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PubMed1979

Clinical evaluation of spiramycin and erythromycin in control of periodontal disease.

Two studies are reported. Each was double-blind in which Spiramycin was compared to Erythromycin and a placebo, to determine the value of Spiramycin as a therapeutic agent in the control of periodontal disease. In Study 1, 48 adults with varying degrees of periodontal disease were randomly assigned to treatment and control groups. Assessments of gingival index, plaque height, pocket depth, crevicular fluid volume and wet plaque weight were made. During this 4-week clinical trial, the patients maintained their usual oral hygiene. The medication was administered systemically for 5 days, starting at the conclusion of week 2. Spiramycin significantly reduced the scores for the five parameters recorded. When comparison were made, the greatest recorded effect with Spiramycin treatment was found in patients with advanced periodontal disease. The indication of this trend favouring Spiramycin led to an extension of this clinical trial involving only patients with advanced periodontal lesions. This second study comprised 54 adults. The same parameters were measured over the same time period as in Study 1. Spiramycin again was responsible for the greatest reduction in the recorded scores. For example, average pocket depth was decreased by approximately 30%, whereas Erythromycin produced a reduction of 15%. It would appear that Spiramycin is of definite benefit in the management of periodontal disease, especially in the more advanced cases.

Administration, Oral↗
PubMed1989

Periodontal disease and oral microbial successions during myelosuppressive cancer chemotherapy.

Factors contributing to the succession of opportunistic pathogens at oral sites, including the periodontium, during myelosuppressive chemotherapy are poorly understood. This study examined the relation of periodontal disease to qualitative and proportional shifts in the oral microflora of 21 acute nonlymphocytic leukemia patients (7 male and 14 female, mean age (range) = 51.0 (25-81 years) observed during standardized myelosuppressive regimens. Supra- and subgingival microbial plaque specimens were individually collected from 2 contralateral oral sites (distobuccal of teeth 1-6 and 3-6) in each participant at hospital admission (day 1) and during point of maximal myelosuppression (day 14). Periodontal disease indices obtained at day 1 included site-specific measures of attachment loss and clinical assessment of disease status. Using a residualized change score analysis, periodontal disease status and attachment loss were positively correlated with increases in the proportional recovery of Staphylococcus sp. from supragingival sites and total yeast from supra- and subgingival sites. When age-related covariation in the microbial shifts was controlled in the analysis, periodontal disease status and attachment loss demonstrated no significant correlation with increases in total yeast at supragingival sites. These findings suggest that host factors such as periodontal disease may contribute to patterns of oral microbial successions during cancer chemotherapy.

Adult↗
PubMed1976

Vitamin E and periodontal disease.

Vitamin E levels in patients with and without periodontal disease were measured. There was no significant difference in the levels of serum vitamin E between these two groups. These data do not provide support for the treatment of inflammatory periodontal disease with vitamin E.

Adult↗
PubMed1994

Assessment of interleukin-6 in the pathogenesis of periodontal disease.

This study was performed to investigate the aspects of interleukin-6 (IL-6) production in both the gingival tissue and the peripheral blood of patients with periodontal disease and of periodontally healthy subjects. In addition, IL-6 expression in human gingival tissues was studied by reverse transcription-polymerase chain reaction analysis and by immunoperoxidase staining with anti-IL-6 monoclonal antibody. The levels of IL-6 in the culture supernatants from peripheral blood mononuclear cells (PBMC) stimulated with lipopolysaccharide and in serum were examined by bioassay. We detected IL-6 mRNA expression in all inflamed gingival tissues (17/17) examined and in 2/4 in healthy gingival tissues. IL-6 protein was detected mainly in endothelial cells, fibroblasts, and macrophages but not in the area containing T or B cells in the inflamed gingival tissues, and was not detected at all in healthy gingival tissues. There was no significant difference between the subjects with periodontal disease and those with healthy gingival tissues either in serum IL-6 levels or in the amount of IL-6 produced by PBMC. These results suggest that non-lymphoid cells in inflamed gingival tissue may contribute to the pathogenesis of periodontal disease via IL-6 production, and that the IL-6 produced in gingival tissue may not reflect the IL-6 levels in peripheral blood.

Adult↗
PubMedDate not supplied

[Periodontal disease in juvenile diabetics and non-diabetics].

