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PubMed2005

Factors influencing the diagnosis and treatment of periodontal disease by dental practitioners in Victoria.

BACKGROUND: Healthy periodontal tissues are essential to overall dental health. Therefore, the detection and management of periodontal disease is an integral part of general dental practice. The aim of this study was to investigate confidence in diagnosis and management of periodontal disease by general dental practitioners (GDPs), assess if the Dental Practice Board guidelines on periodontal record keeping are being addressed, and, if necessary, try to find ways of improving the periodontal knowledge of GDPs. METHODS: A survey assessing practitioner confidence in diagnosing and treating periodontal disease was sent to a random selection of 550 dental care providers registered with the Dental Practice Board of Victoria. RESULTS: Two hundred and eighty five (51.8 per cent) of questionnaires were returned completed. It was found that 79.7 per cent of the sampled population screened all new patients for periodontal disease. The majority of respondents felt confident to diagnose and treat gingivitis and initial periodontitis. However, only 61.9 per cent felt confident to diagnose aggressive/early onset periodontitis, and many were not confident in treating advanced periodontitis (36.3 per cent) or aggressive periodontitis (51.6 per cent). The majority of dentists reported that they provided most of the non surgical periodontal therapy to their patients, while most surgical treatments were referred to specialist periodontists. Factors deemed to be important in influencing the decision to provide periodontal treatment included level of training and ability to motivate patients to improve oral hygiene. Many responents requested periodontic continuing education (CE) courses be run. CONCLUSIONS: Most of the dentists surveyed were confident to diagnose periodontal disease and to treat the more common presentations of periodontal disease. There is some evidence to suggest that some practitioners are not following the minimum requirements set by the Dental Practice Board of Victoria in relation to periodontal record keeping. The results also indicate a need for more periodontic CE courses in Victoria.

Clinical Competence↗
PubMed1997

Treatment of periodontal disease in diabetics reduces glycated hemoglobin.

Periodontal disease is a common infection-induced inflammatory disease among individuals suffering from diabetes mellitus. The purpose of this study was to assess the effects of treatment of periodontal disease on the level of metabolic control of diabetes. A total of 113 Native Americans (81 females and 32 males) suffering from periodontal disease and non-insulin dependent diabetes mellitus (NIDDM) were randomized into 5 treatment groups. Periodontal treatment included ultrasonic scaling and curettage combined with one of the following antimicrobial regimens: 1) topical water and systemic doxycycline, 100 mg for 2 weeks; 2) topical 0.12% chlorhexidine (CHX) and systemic doxycycline, 100 mg for 2 weeks; 3) topical povidone-iodine and systemic doxycycline, 100 mg for 2 weeks; 4) topical 0.12% CHX and placebo; and 5) topical water and placebo (control group). Assessments were performed prior to and at 3 and 6 months after treatment and included probing depth (PD), clinical attachment level (CAL), detection of Porphyromonas gingivalis in subgingival plaque and determination of serum glucose and glycated hemoglobin (HbA1c). After treatment all study groups showed clinical and microbial improvement. The doxycycline-treated groups showed the greatest reduction in probing depth and subgingival Porphyromonas gingivalis compared to the control group. In addition, all 3 groups receiving systemic doxycycline showed, at 3 months, significant reductions (P < or = 0.04) in mean HbA1c reaching nearly 10% from the pretreatment value. Effective treatment of periodontal infection and reduction of periodontal inflammation is associated with a reduction in level of glycated hemoglobin. Control of periodontal infections should thus be an important part of the overall management of diabetes mellitus patients.

Adult↗
PubMed1999

Calprotectin in gingival crevicular fluid correlates with clinical and biochemical markers of periodontal disease.

Clinical and biochemical markers of periodontal disease have been used for precise objective diagnosis of periodontal inflammation. Interleukin 1beta (IL-1beta) and prostaglandin E2 (PGE2), inflammatory factors, levels in gingival crevicular fluid (GCF) of patients with periodontal disease are elevated and have been studied as biochemical markers. The levels of calprotectin, a leukocyte protein, in body fluids of patients with some inflammatory diseases are raised. Recently, we detected calprotectin in GCF and its concentrations in periodontal pockets were higher than those in healthy gingival crevices. In this study, we investigated the correlations between GCF calprotectin levels and clinical indicators (probing depth and bleeding on probing, BOP), and the IL-1beta or PGE2 levels in GCE Probing depth and BOP at 130 sites of 110 subjects with periodontal or other oral diseases were examined, then GCF samples were collected and their calprotectin, IL-1beta and PGE2 were determined by ELISA. The calprotectin level correlated positively with the probing depth and was significantly higher at BOP-positive than BOP-negative sites. There were significant, positive correlations between the calprotectin and IL-1beta or PGE2 concentrations. These results indicate that the calprotectin level in GCF correlates well with clinical and biochemical markers of periodontal disease and suggest that calprotectin may be useful for evaluating the extent of periodontal inflammation.

