingivalis, Fusobacterium nucleatum ss vincentii, and Streptococcus gordonii exhibited odds ratios of 12.4, 9.3, 8.1, and 6.7, respectively of detecting ICTP. These results suggest a relationship between elevated ICTP levels at implant sites and some species associated with disease progression. Longitudinal studies are necessary to determine whether elevated ICTP levels may predict the development of peri-implant bone loss.  (+info)

(4/161) The oral cleanliness and periodontal health of UK adults in 1998.

Periodontal disease continues to be a major concern for dentists and patients. This paper reports the findings of the 1998 UK Adult Dental Health survey in relation to plaque, calculus, periodontal pocketing and loss of attachment. It is apparent from this study that moderate periodontal disease remains commonplace amongst UK adults and that the associated risk factors of plaque and calculus are in abundance, even amongst those who profess to be motivated about their oral health and attend the dentist regularly. The continued high prevalence of disease needs to be seen in the context of the far larger number of people who are now potentially at some risk, particularly in the older age groups, because of improvements in tooth retention. However, the cumulative effect of disease means that control of the periodontal diseases, even mild and slowly progressing disease, will be a key issue if large numbers of teeth are to be retained into old age. If that level of control is to be achieved we need a widespread improvement in our management of the disease, particularly in our ability to improve the oral cleanliness of the UK population.  (+info)

(5/161) Tissue reaction to orthodontic tooth movement--a new paradigm.

Direct or indirect resorption are both perceived as a reaction to an applied force. This is in contrast to orthopaedic surgeons who describe apposition as 'the reaction to loading of bone'. The article reviews the literature on intrusion of teeth with periodontal breakdown, and on the basis of clinical and experimental studies. The conclusion is reached that intrusion can lead to an improved attachment level, and that forces have to be to low and continuous. The tissue reaction to a force system generating translation of premolars and molars in the five Macaca fascicularis monkeys is described. Three force levels, 100, 200, and 300 cN were applied for a period of 11 weeks. Undecalcified serial sections were cut parallel to the occlusal plane and a grid consisting of three concentric outlines of the root intersected by six radii was placed on each section so that areas anticipated to be subject to differing stress/strain distributions were isolated. A posteriori tests were utilized in order to separate areas that differed with regard to parameters reflecting bone turnover. Based on these results and a finite element model simulating the loading, a new hypothesis regarding tissue reaction to change in the stress strain distribution generated by orthodontic forces is suggested. The direct resorption could be perceived as a result of lowering of the normal strain from the functioning periodontal ligament (PDL) and as such as a start of remodelling, in the bone biological sense of the word. Indirect remodelling could be perceived as sterile inflammation attempting to remove ischaemic bone under the hyalinized tissue. At a distance from the alveolus, dense woven bone was observed as a sign of a regional acceleratory phenomena (RAP). The results of the intrusion could, according to the new hypothesis, be perceived as bending of the alveolar wall produced by the pull from Sharpey's fibres.  (+info)

(6/161) Inflammation and tissue loss caused by periodontal pathogens is reduced by interleukin-1 antagonists.

Periodontal disease is a significant cause of tooth loss among adults. It is initiated by pathogenic bacteria, which trigger an inflammatory response that is effective in preventing significant microbial colonization of the gingival tissues. In some individuals, the reaction to bacteria may lead to an excessive host response, resulting in periodontal tissue destruction. Recent developments suggest that interleukin (IL)-1 genetic polymorphisms may identify certain individuals who have a predisposed susceptibility to periodontal breakdown and that elevated levels of IL-1 are found in individuals with periodontal disease. However, there is no direct evidence that IL-1 per se is responsible for the critical events that occur in periodontitis. We investigated the role of IL-1 in periodontal disease in a Macaca fascicularis primate model, using human soluble IL-1 receptor type I as a specific inhibitor. The results indicate that inhibition of IL-1 alone significantly reduces inflammation, connective tissue attachment loss, and bone resorption that are induced by periodontal pathogens.  (+info)

(7/161) Antibody-based diagnostic for 'refractory' periodontitis.

OBJECTIVE: About 10-15% of US adults are 'refractory' to therapy for chronic periodontitis. Recently, studies suggest that these patients have elevated lysine decarboxylase activity in the sulcular microbiota. The aim of this study was to determine whether an elevated IgG antibody response to lysine decarboxylase, alone or with antibody to other bacterial antigens and baseline clinical measurements, would predict 'refractory' patients with high accuracy. METHODS: Chronic periodontitis patients were treated using scaling and root planing (SRP) followed by maintenance SRP and 3-monthly re-examinations. If there was a loss of mean full mouth attachment or more than three sites appeared with > 2.5 mm new loss within a year, the subjects were re-treated (modified Widman flap surgery and systemically administered tetracycline). If attachment loss as above recurred, the subjects were 'refractory'. Baseline clinical measurements and specific antibody responses were used in a logistic regression model to predict 'refractory' subjects. RESULTS: Antibody to a peptide portion of lysine decarboxylase (HKL-Ab) and baseline bleeding on probing (BOP) prevalence measurements predicted attachment loss 3 months after initial therapy [pIAL = loss (0) or gain (1)]. IgG antibody contents to a purified antigen from Actinomyces spp. (A-Ab) and streptococcal d-alanyl glycerol lipoteichoic acid (S-Ab) were related in 'refractory' patients (R2 = 0.37, p < 0.01). From the regression equation, the relationship between the antibodies was defined as linear (pLA/S-Ab = 0) or non-linear pLA/S-Ab = 1). Using pLA/S-Ab, pIAL and age, a logistic regression equation was derived from 48 of the patients. Of 59 subjects, 37 had 2-4 mm attachment loss and were assigned as 'refractory' or successfully treated with 86% accuracy. CONCLUSION: HKL-Ab facilitated an accurate prediction of therapeutic outcome in subjects with moderate periodontitis.  (+info)

(8/161) Periodontal disease as a risk factor for ischemic stroke.

BACKGROUND AND PURPOSE: Chronic infectious diseases may increase the risk of stroke. We investigated whether periodontal disease, including periodontitis and gingivitis, is a risk factor for cerebral ischemia. METHODS: We performed a case-control study with 303 patients examined within 7 days after acute ischemic stroke or transient ischemic attack, 300 population controls, and 168 hospital controls with nonvascular and noninflammatory neurological diseases. All subjects received a complete clinical and radiographic dental examination. The individual mean clinical attachment loss measured at 4 sites per tooth served as the main indicator for periodontitis. RESULTS: Patients had higher clinical attachment loss than population (P<0.001) and hospital (P=0.010) controls. After adjustment for age, sex, number of teeth, vascular risk factors and diseases, childhood and adult socioeconomic conditions, and lifestyle factors, the risk of cerebral ischemia increased with more severe periodontitis. Subjects with severe periodontitis (mean clinical attachment loss >6 mm) had a 4.3-times-higher (95% confidence interval, 1.85 to 10.2) risk of cerebral ischemia than subjects with mild or without periodontitis (+info)