Periodontal Disease

Oral bacteria and cancer.

“Perhaps the most likely carcinogenic link with oral bacteria is with oral squamous cell carcinoma (OSCC), one of the most common cancers worldwide. OSCC surfaces have been reported to harbor significantly higher levels of Porphyromonas and Fusobacterium compared with contiguous healthy mucosa [3]. Moreover, immunohistochemistry with P. gingivalis antibodies revealed higher levels of detection and intensity of staining in gingival carcinomas compared with healthy gingival tissue, although only a small number of cases were examined [4]. A striking association has also been demonstrated between P. gingivalis infection and pancreatic cancer. In a prospective cohort study of over 400 cases and controls, a >2-fold increase in risk of pancreatic cancer was observed among those with high levels of antibodies to P. gingivalis, after adjusting for known risk factors [5]. Similarly, in the extensive National Health and Nutrition Examination Survey III, orodigestive cancer mortality was found to be related to the levels of P. gingivalis antibodies, independent of periodontal disease [6]. Several recent studies have shown a strong association between F. nucleatum and colorectal cancer (CRC) [7]–[10]. F. nucleatum was found to be one of the more abundant species within and around CRC neoplasms, and levels of F. nucleatum correlated with the presence of lymph node metastases.”

By |2018-07-11T15:46:58+00:00January 1st, 2014|Periodontal Disease|

The link between periodontal disease and rheumatoid arthritis: an updated review.

Porphyromonas gingivalis is a leading pathogen in chronic periodontitis, a disease process involving progressive destruction of the tissues that support the teeth. Recently, the organism has been reported to produce a unique bacterial enzyme, P. gingivalis peptidyl-arginine deiminase (PPAD), which has the ability to convert arginine residues in proteins to citrulline. Protein citrullination alters protein structure and function; hence, PPAD may be involved in deregulation of the host’s signalling network and immune evasion. Further, accumulating evidence suggests a role for autoimmunity against citrullinated proteins in the development of rheumatoid arthritis (RA). As inflammatory conditions in the lungs of cigarette smokers contribute to the breakdown of immune tolerance to citrullinated epitopes, chronic exposure to citrullinated proteins at periodontitis sites may also predispose susceptible individuals to the development of autoantibodies and the initiation of RA. In this review, we discuss evidence that PPAD may represent a mechanistic link between periodontitis and RA, diseases that are known to be significantly associated at the epidemiological level.

By |2019-06-09T00:38:12+00:00January 1st, 2014|Periodontal Disease|

Ozone and its use in periodontal treatment

“Objectives: To evaluate the effects of ozone in perio- dontal treatment in dental practice. Methods: An eva- luation of the current state of knowledge regarding the application of ozone in periodontal treatment re- vealed limited available literature. Therefore an audit was conducted in dental practice in order to evaluate the effects of ozone in periodontal treatment. Twenty- five patients were treated with gaseous ozone after having had failed conventional periodontal treatment. BPE scores and the six deepest pockets were meas- ured in each patient before and after the use of ozone.

Results: From the initial number of twenty-nine pa- tients selected, twenty-five patients attended both fol- low up appointments. Based on BPE scores, twenty of the patients have overall improvement while five of the patients continued to have deterioration. Eight patients had an improvement in depths of periodontal pockets by three millimetres, sixteen patients had im- provement by one to two millimetres and one patient did not improve. The depth of pockets after the use of ozone decreased significantly (P < 0.001).

Conclusion: The audit revealed that gaseous ozone significantly (P < 0.001) reduced the depth of pockets in patients with periodontal disease. The positive results encourage further investigation in the subject.”

By |2018-06-12T22:37:38+00:00January 1st, 2013|Periodontal Disease|

Periodontal disease and overall health: An update.

“Periodontitis is a chronic inflammatory disease caused by a mixed microbial infection. The disease is a result of a complex interaction between the bacteria and the susceptible host. The host reaction to the microbial flora leads to a release of pro?inflammatory cytokines and a low grade inflammatory response that has an effect on the overall health status of the patient. Periodontitis has been associated with several systemic conditions such as cardiovascular disease, diabetes, adverse pregnancy outcomes and respiratory infections. In recent years, the relationship of periodontitis to overall health has been explored by numerous researchers who have expanded our understanding of periodontal disease as it affects the overall health of human subjects. This article further examines the relationship of periodontitis to overall health and throws a light on recent associations.”

The association of tooth scaling and decreased cardiovascular disease: a nationwide population-based study

OBJECTIVE:

Poor oral hygiene has been associated with an increased risk for cardiovascular disease. However, the association between preventive dentistry and cardiovascular risk reduction has remained undetermined. The aim of this study is to investigate the association between tooth scaling and the risk of cardiovascular events by using a nationwide, population-based study and a prospective cohort design.

METHODS:
Our analyses were conducted using information from a random sample of 1 million persons enrolled in the nationally representative Taiwan National Health Insurance Research Database. Exposed individuals consisted of all subjects who were aged ≥ 50 years and who received at least 1 tooth scaling in 2000. The comparison group of non-exposed persons consisted of persons who did not undergo tooth scaling and were matched to exposed individuals using propensity score matching by the time of enrollment, age, gender, history of coronary artery disease, diabetes, hypertension, and hyperlipidemia.
RESULTS:
During an average follow-up period of 7 years, 10,887 subjects who had ever received tooth scaling (exposed group) and 10,989 age-, gender-, and comorbidity-matched subjects who had not received tooth scaling (non-exposed group) were enrolled. The exposed group had a lower incidence of acute myocardial infarction (1.6% vs 2.2%, P<.001), stroke (8.9% vs 10%, P=.03), and total cardiovascular events (10% vs 11.6%, P<.001) when compared with the non-exposed group. After multivariate analysis, tooth scaling was an independent factor associated with less risk of developing future myocardial infarction (hazard ratio [HR], 0.69; 95% confidence interval [CI], 0.57-0.85), stroke (HR, 0.85; 95% CI, 0.78-0.93), and total cardiovascular events (HR, 0.84; 95% CI, 0.77-0.91). Furthermore, when compared with the non-exposed group, increasing frequency of tooth scaling correlated with a higher risk reduction of acute myocardial infarction, stroke, and total cardiovascular events (P for trend<.001).
CONCLUSION:
Tooth scaling was associated with a decreased risk for future cardiovascular events.