BACKGROUND: Knowing the prevalence of periodontal disease, to identify some associated variables in youth population. Insulin dependent diabetes mellitus (DMID) has been included as a common variable. METHODS: Cross-sectional study over 383 individuals, 11 to 18 years old. Chi square and Odds ratio (95% confidence limits) have been determined. RESULTS: Periodontal disease prevalence is 37.53%. An epidemiological and statistical association were found with: Insulin-dependent diabetes mellitus, low social class, poor dental hygiene and plaque index over 0.20. CONCLUSIONS: Juvenile diabetic population must be considered as a high risk group for periodontal disease.

Adolescent↗
PubMed2001

Elevated blood glucose levels in patients with severe periodontal disease.

BACKGROUND, AIMS: The rôle of diabetes mellitus in various forms of periodontal disease was investigated intensively in the past; some studies have also indicated an impact of periodontal inflammation on diabetic balance. The purpose of this study was to evaluate the reciprocal relationship between abnormal serum glucose levels and elevated CPITN scores in non-diabetic patients. MATERIAL AND METHODS: 10,590 subjects were analyzed for normal and abnormal (higher than 120 mg/dl) serum glucose levels, their periodontal status reflected as CPITN was correlated with their glucose level category. RESULTS: The results of the present study reflect a significant association between elevated blood glucose levels (higher than 120 mg/dl) and CPITN scores of 4.5 with an odds ratio of 2.46. CONCLUSION: A strong association exists between abnormal serum glucose level and periodontal disease as manifested by CPITN score.

Age Factors↗
PubMed2001

Periodontal disease in pregnancy complicated by type 1 diabetes mellitus.

BACKGROUND: Systemic disease and hormonal changes have been implicated as complicating factors for periodontal disease. Diabetes has been identified as a risk factor for periodontal disease, and diabetics can experience periodontal destruction at an earlier age than non-diabetic individuals. Increased hormone levels during pregnancy can contribute to increased gingival inflammation. The purpose of this study was to examine the association of type 1 diabetes mellitus (DM) on the periodontal status of pregnant women. METHODS: Thirty-three (13 diabetic and 20 non-diabetic) subjects, 20 to 39 weeks gestation, participated in this study. The mean age of the diabetics and non-diabetics was 28.5 +/- 7.1 (SD) and 27.0 +/- 7.3 years, respectively. The following parameters were assessed at Ramfjord's reference teeth: plaque index (PI), gingival inflammation (GI), probing depth (PD), gingival margin (GM) location, and clinical attachment level (CAL). RESULTS: Diabetic subjects had significantly (P<0.001) higher PI (1.48 +/- 0.69) and GI (1.77 +/- 0.44) scores than non-diabetics (PI = 0.63 +/- 0.38; GI = 0.93 +/- 0.48). Mean PD for diabetics (2.95 +/- 0.69 mm) was significantly different (P<0.024) from that of non-diabetics (2.44 +/- 0.32 mm). Although mean GM location was coronal to the cemento-enamel junction (CEJ) in both groups, gingival margins were at a more apical position (P<0.001) in the diabetics (-0.20 +/- 1.24 mm) compared to non-diabetics (-1.76 +/- 0.53 mm). Mean CAL values also varied significantly (P<0.001) between diabetics (2.60 +/- 1.54 mm) and non-diabetics (0.68 +/- 0.65 mm). Significant differences were seen for GI (P<0.001), PD (P=0.005), GM location (P<0.001), and CAL (P<0.001) when assessing the effect of diabetes and controlling for plaque. When assessing the effect of plaque and controlling for diabetes, the only significant difference was GI (P=0.001). CONCLUSIONS: The results of this study demonstrate that periodontal inflammation and destruction are increased in pregnant diabetics as compared to non-diabetic pregnant patients. These findings may have implications for diabetic control and, hence, maternal and fetal outcomes in pregnant diabetic patients.

Adult↗
PubMed1975

[The uptake of oxygen and glucose by the gingiva in diabetes mellitus with various forms of periodontal diseases].

Gingiva biopsy samples from healthy individuals and from diabetics with different forms of periodontal disease were incubated in the Warburg apparatus for 2 hours. Considerable reduction in oxygen consumption and glucose uptake was found in each type of periodontal disease, the most marked reduction being stated in case of parodontopathia dystrophica. The extent of the metabolic disturbance as well as the appearence of periodontal disease correlated with the duration of diabetes on the one hand with the frequency and severity of diabetic retinopathy on the other hand.

Adult↗
PubMed2003

Association between interleukin-1 genotype and periodontal disease in a diabetic population.

