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Risk for periodontal disease in patients with longstanding rheumatoid arthritis.

OBJECTIVE: To quantify periodontal disease in rheumatoid arthritis (RA) patients and controls, and to correlate the degree of destruction from periodontal disease and from RA. METHODS: Fifty RA patients were matched for age, sex, smoking status, and oral hygiene with 101 controls. Correlations between indices of chronic destruction in periodontal disease (gingival attachment loss) and in RA (Larsen radiographic score) were determined. RESULTS: Patients with longstanding active RA (mean +/- SD 13 +/- 8 years) who were receiving treatment with disease-modifying antirheumatic drugs (n = 46), corticosteroids (n = 38), or nonsteroidal antiinflammatory drugs (n = 43) had a higher rate of gingival bleeding (increased by 50%), greater probing depth (increased by 26%), greater attachment loss (increased by 173%), and higher number of missing teeth (increased by 29%) compared with controls. No correlation was found between the Larsen radiographic score and gingival attachment. CONCLUSION: Patients with longstanding active RA have a substantially increased frequency of periodontal disease, including loss of teeth, compared with controls. Antiinflammatory treatment interferes with periodontal disease and might have masked a possible correlation between the indices of chronic destruction in RA and periodontal disease.

Adult↗

Etiology and pathogenesis of periodontal diseases.

The two most prevalent and most investigated periodontal diseases are dental plaque-induced gingivitis and chronic periodontitis. The last 10 to 15 years have seen the emergence of several important new findings and concepts regarding the etiopathogenesis of periodontal diseases. These findings include the recognition of dental bacterial plaque as a biofilm, identification and characterization of genetic defects that predispose individuals to periodontitis, host-defense mechanisms implicated in periodontal tissue destruction, and the interaction of risk factors with host defenses and bacterial plaque. This article reviews current aspects of the etiology and pathogenesis of periodontal diseases.

Biofilms↗

[Measuring of thresholds of the periodontal diseased teeth by electric pulp tester].

Studying of influence of periodontal disease on vitality of pulp, the response thresholds of 421 teeth (250 normal teeth, 171 periodontal diseased teeth) were examined electronically by means of an automatic pulptester. (ANALYTIC TECHNOLOGY CO.) The pulp tester values of three experiments were averaged. The average value of normal teeth was 36.3 and that of periodontal diseased teeth 31.4. The response thresholds of periodontal diseased teeth were lower than those of normal teeth. This indicated that pulp was inflamed by periodontal disease and pulp vitality became weak.

Dental Pulp Diseases↗

[Periodontal disease and implant-supported prostheses].

Periodontal disease is one of the most common dental pathologies which is found in more than 80% of the Japanese adult population. It is also one of the major causes of tooth loss where more than 50% of the tooth are lost due to the periodontal disease. To reconstruct the dental defects, and re-establish the lost functions due to the periodontal disease are very important aspects of the clinical dentistry. Because of the aging society, these services will become even more critical. To lose a tooth not only means a compromised masticatory efficiency, but it has a profound effect on the patient's QOL and ADL. That is why the rehabilitation of the dental function becomes so important. There are two major clinical procedures for the reconstruction of the lost dental functions. They are (1) bridge or partial denture, and (2) implant-supported prostheses. Among other problems, the crown-root ratio of the periodontally involved teeth are less than adequate to serve as an abutment tooth for a bridge, or a clasped tooth for a partial denture. Their prognosis is questionable because of an excessive load over the diseased tooth. Implant-supported prostheses, in contrast, have an excellent long term prognosis because the prosthetic appliances are directly supported by the jaw bone.

English Abstract↗

Periodontal diseases in HIV-infected patients.

Periodontal diseases may be the first clinical sign of human immunodeficiency virus (HIV)-infection. Since the immunosuppression and subsequent susceptibility may alter the responses of the oral tissues as well as the microflora, both periodontal treatment and result of therapy may be modified. The periodontal diseases in HIV-seropositive patients include common as well as less conventional forms of gingivitis and periodontitis, and bacterial, mycotic and viral infections are seen. Neoplasias may also involve the periodontium; most common are Kaposi's sarcoma and non-Hodgkin's lymphoma. Recent studies of unselected groups of patients indicate that periodontal health in at least some groups of HIV-seropositive patients is better than previously reported.

Gingival Neoplasms↗

Periodontal disease in adult insulin-dependent diabetics.