Adult↗
PubMed1998

Epidemiological and clinical aspects of periodontal diseases in diabetics.

The association between diabetes mellitus and periodontal disease has long been discussed, with conflicting conclusions. On the one hand, numerous reports indicate a high prevalence of periodontal disease in diabetics compared to healthy controls, while others fail to show such a relationship. Clarification of this dilemma has been occurring as the diagnostic criteria for periodontal disease destruction improve and the number and size of the populations surveyed grow. This review is based on a selective review of the literature from the present decade. To date, based mainly on an extensive study of the Pima Indians who have an extremely high incidence of non-insulin-dependent diabetes mellitus (NIDDM), it seems to be clear that patients with NIDDM have a higher prevalence and severity of periodontal disease destruction than non-diabetics in the same population. However, it must be borne in mind that these data are for a special population. Studies on patients with insulin-dependent diabetes mellitus (IDDM) indicate results similar to those found in studies on NIDDM. There is an increase in prevalence and severity of periodontitis compared to controls. For both IDDM and NIDDM, there does not appear to be any correlation between the prevalence or the severity of periodontal disease and the duration of diabetes. Well-controlled diabetic patients as measured by blood glycated hemoglobin levels have less severe periodontal disease than poorly controlled diabetics. The principles of treatment of periodontitis in diabetics are the same as those for non-diabetic patients and are consistent with our approach to all high-risk patients who have already developed periodontal disease. The major efforts should be directed at the prevention of periodontitis in patients at risk of developing diabetes. Another important clinical question relates to the influence of periodontal disease on the control of the diabetic state. Here again the literature is unclear; however, a recent development suggests that effective control of periodontal infection in patients with diabetes reduces the level of advanced glycosylation end products in the serum. If future studies can confirm this effect, then periodontal infection control must be considered an integral part of diabetic control.

Diabetes Complications↗
PubMed1993

Periodontal disease in an Amish population.

Epidemiological studies of periodontal disease have attempted to focus on defined groups in which the variables thought to be responsible for disease could be controlled or more easily identified. This study documents periodontal disease parameters in a unique population of Amish farmers. A total of 371 Amish were contacted and 282 were examined in their homes giving a participation rate of 76%. Ages ranged from 18 to 79 years. Overall means for periodontal conditions were 1.54 mm for attachment loss, 2.63 mm for pocket depth, 0.17 for calculus, 0.63 for plaque and 0.61 for gingivitis. One dental examiner conducted all examinations. Prevalence of periodontal disease tended to be higher among males and increased with age. The majority of Amish examined had little evidence of destructive periodontal disease; about 3.4% of teeth examined had attachment loss of 6 mm or more. These findings indicate a modest level of periodontal disease among the Amish. It is of interest that this population does not generally seek routine dental care. Preliminary analyses of health behavior data collected indicate a lack of regular oral hygiene practices. It appears that the Amish may have protective factors which affect their level of disease.

Adolescent↗
PubMed1999

Periodontal tissue disposition of azithromycin in patients affected by chronic inflammatory periodontal diseases.

BACKGROUND: The recognition that periodontal diseases are associated with specific pathogens has led to interest in the use of antibacterial drugs for inhibition of these microorganisms. On these bases, the present study was aimed at evaluating the tissue distribution of the new macrolide antibiotic azithromycin in patients subjected to oral surgery for chronic inflammatory diseases of both marginal and periapical periodontium. METHODS: Thirty-two patients were treated with azithromycin 500 mg/day orally for 3 consecutive days, and drug concentrations in plasma, saliva, normal gingiva, and pathological periodontal tissues were evaluated. For this purpose, samples of blood, saliva, normal gingiva, granulation tissue, and radicular granuloma or cyst wall (from dentigerous cyst) were collected during oral surgery or 0.5, 2.5, 4.5, and 6.5 days after the end of pharmacological treatment; then, azithromycin levels were measured by a microbiological plate assay, using Micrococcus luteus NCTC 8440 as the indicator organism. RESULTS: The concentrations of azithromycin in plasma, saliva, normal gingiva, and pathological tissues reached the highest values 12 hours after the last dose (0.37+/-0.05 mg/l, 2.12+/-0.30 mg/l, 6.30+/-0.68 mg/kg, and 11.60+/-1.50 mg/kg, respectively) and then declined gradually. Consistent levels of the drug in normal gingiva and pathological tissues could be detected, however, up to 6.5 days, indicating that azithromycin was retained in target tissues for a long time after the end of treatment. Moreover, azithromycin levels in both normal gingiva and pathological tissues exceeded the minimum inhibitory concentrations of most pathogens involved in the pathophysiology of chronic inflammatory periodontal diseases. Notably, azithromycin levels in pathological tissues were significantly higher than those in normal gingiva 0.5, 2.5, and 4.5 days after the last dose. CONCLUSIONS: The present results indicate a marked penetration of azithromycin into both normal and pathological periodontal tissues, suggesting that azithromycin represents a promising option in both adjunctive and prophylactic treatments of chronic inflammatory periodontal diseases.