BACKGROUND: Recently, it has become evident that for many common chronic diseases, modifying factors amplify disease mechanisms to make the clinical condition more severe. The aims of this report were 1) to investigate the prevalence of periodontitis in a diabetic population, 2) to evaluate the association of periodontitis with metabolic control, and 3) to evaluate periodontitis in diabetics with different interleukin (IL)-1 genotypes. METHODS: One hundred diabetic patients were screened. Type and duration of diabetes, level of control (glycosylated hemoglobin), and demographic data were recorded. Periodontal disease was defined as two or more teeth with clinical attachment loss (CAL) > or = 5 mm. Poorly controlled diabetes was defined as glycosylated hemoglobin values > 8%. Finger-stick blood samples were collected and analyzed for genotyping of IL-1A (+4845), IL-1B (+3954), IL-1B (-511), and IL-1RN (+2018) polymorphisms. RESULTS: Among the diabetic patients in the study, 66% showed periodontal destruction, and 43% of those could be characterized as severe. The prevalence of severe attachment loss increased with decreasing control of diabetes. Only the IL-1B (-511) genotype was found to be associated with periodontal disease in the African American patients (P<0.05). The frequency of allele 1 was 0.77 in periodontitis affected versus 0.33 in healthy African American diabetics. A borderline significant association between IL-1B (+3954) and periodontal disease also was noted in Caribbean periodontal patients (P=0.06); however, the allele 2 frequency in this population was only 10%. CONCLUSIONS: These data confirm the high prevalence and severity of periodontitis in the diabetic population, and support the association between poor glycemic control and periodontal disease. The low prevalence of some of the IL-1 gene polymorphisms in the ethnic groups included in this study limits the validity of conclusions on genotype associations with clinical findings, but there was a trend suggesting that allele 1 at IL-1B (-511) and IL-1B (+3954) was overrepresented among diabetics with periodontal disease.

Adult↗
PubMed1975

Standardization of the epidemiologic assessment of periodontal diseases. Surveys in the South Pacific.

Attempts of introducing uniform techniques for the collection of statistical data on the prevalence of periodontal diseases have been made by FDI and WHO in order to arrive at valid, reproducible, and internationally comparable results. The WHO Manual of the International Classification of Diseases. Application to Dentistry offers a five digit classification of all oral diseases for statistical purposes. In contrast to morbidity statistics, epidemiological surveys must be based on adequate samples, representative for the entire population or distinct strata thereof. FDI is actually preparing guidelines for the conduct of clinical trials in periodontal diseases, comparable to those on caries incidence, indicating the proper use of indices. For the epidemiological assessment of periodontal diseases, the WHO Basic Methods (1962, 1971) have recommended the use of simple ratios of persons affected with signs of the disease. Data collected in four extensive dental surveys in Polynesian and Melanesian populations in the South Pacific served as an example to show the variety of valid information provided by these basic methods. The main results showed an early appearance of pocket formation at ages 10 to 14, preceded in a statistically significant way by calculus formation and gingivitis. A constant pattern in the sequence of attack of the various teeth by pocket formation was shown to be specific for these island populations; males were consistently more affected than females. The character of periodontal diseases prevalent among Polynesians and Melanesians was recognized to be a "dirt pyorrhea" accompanied by progressive subgingival calculus deposition and destructive periodontitis.

Adolescent↗
PubMed2002

Gender and smoking-related risk reduction of periodontal disease with variant myeloperoxidase alleles.

Myeloperoxidase (MPO) is an oxidative enzyme expressed in polymorphonuclear leukocytes. It is involved in the defence against periodontal bacteria, and is also able to mediate inflammatory tissue destruction in periodontal disease. A G/A polymorphism in the promoter region of the MPO gene at position -463 has been assumed to exert profound effects on the expression of the enzyme. It is the aim of this study to evaluate whether this polymorphism may influence the risk of periodontal diseases. A total of 3148 subjects were randomly selected from the general population in the SHIP study (Study of Health in Pomerania). Periodontal status, health-related and socio-economic items were assessed. All subjects aged 40-60 years (n = 1103) were included in this study, and 1083 genotyped for the MPO -463 G/A polymorphism by PCR and RFLP methods. The genotype frequencies determined were homozygous wild type G/G 65.9% (95% CI 63.5-68.6), heterozygous A/G 31.4% (28.8-34.4), and homozygous variant A/A 2.7% (2.0-3.8). Only female subjects have a significantly reduced risk of severe periodontal disease when bearing the variant genotypes A/G or A/A. In female subjects the reduction in periodontal risk was significant for non-smokers (OR = 0.48; 95% CI 0.23-0.96); the smoke-related increase in risk was also reduced (OR = 0.50; 95% CI 0.22-1.10). When adjusted for age, smoking, and education the odds ratios were calculated as 0.52 (P = 0.01) and 0.97 (P = 0.90) for female and male subjects, respectively. The results of this study confirm the assumption that the MPO -463A allele variants are protective in the pathogenesis of periodontal diseases. This holds true only with women but not with men. The results are discussed with respect to the known influences of sexual hormones on MPO activity.