The overall objective with the present investigations was to study the influence of insulin-dependent diabetes mellitus (IDDM) on periodontal conditions and to identify factors that may be predictors for severe periodontal disease in individuals with IDDM. Periodontal conditions were studied in two cross-sectional studies of adult, insulin-dependent diabetics and age-and sex-matched controls. In one study 72 diabetics with short-(SD) and 82 with long-duration (LD) diabetes and 77 controls participated. In the other study 83 LD diabetics and 99 controls took part. The portion of individuals exhibiting severe periodontal disease was larger in the diabetic group than in the control group. Advanced periodontal disease appeared in earlier ages (40-49 years) in the LD diabetics compared to the SD diabetics and controls. In fact, the 40-49-year-old LD diabetics had alveolar bone loss equal to the older controls (60-69 years). LD diabetics exhibited more severe periodontitis than SD diabetics. Some salivary factors were studied in 72 SD and 82 LD diabetics and 77 controls. LD and SD diabetics had a lower stimulated salivary secretion rate and an increased glucose content compared to the controls. The reduction in flow rate, however, was moderate, and all mean values were within the normal limits. The moderately increased glucose content did not result in higher mean numbers of Candida albicans, lactobacilli, and mutans streptococci. The subgingival bacterial species currently considered to be associated with periodontitis were studied in 30 LD diabetics and 34 controls. All these bacterial species were recovered in diabetics as well as controls. More LD diabetics than controls harboured Porphyromonas gingivalis. In the control group the periopathogens were recovered more often in deep periodontal pockets. In the LD group, however, these bacterial species were recovered as often in shallow as in deep periodontal pockets. The medical status of 39 matched pairs of LD diabetics was analysed. One in each pair had severe periodontal disease while the other had no/minor symptoms of periodontal disease. Biochemical analyses and clinical variables routinely used in monitoring diabetics failed to discriminate between diabetics with severe and minor periodontal disease. Diabetics with severe periodontal disease, however, showed a higher prevalence of renal disease and cardiovascular complications such as stroke, transient ischemic attacks, angina, myocardial infarct, heart failure, and claudicatio intermittens than diabetics with only minor periodontal disease. This indicates that closer cooperation between the diabetologist and the dentist is necessary in monitoring the diabetic patient.

Adult↗

Osteoporosis and periodontal disease: a review.

A review of the literature on the relationship between osteoporosis and periodontal disease is presented. Osteoporosis, a metabolic disease, and periodontal disease, which is infectious, are both major health problems with multifactorial etiologies. There is histologic and radiographic evidence from animals and humans that osteoporosis does affect alveolar bone by decreasing bone mass and trabeculation. The literature reviewed in this paper suggests, but does not yet provide conclusive evidence for, a direct relationship between osteoporosis and periodontal disease.

Aged↗

Periodontal disease as a specific, albeit chronic, infection: diagnosis and treatment.

Periodontal disease is perhaps the most common chronic infection in adults. Evidence has been accumulating for the past 30 years which indicates that almost all forms of periodontal disease are chronic but specific bacterial infections due to the overgrowth in the dental plaque of a finite number of mostly anaerobic species such as Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola. The success of traditional debridement procedures and/or antimicrobial agents in improving periodontal health can be associated with the reduction in levels of these anaerobes in the dental plaque. These findings suggest that patients and clinicians have a choice in the treatment of this overgrowth, either a debridement and surgery approach or a debridement and antimicrobial treatment approach. However, the antimicrobial approach, while supported by a wealth of scientific evidence, goes contrary to centuries of dental teaching that states that periodontal disease results from a "dirty mouth." If periodontal disease is demonstrated to be a risk factor for cardiovascular disease and stroke, it will be a modifiable risk factor since periodontal disease can be prevented and treated. Since the antimicrobial approach may be as effective as a surgical approach in the restoration and maintenance of a periodontally healthy dentition, this would give a cardiac or stroke patient and his or her physician a choice in the implementation of treatment seeking to improve the patient's periodontal condition so as to reduce and/or delay future cardiovascular events.

Anaerobiosis↗

Is periodontal disease during orthodontics preventable?

Periodontal disease during orthodontic therapy is preventable and is controllable and in continuous studies after orthodontic therapy has been completed, it has been shown that under the properly controlled regimen of treatment the destruction to the periodontal tissues of the teeth is not accentuated to a statistically significant degree as greater than that which occurs during the same interim without orthodontic therapy. This encourages us; however, the difficulties cited in the paper above challenges us and our finest professional skills in the proper care of the orthodontic patients with periodontal complications.

Humans↗

[Periodontal disease and atherosclerosis: an underestimated link?].

Periodontal disease is a common bacterial and destructive disorder of oral tissues. We reviewed epidemiological and experimental to data studies demonstrating close associations between chronic periodontitis and development of generalized inflammation, vascular endothelial injury, and atherosclerosis. Periodontal disease has been convincingly emerging as an important independent cardiovascular risk factor. It deserves timely treatment also as a likely part of primary prevention of ischemic heart disease, stroke, and peripheral vascular disease.