Adolescent↗
PubMed1978

The use of extracted teeth to evaluate clinical measurements of periodontal disease.

Clinical indicators of periodontal disease, Gingivitis Index, Gingival crevicular fluid and pocket depth measurements were obtained from the gingiva surfaces of 30 teeth. The gingival margins were marked on the surfaces of the teeth prior to extraction. The extracted teeth were stained with hematoxylin and air dried, and the distances from the groove to the base of the calculus, plaque, and connective tissue attachment were obtained. The plaque-free zone was also measured. Comparisons were made between clinical and tooth surface measurements. A high correlation was found between clinical pocket depth measurements and tooth surface parameters. The correlations between all tooth surface parameters and GCF were statistically significant. The G.I. was significantly correlated only with the penetration of calculus into the pocket. The clinical pocket depth was statistically the same as the distance from the gingival groove to the coronal connective tissue attachment. The plaque-free zone appeared to represent the junctional epithelium.

Dental Calculus↗
PubMed1996

Periodontal disease and cardiovascular disease.

It is our central hypothesis that periodontal diseases, which are chronic Gram-negative infections, represent a previously unrecognized risk factor for atherosclerosis and thromboembolic events. Previous studies have demonstrated an association between periodontal disease severity and risk of coronary heart disease and stroke. We hypothesize that this association may be due to an underlying inflammatory response trait, which places an individual at high risk for developing both periodontal disease and atherosclerosis. We further suggest that periodontal disease, once established, provides a biological burden of endotoxin (lipopolysaccharide) and inflammatory cytokines (especially TxA2, IL-1 beta, PGE2, and TNF-alpha) which serve to initiate and exacerbate atherogenesis and thromboembolic events. A cohort study was conducted using combined data from the Normative Aging Study and the Dental Longitudinal Study sponsored by the United States Department of Veterans Affairs. Mean bone loss scores and worst probing pocket depth scores per tooth were measured on 1,147 men during 1968 to 1971. Information gathered during follow-up examinations showed that 207 men developed coronary heart disease (CHD), 59 died of CHD, and 40 had strokes. Incidence odds ratios adjusted for established cardiovascular risk factors were 1.5, 1.9, and 2.8 for bone loss and total CHD, fatal CHD, and stroke, respectively. Levels of bone loss and cumulative incidence of total CHD and fatal CHD indicated a biologic gradient between severity of exposure and occurrence of disease.

Alveolar Bone Loss↗
PubMedDate not supplied

The use of systemic antibiotics in the treatment of aggressive periodontal disease.

General dentists frequently encounter patients with aggressive periodontal disease and should be able to diagnose and manage this disease properly. Periodontal care in the absence of a comprehensive treatment plan and proper therapy can result in the rapid progression of the disease and, ultimately, tooth loss. It is important for the general dentist to diagnose, inform, and treat the periodontal patient accurately, using referral and nonsurgical, surgical, and antimicrobial/antibiotic therapy. This article provides a brief history of the classification of aggressive periodontal disease, describes the microorganisms associated with aggressive periodontal disease, discusses the selection and use of systemic antibiotics in therapy, and lists the various antibiotic regimens for treating aggressive periodontal disease.

Administration, Oral↗
PubMed1998

[Stess analysis of conical telescope denture using on the prosthodontic treatment for basic teeth combined periodontal diseases]

OBJECTIVE:Periodontal splints were made both on patients with peridontal absorption of three different degrees and on normal situation respectively followed by finite element calculation.The result sugree that the stesses of the supporting tissues redistributed during mastication in accordance with different degrees of periodontal absorption.The more obvious of the pcriodontal absorption is the more stress value of the periodontal supporting tissue decrease,while those of the subbasal supporting tissues increase.

