Longitudinal data were collected over a period of at least 18 months and up to 3 years on 41 adult periodontitis patients (AAP Type III and IV). Ramfjord attachment level measurements and sampling of crevicular fluid (CF) at each tooth were repeated every 3 months. A mean full mouth CF prostaglandin E2 (MCF‐PGE) value was determined for each patient at each visit. The three‐month monitoring was continued until a single site demonstrated a statistically and clinically significant attachment loss (ALOSS) episode. Results indicated that in ALOSS patients the MCF‐PGE was significantly elevated at the ALOSS visit as compared to previous levels. Furthermore, the sites which had the ALOSS had elevated levels as compared to the contralateral no ALOSS control sites (305.6±56.5 vs. 65.7±6.89 ng/ml, mean ± SEM). One month following treatment the CF‐PGE level dropped to 16.9±3.4 ng/ml at the ALOSS sites. Since the MCF‐PGE level increases preceding the attachment loss episode, reaches a maximum at the sites which actually undergo ALOSS, and subsides following treatment, the possibility of using the MCF‐PGE level to predict an oncoming future ALOSS episode was examined. The ALOSS patients had a MCF‐PGE level of 113.4±9.0 ng/ml 6 months prior to the ALOSS episode, which was significantly higher than the no ALOSS patients’MCF‐PGE level of 50.1±7.1. Analysis of MCF‐PGE levels as a screening test indicate that this measurement has a high degree of sensitivity, specificity, and a predictive value of 0.92–0.95. Thus, this method has significant merit as a diagnostic tool to determine if a patient is in a state of remission or about to undergo an attachment loss episode.
Dental caries and periodontitis account for a vast burden of morbidity and healthcare spending, yet their genetic basis remains largely uncharacterized. Here, we identify self-reported dental disease proxies which have similar underlying genetic contributions to clinical disease measures and then combine these in a genome-wide association study meta-analysis, identifying 47 novel and conditionally-independent risk loci for dental caries. We show that the heritability of dental caries is enriched for conserved genomic regions and partially overlapping with a range of complex traits including smoking, education, personality traits and metabolic measures. Using cardio-metabolic traits as an example in Mendelian randomization analysis, we estimate causal relationships and provide evidence suggesting that the processes contributing to dental caries may have undesirable downstream effects on health.
A paucity of epidemiologic research exists regarding systemic health consequences of endodontic disease. This study evaluated whether incident radiographically evident lesions of endodontic origin were related to development of coronary heart disease (CHD) among 708 male participants in the VA Dental Longitudinal Study. At baseline and every three years for up to 32 years, participants (who were not VA patients) received complete medical and dental examinations, including full-mouth radiographs. Cox regression models estimated the relationship between incident lesions of endodontic origin and time to CHD diagnosis. Among those < or = 40 years old, incident lesions of endodontic origin were significantly associated with time to CHD diagnosis (p < 0.05), after adjustment for covariates of interest, with hazard ratios decreasing as age increased. Among those > 40 years old, no statistically significant association was observed. These findings are consistent with research that suggests relationships between chronic periodontal inflammation and the development of CHD, especially among younger men.
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