Search PubMed⌕ Search

Biomedical subjects

Y Buyle-Bodin

Publications and source records attributed to Y Buyle-Bodin.

15 recordsLinked to original sources
PubMed1997

Short-chain carboxylic acid concentration in human gingival crevicular fluid.

Short-chain carboxylic acids (e.g., lactic acid, propionic acid, butyric acid) are metabolic by-products of bacterial metabolism which can accumulate in the gingival crevice. It is of no small consequence, therefore, that 1- to 5-mM concentrations of these acids exhibit significant biological activity, including the ability to alter cell proliferation and gene expression in cells of importance to the periodontium. This communication reports on the in vivo concentrations of propionic and butyric acid in the gingival crevices of periodontal subjects with severe and mild disease. The results indicated that severely diseased subjects exhibited a > 10-fold increase in the mM concentration of these acids when compared with mildly diseased subjects (mean propionic acid-severe = 9.5 +/- 1.8 mM, and mild = 0.8 +/- 0.3 mM; mean butyric acid-severe = 2.6 +/- 0.4 mM, and mild = 0.2 +/- 0.04 mM). These differences (mean +/- SE) were significant (p < 0.0001). The propionic and butyric acid concentrations were below detection limits in healthy sites of mildly diseased subjects. The propionic and butyric acid concentrations also associated significantly with clinical measures of disease severity (e.g., pocket depth, attachment level) and inflammation (e.g., subgingival temperature, % of sites bleeding when probed), and with the total microbial load (all p < 0.05). Taken together, these data suggest that short-chain carboxylic acids play a mediating role in periodontal disease pathogenesis.

Aggregatibacter actinomycetemcomitans↗
PubMed1996

The relationship of gingival crevicular fluid short chain carboxylic acid concentration to gingival inflammation.

Short-chain carboxylic acids (SCCA; C < or = 5; e.g., lactic acid, propionic acid, butyric acid) are metabolic by-products of bacterial metabolism which accumulate in the gingival crevice, and exhibit significant biological activity, including the ability to alter gene expression. It has been hypothesized that among the activities of SCCAs are their ability to contribute to gingival inflammation. This concept complements the notion that specific periodontal pathogens are the causative agents of gingival inflammation. To begin testing these 2 hypotheses, we examined the relationship between SCCA concentrations, specific putative periodontal pathogens, and gingival inflammation in medically healthy periodontally diseased subjects. We reasoned that if SCCAs and/or specific periodontal pathogens were causative gingival inflammatory agents, gingival inflammation should increase with increasing concentration of the inflammatory mediator. We also recognized that other clinical variables needed to be controlled for, and an objective quantitative assessment of gingival inflammation used. To accomplish these tasks, sites within subjects were stratified by location and pocket depth, and the following quantified: bacterial presence; SCCA concentration; and gingival inflammation. The results indicated that gingival inflammation directly and significantly correlated with SCCA concentrations in the maxillary and mandibular molars, incisors and canines (all r > or = 0.47; all p < or = 0.015; too few bicuspids were available for complete analysis). The relationship between gingival inflammation and SCCA concentration was best described by a natural log relationship. Gingival inflammation did not, however, correlate positively with either the total number of specific putative periodontal pathogens, or the sum of subsets of these pathogens (-0.31 < or = r < or = 0.39; 0.08 < or = p < or = 0.75) for any of the locations. Finally, the SCCA concentration did not correlate with the level of individual or groups of pathogens. These data, together with historical work and other preliminary data, support the hypothesis that SCCA, rather than specific putative periodontal pathogens, may be a causative agent in gingival inflammation. This work may, in part, begin to explain the apparent lack of a direct relationship between current gingival inflammation and the prediction of bacterially mediated periodontal attachment loss.

Aggregatibacter actinomycetemcomitans↗
PubMed1995

Subgingival temperature as a gingival inflammatory indicator.

Elevated temperature is one of 4 cardinal inflammatory signs. Previous work indicates that subgingival temperature assessments are accurate and re- liable, and provide objective, quantitative information over a broad 10 degrees C range, in small 0.1 degrees C increments with a direct, immediate report on the inflammatory status at the pocket base. However, complicating the use and interpretation of subgingival temperature assessments are its 3 forms: actual subgingival temperature, sublingual temperature minus subgingival temperature (temperature differential), and a temperature indicator light. We reasoned that if one could determine which of the temperature assessments reflected the periodontal condition, and which were independent variables, they would provide new and unique information about the inflammatory status of the periodontium. We also reasoned that by providing objective, quantitative data over a broad range, subgingival temperature should reduce the sample size required to obtain significance in clinical trials. Therefore, the purpose of this study was 2-fold: (1) to determine whether the 3 subgingival temperature assessments could differentiate between clinically defined periodontal health and disease; (2) to determine whether the 3 assessments were dependent or independent clinical variables. The data indicated that all 3 subgingival temperature assessment methods differentiated between clinically-defined periodontal health and disease (all p<0.02). All 3 assessments also correlated significantly (all p<0.03), but modestly (all r>0.49), with bleeding on probing. Based on scatter-plot matrices and common factor analysis, the data indicated that only actual subgingival temperature and temperature differential were independent variables. Taken together, this data indicates that subgingival temperature and temperature differential provide unique information about the periodontal inflammatory state. Power calculations indicated that the temperature differential may significantly reduce the subject number required to achieve significance in clinical trials examining gingival inflammation. Because of the body's rapid temperature response, these assessments may also significantly reduce the time required for gingival inflammation trials.

Analysis of Variance↗
PubMed1977

[The morphologic relation between the temporomandibular joint and other components of the masticatory apparatus in catarrhine simians and humans].

The articular temporo-mandibular structures and their osseous and dental environment were studied in some catarhinians Simians (Cynomorphs and Anthropomorphs) and some representatives of the human lineage. The study of measurable and descriptive characters showed a relative stability of the temporo-mandibular joint compared to the dynamism of the other components of the masticatory system. The functional specificity of the actual human temporo-mandibular joint seemed to be tightly associated to the main processes leading toward human evolution (facial regression, increase of the cranial capacity). On the other hand, this study casts some doubts regarding the utilization of Primates for experiments in this field.

Animals↗
PubMed1976

[Acquisition of masticatory structures in mammalian reptiles (preliminary study].

Possession of the masticatory function and apparatus appears as essential for the passage from Reptiles to Mammals. The present study, based on material of the Museum of d'Histoire Naturelle of Paris and on the literature, tries to distinguish the different stages of modification and specialization of feeding device in the cynodont theriodonts, leading to the mammalian stomatognathic system. The relationship between bone components (lateral skull and lower jaw), teeth and muscles are discussed. Induction of these changes comes from the external adductor muscular system in which the transformation from a primitive mass to mammalianlike masticatory muscles, directs this evolution. The conditions of feeding specialization of the Gomphodonts are discussed, as well as their evolutionary failure. Lastly, without taking up the quarrel about the double jaw-joint, it seems for the authors that the jaw-joint transformation appears as the most determinative element for assigning mammalian origins to the Cynodonts.

Animals↗