Journal Article↗
PubMedDate not supplied

[The use of an ortofen-containing paste in the combined treatment of periodontal diseases].

A periodontal dressing for the treatment of gingivitis and periodontitis, characterized by antiinflammatory and antibacterial action, was developed and clinically tried. Application of this dressing cut down the periods of treatment of chronic gingivitis and periodontitis, shortens the period of preparation to surgery, and provides a smooth course of the postoperative period.

Adult↗
PubMed1976

Controversies, perspectives, and clinical implications of nutrition in periodontal disease.

Many controversies concerning the role of nutrition in periodontal disease and problems in the design and analysis of nutrition-periodontal disease studies have been reviewed. In addition, recent advances in the interactions of nutrition, host defense, and infection have been conceptually related to the pathogenesis of periodontal disease. Finally, nutritional factors relevant to the diagnosis and clinical management of patients with periodontal disease have been discussed. The concepts developed with respect to experimental design and the host defenses approach to periodontal disease, will hopefully serve to encourage definitive studies which may delineate a more precise role for nutrition in periodontal disease.

Animals↗
PubMed1998

Interactions between non-immune host cells and the immune system during periodontal disease: role of the gingival keratinocyte.

Periodontal disease and inflammatory dermatoses, such as psoriasis, are characterized by the accumulation of dense inflammatory infiltrates immediately beneath the epithelial cell layer of the gingiva and skin, respectively. Dermatologists are increasingly aware that the epidermal keratinocyte probably contributes to inflammatory disease progression by secreting a number of pro-inflammatory cytokines and expressing various adhesion molecules. In psoriatic lesions, it is now believed that epidermal keratinocytes may also act as antigen-presenting cells and participate directly in the superantigenic activation of T-cell clones, some of which may initiate, contribute to, or maintain the disease process. Although the role of the host response in periodontal disease has been extensively studied over the years, very little is known about the contribution of the gingival keratinocyte to the inflammatory response. The available published information is discussed in this review, and we suggest that, like its epidermal counterpart, the gingival keratinocyte may participate actively in the pathogenesis of periodontal disease.

Antigen-Presenting Cells↗
PubMed2001

Postnatal glutamate-induced central nervous system lesions alter periodontal disease susceptibility in adult Wistar rats.

BACKGROUND: Inability to mount a suitable brain-neuroendocrine response to bacterial or other antigenic challenges has been found to play an important rôle in infectious and inflammatory disease susceptibility and progression, including periodontal disease. OBJECTIVE: The present study was designed to determine the effects of glutamate administration to new-born Wistar rats on the development and progression of naturally occurring and ligature-induced periodontal disease in the rats as adults. Postnatal glutamate administration is known to permanently damage neurones in the hypothalamic arcuate nucleus. METHOD: New-born rats were treated 1x daily subcutaneously with 2 mg/g of monosodium-L-glutamate (MSG) for 5 days from day 3 to 6. Control animals were injected with similar amounts of saline. Experimental ligature-induced periodontal disease was induced in the rats at the age of 12 weeks at maxillary right 2nd molar teeth. The contralateral maxillary left 2nd molars served as control teeth, and for assessment of naturally occurring periodontal disease. Disease progression was evaluated histometrically. RESULTS: The results revealed that the glutamate-lesioned rats developed significantly more periodontal tissue destruction compared to sham-lesioned control rats in both the ligated and non-ligated teeth. CONCLUSIONS: This study supports our recent findings indicating that inappropriate brain-neuroendocrine-immune regulation may play a rôle in periodontal disease susceptibility and progression.

Animals↗
PubMed2006

[Proinflammatory cytokines in pathogenesis of periodontal disease].

The pathologic mechanisms of periodontal disease are still not completely understood. Current knowledge concerning the pathogenesis of periodontitis suggests an interaction between putative periodontal pathogens and the host defense system which results in the inflammation and eventual destruction of supporting periodontal tissues, including connective tissue and alveolar bone. Bacterial products stimulating host cells lead to a release of inflammatory mediators such as cytokines. These regulators have attracted particular research attention and are suspected to be involved in both inflammation-related alteration and repair of the periodontal tissues. This study - based on current literature - shows the modern understanding of the role of proinflammatory cytokines in periodontal disease pathogenesis.

Cytokines↗
PubMed1999

[Epidemiological study on association of periodontal disease and total and differential leukocyte counts].