Genetic predisposition to persistent apical periodontitis.

INTRODUCTION:
The proinflammatory cytokine interleukin (IL)-1 is a key regulator of host responses to microbial infection and a major modulator of extracellular matrix catabolism and bone resorption. Allele2 of IL-1β is associated with a four-fold increase in IL-1β production. The aim of this case-control study was to evaluate the gene polymorphism of IL-1β in the pathogenesis of endodontic failure. We hypothesized that the gene polymorphism (allele2 of IL-1β) would influence host response and enhance inflammatory reactions predisposing to persistent apical periodontitis (PAP).

MATERIALS AND METHODS:
Subjects with at least 1 year of follow-up after root canal therapy (RCT) were recalled. Inclusion and exclusion criteria were applied, and 34 subjects with signs/symptoms of PAP with otherwise acceptable RCT were included. Sixty-one controls showed healing with acceptable RCT. Genomic DNA from buccal mucosa was amplified by polymerase chain reaction followed by restriction fragment length polymorphism to distinguish the alleles of IL-1β gene polymorphism.

RESULTS:
A significant difference in the distribution of the polymorphic genotype among cases (70.6%) and controls (24.6%) (P < .001, Pearson χ(2)) was shown.

CONCLUSIONS:
These findings suggest that specific genetic markers associated with increased IL-1β production may contribute to increased susceptibility to PAP.

Use of PCR to detect Entamoeba gingivalis in diseased gingival pockets and demonstrate its absence in healthy gingival sites.

“Investigators using light microscopy have identified the protozoan parasite Entamoeba gingivalis from diseased gingival pockets for nearly 100 years. The objective of the present investigation was to develop a molecular biology approach for determining the presence of E. gingivalis in both diseased gingival pockets and healthy gingival sites. For this, a previously developed conventional polymerase chain reaction (PCR) was evaluated and a real-time polymerase chain reaction assay was developed. Paper points were inserted into the base of the sulcus of both diseased gingival pockets and healthy gingival sites. DNA was extracted using the QIAamp DNA mini kit, and subsequently analyzed using conventional and real-time PCR analysis. A previously described primer set specific for the small subunit ribosomal RNA gene (SSU rDNA) of E. gingivalis was used for the conventional PCR. For the real-time PCR, a primer set was designed to amplify a 135-bp fragment inside the SSU rDNA of E. gingivalis. A conventional PCR assay detected E. gingivalis in 27% of diseased gingival pockets. The real-time PCR using a different primer set detected protozoa in 69% of diseased pocket sites. Thus, the latter technique proved more sensitive for detection of E. gingivalis. No E. gingivalis were detected in any of the healthy gingival pocket sites using either type of PCR assay. Results support a concept that the presence of E. gingivalis is associated only with diseased gingival pocket sites. The newly described methodology may also serve to provide a novel eukaryotic cell marker of disease status in gingival pockets.”

Periodontal disease may associate with breast cancer.

“The main purpose was to evaluate the association between periodontal disease and the incidence of breast cancer in a prospective study of 3273 randomly selected subjects aged 30–40 years at baseline. Breast cancer incidence was registered from 1985 to 2001 according to the WHO International Classification of Diseases criteria. At baseline, 1676 individuals also underwent a clinical oral examination (Group A) whereas 1597 subjects were not clinically examined but were registered (Group B). The associations between breast cancer, periodontal disease, and missing molars were determined using multiple logistic regression models with several background variables and known risk factors for cancer. In total 26 subjects in group A and 15 subjects in group B had breast cancer. The incidence of breast cancer was 1.75% in subjects who had periodontal disease and/or any missing molars, and 0 in subjects who had periodontal disease but had no missing molars. For periodontally healthy subjects with no missing teeth the breast cancer incidence was 1%. For group B the respective incidence was 0.94%. Female gender (odds ratio (OR) 13.08) and missing any molar in the mandible (OR 2.36) were explanatory variables for breast cancer. Of the subjects with periodontal disease and any missing molars in the mandible 5.5% had breast cancer in comparison to 0.5% of the subjects who had periodontal disease but no missing molars in the mandible (P < 0.02). Chronic periodontal disease indicated by missing molars seemed to associate statistically with breast cancer.”

Periodontitis and atherosclerotic vascular disease

Recent scientific statement by the American Heart Association (AHA) titled “Periodontal Disease and Atherosclerotic Vascular Disease: Does the Evidence Support an Independent Association?”1 has stimulated a wave of media attention on this important subject. Unfortunately, a misleading press release that has since been corrected and re-issued resulted in dissemination of inaccurate information in the print and electronic media and has generated more confusion about a topic that needed clarity. For this reason, it is a good time to take a closer look at what we have learned from a wide body of literature in which researchers have examined the association between periodontitis and atherosclerotic vascular disease (AVD); what gaps in knowledge must be addressed in further research; what we, as health care professionals, can and should tell our patients today about this important topic.

By |2019-06-03T02:13:42+00:00January 1st, 2010|Periodontal Disease|
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