C-Reactive Protein↗

Progressive periodontal disease and risk of very preterm delivery.

OBJECTIVE: The goal was to estimate whether maternal periodontal disease was predictive of preterm (less than 37 weeks) or very preterm (less than 32 weeks) births. METHODS: A prospective study of obstetric outcomes, entitled Oral Conditions and Pregnancy (OCAP), was conducted with 1,020 pregnant women who received both an antepartum and postpartum periodontal examination. Predictive models were developed to estimate whether maternal exposure to either periodontal disease at enrollment (less than 26 weeks) and/or periodontal disease progression during pregnancy, as determined by comparing postpartum with antepartum status, were predictive of preterm or very preterm births, adjusting for risk factors including previous preterm delivery, race, smoking, social domain variables, and other infections. RESULTS: Incidence of preterm birth was 11.2% among periodontally healthy women, compared with 28.6% in women with moderate-severe periodontal disease (adjusted risk ratio [RR] 1.6, 95% confidence interval [CI] 1.1-2.3). Antepartum moderate-severe periodontal disease was associated with an increased incidence of spontaneous preterm births (15.2% versus 24.9%, adjusted RR 2.0, 95% CI 1.2-3.2). Similarly, the unadjusted rate of very preterm delivery was 6.4% among women with periodontal disease progression, significantly higher than the 1.8% rate among women without disease progression (adjusted RR 2.4, 95% CI 1.1-5.2). CONCLUSION: The OCAP study demonstrates that maternal periodontal disease increases relative risk for preterm or spontaneous preterm births. Furthermore, periodontal disease progression during pregnancy was a predictor of the more severe adverse pregnancy outcome of very preterm birth, independently of traditional obstetric, periodontal, and social domain risk factors. LEVEL OF EVIDENCE: II-2.

Adolescent↗

Periodontal disease and NIDDM in Pima Indians.

The goal of this study was to determine the prevalence and incidence of periodontal disease and its relationship with non-insulin-dependent diabetes mellitus (NIDDM). Two thousand two hundred seventy-three Pima Indians (949 men, 1324 women) aged greater than or equal to 15 yr from the Gila River Indian Community in Arizona were examined between 1983 and 1989. Periodontal disease was diagnosed by tooth loss and by percentage of interproximal crestal alveolar bone loss ascertained from panoramic radiography. Subjects with little or no evidence of periodontal disease were classified as nondiseased. Thus, the incidence of advanced periodontal disease was determined. The age- and sex-adjusted prevalence of periodontal disease at first dental examination was 60% in subjects with NIDDM and 36% in those without. Twenty-two new cases developed in a subset of 701 subjects (272 men, 429 women) aged 15-54 yr who initially had little or no evidence of periodontal disease and had at least one additional dental examination. The incidence of periodontal disease in this group was similar in men and women (incidence-rate ratio 1.0, 95% confidence interval [Cl] 0.5-1.9, controlled for age and diabetes). Higher age predicted a greater incidence of periodontal disease (chi 2 = 30.6, df = 3, P less than 0.001, controlled for sex and diabetes). The rate of periodontal disease in subjects with diabetes was 2.6 times (95% Cl 1.0-6.6, controlled for age and sex) that observed in those without. Although periodontal disease was common in nondiabetic Pima Indians, in whom most of the incident cases occurred, diabetes clearly conferred a substantially increased risk. Thus, periodontal disease should be considered a nonspecific complication of NIDDM.

Adolescent↗

[The relationship between periodontal diseases and prostacyclin in saliva of periodontal patients by RIA]

The purpose of this investigation was to measure the changes of Prostacyclin(PG12) occuring in gingivitis and periodontitis.Fifteen cases of periodontitis,ten cases of gingivitis and ten cases of healthy participated in this study,Saliva was taken before treatment,Prostacyclin in saliva was measure by radioimmunoassay(RIA).The results showed that prostacyclin of human saliva is increased from healthy gingivitis to periodontitis.There is a statistical difference between groups,6-k-PGF1alpha in saliva of periodontitis is 3.6 folds of healthy.Gingivitis is 2.6 folds of healthy.There is also a significant difference between adult periodontitis our findings suggested that prostacyclin may play an important role in etiology of periodontal disease.Measured 6-k-PGF1alpha in saliva may indicate the severity of periodontal disease.

Journal Article↗

[Nomenclature of regional tissue changes in periodontal diseases].

The nomenclature of periodontal diseases has undergone repeated alterations in the course of time. An important reason for this was the difficulty of reconciling the clinical symptomatology, which must always be the basis of a classification, with the nature of the tissue changes, i.e. with the pathogenetic principles underlying them.

Humans↗