Periodontal disease is defined as inflammation that is caused by bacteria in dental plaque. This disease is liable to be a factor contributing to the high leukocyte count over an extended period. Furthermore, a number of prospective epidemiologic studies have shown that the leukocyte count is a good predictor of ischemic heart disease (IHD). However there have been few epidemiological studies of the relationship between periodontal disease and the leukocyte count. The purpose of this study was to investigate the relationship between the total and differential leukocyte counts and oral conditions of Japanese factory workers who were classified according to their smoking habits. The 1,167 subjects were male factory workers employed with a chemical factory in Osaka, Japan. The oral conditions recorded were periodontal status (Community Periodontal Index of Treatment Needs, CPITN). The relationship between the total and differential leukocyte counts and the CPITN score of subjects who were classified according to their smoking habits was investigated in 1996 and 1997. In both the current smokers and nonsmokers, the subjects with severe periodontal disease, in contrast to the normal subjects, exhibited total leukocyte, neutrophil and monocyte counts that were significantly high for 1 year during follow-up studies. The periodontal disease is shown that causes the total leukocyte and neutrophil counts related to the development of IHD to remain at a high level.

Adult↗
PubMed2003

Alveolar bone response in an experimental model of renal failure and periodontal disease: a histomorphometric and histochemical study.

BACKGROUND: Chronic destructive periodontal disease is characterized by gingival inflammation, periodontal pocket formation, and bacterial plaque that lead to alveolar bone destruction. Polymorphonuclear neutrophil leukocytes (PMNs) are the first line of defense against infection caused by dental plaque bacteria. Renal patients present functional abnormalities of PMN, including impaired chemotaxis, phagocytosis, and intracellular killing of bacteria. In view of the above, the aim of this work was to evaluate the effect of renal failure on bone damaged by periodontal disease using histomorphometric and histochemical parameters. METHODS: Twenty male Wistar rats weighing 250 g were assigned to one of the following four groups: 1) control (no treatment); 2) renal failure (RF); 3) periodontal disease (PD); and 4) renal failure plus periodontal disease (RF+PD). All the animals were sacrificed 31 days after the onset of the experiment. Mesio-distally oriented sections of the first lower molar were obtained for histomorphometric and histochemical evaluation. RESULTS: Total erosion, active erosion, and total number of tartrate-resistant acid phosphatase-positive (TRAP+) osteoclasts were found to be increased in the RF+PD group compared with the PD group. CONCLUSION: Our results demonstrate increased bone resorption in animals with untreated renal failure and periodontal disease, and thus indicate that the release of different factors by inflammatory cells is magnified, accelerating the progression of the disease in this animal model.

Acid Phosphatase↗
PubMed2000

Passive immunization against dental caries and periodontal disease: development of recombinant and human monoclonal antibodies.

Indigenous micro-organisms in the oral cavity can cause two major diseases, dental caries and periodontal diseases. There is neither agreement nor consensus as to the actual mechanisms of pathogenesis of the specific virulence factors of these micro-organisms. The complexity of the bacterial community in dental plaque has made it difficult for the single bacterial agent of dental caries to be determined. However, there is considerable evidence that Streptococcus mutans is implicated as the primary causative organism of dental caries, and the cell-surface protein antigen (SA I/II) as well as glucosyltransferases (GTFs) produced by S. mutans appear to be major colonization factors. Various forms of periodontal diseases are closely associated with specific subgingival bacteria. Porphyromonas gingivalis has been implicated as an important etiological agent of adult periodontitis. Adherence of bacteria to host tissues is a prerequisite for colonization and one of the important steps in the disease process. Bacterial coaggregation factors and hemagglutinins likely play major roles in colonization in the subgingival area. Emerging evidence suggests that inhibition of these virulence factors may protect the host against caries and periodontal disease. Active and passive immunization approaches have been developed for immunotherapy of these diseases. Recent advances in mucosal immunology and the introduction of novel strategies for inducing mucosal immune responses now raise the possibility that effective and safe vaccines can be constructed. In this regard, some successful results have been reported in animal experimental models. Nevertheless, since the public at large might be skeptical about the seriousness of oral diseases, immunotherapy must be carried out with absolute safety. For this goal to be achieved, the development of safe antibodies for passive immunization is significant and important. In this review, salient advances in passive immunization against caries and periodontal diseases are summarized, and the biotechnological approaches for developing recombinant and human-type antibodies are introduced. Furthermore, our own attempts to construct single-chain variable fragments (ScFv) and human-type antibodies capable of neutralizing virulence factors are discussed.

Adhesins, Bacterial↗