Adult↗
PubMed1994

Cybernetic hypothesis of periodontal disease in mammalian carnivores.

Factors known to govern the pathogenesis of periodontal disease of carnivores are reinterpreted from an ecological perspective. A cybernetic hypothesis is generated which predicts and explains population control mechanisms. Sensitivity to prevailing conditions and the ability to exert a powerful influence upon those conditions is central to the hypothesis. Natural and domestic situations are contrasted with demonstration of a range of immune-mediated conditions arising from a permanent septic focus in the mouths of domestic cats and dogs. The hypothesis is expected to withstand critical scrutiny. In which case a new theory at the heart of a new paradigm will set the future course.

Animal Feed↗
PubMed1997

Oral malodor in beagles: association with indicators of periodontal disease.

The study of oral malodor continues to receive attention. Most bad breath is of oral origin and can be corrected with proper oral hygiene. Studies performed with saliva from people with periodontal disease and from healthy individuals showed that saliva from diseased patients produced a more objectionable odor faster than that of healthy people, and that the volatile sulfur components (VSC) produced may actually play a role in the etiology of periodontal disease. However, not all people or animals with bad breath have periodontal disease. The objectives of this study were to determine if a trained panel could discriminate between 10 dogs with clinically defined periodontal disease and those with relatively healthy periodontium. Second, this study attempted to establish a correlation between odor intensity and six clinical parameters of oral health. The judges were able to differentiate between the two groups of dogs based only on oral malodor (p < 0.02). There were strong associations of the intensity of oral malodor with oral health index scores. The correlations established between odor and gingivitis (r = 0.81) and between odor and furcation exposure (r = 0.88) were very high and statistically significant. Similarly, probing depth (r = 0.73), plaque (r = 0.07) and tooth mobility (r = 0.66) showed clear, positive relationships with oral malodor.

Animals↗
PubMed1998

Cigarette smoking and periodontal diseases: etiology and management of disease.

Cigarette smoking has long been suspected to be associated with a variety of oral conditions including periodontal diseases. Experimental evidence accumulated over the last 2 decades has indicated that cigarette smoking is probably a true risk factor for periodontitis. This environmental exposure has been associated with 2- to 3-fold increases in the odds of developing clinically detectable periodontitis. Smokers have both increased prevalence and more severe extent of periodontal disease, as well as higher prevalence of tooth loss and edentulism, compared to non-smokers. The greater severity of periodontal destruction may be partly accounted for by the reported increases in the rate of periodontal disease progression. The noxious effect of smoking has been shown to be dose dependent and to be particularly marked in younger individuals; in these subjects, up to 51% of the observed risk of periodontitis was associated with smoking. Much of the literature has also indicated that smokers affected with periodontitis respond less favorably to both non-surgical, surgical, and regenerative periodontal treatments. The success rate of dental implants has also been shown to be compromised in smokers. Furthermore, longterm studies have pointed out that smoking was associated with recurrence of periodontitis during periodontal maintenance; the effect appeared to be dose dependent, with heavy smokers (> 10 cigarettes/day) presenting with higher levels of disease progression. The indication that previous smokers have lower levels of risk for periodontitis compared to current smokers is considered to be the strongest available evidence that smoking cessation will result in improved periodontal health and that smoking cessation counseling should be an integral part of periodontal therapy and prevention. So far, however, no randomized controlled clinical trial establishing the effect of smoking cessation and/or reduction on the periodontal outcomes has been reported. Given the present state of uncertainty about the periodontal benefits, but in light of the established general health gains for the patient that could be derived from a smoking cessation program, practitioners are incorporating smoking cessation counseling as an integral part of periodontal therapy. Furthermore, smoking status represents a key parameter to assess the periodontal risk of an individual subject and therefore to make evidence-based clinical decisions.

Health Education, Dental↗