Mechanisms of circumduction and axial rotation of the carpometacarpal joint of the thumb.

Osteoarthritis of the carpometacarpal joint of the thumb (CMCJ) is a frequent clinical problem. The aim of the study was to discuss the mechanisms of circumduction and axial rotation of the CMCJ considering geometrical properties of the articulating surfaces and the configuration of the muscle system acting over the CMCJ. 28 CMCJ from 7 female and 7 male corpses (age: 81 yrs (median), 53-91 yrs (interval), which did not show any sign of arthrosis, were investigated. Contours in flexion/extension: in saddle point O, the contour of the proximal surface is stronger curved. For 23 of the 28 joints the contours showed an eye-catching difference. Contours in ab-/adduction: all 28 joints showed the respective incongruity. Straight lines and their included angles: in both articulating surfaces, the angles between the straight lines through the saddle point showed values which were close to 90 degrees. Out of neutral position a small axial rotation (maximal range: 3.5 degrees) is possible without that the contact at the saddle points is changed. But, when one of the straight lines of the proximal surface meets a respective straight line of the distal surface, the contact "point" is enlarged to a contact "line". When the axial rotation is further increased, the contact "line" splits into two contacts "points", which are located at outer areas of the articulating surfaces.

Expression of N-acetyltransferases in periodontal granulation tissue.

Smoking is a major risk of periodontal diseases. At the site of first contact, the gingiva is exposed to aromatic amines and polycyclic hydrocarbons. These are metabolized by the N-acetyltransferases (NAT), leading to local detoxification and/or activation reactions contributing to the risk of periodontal destruction in smokers. The purpose of this study was to detect the expression of N-acetyltransferase isoenzymes NAT1 and NAT2 in periodontal granulation tissue. In 24 specimens obtained from periodontitis patients or control subjects, mRNA encoding for NAT1 and NAT2 was detected by RT-PCR, and proteins were identified by immunohistochemistry. In periodontal granulation tissues, immunoreactivity for NAT1 and NAT2 was detected in infiltrating leukocytes and fibroblasts. In normal gingiva, both enzymes were found in epithelial cells, whereas NAT1 was also detected in endothelial cells. The results suggest that these enzymes may play a role in the defense against xenobiotics and the accelerated progression of periodontal disease in smokers.

Polymorphisms of Fc gamma-receptors RIIa, RIIIa, and RIIIb in patients with adult periodontal diseases.

Polymorphisms influencing the binding affinity between the Fcgamma receptors and IgG of different subclasses are thought to be of importance in the individual susceptibility to infections with Gram-negative bacteria contributing to periodontal disease. One hundred and fifty-four Caucasian subjects were clinically and radiographically examined for their periodontal status and genotyped for their allelic pattern of FcgammaRIIa, FcgammaRIIIa, and FcgammaIIIb polymorphism. In assessing periodontitis according to mean probing depth and attachment loss, no differences were found in allele frequencies or combined allotypes between the subjects with mild or moderate and those with severe signs of periodontitis. However, the extent and severity of bone loss were significantly associated with the genotype of the receptor FcgammaRIIIa. An increased risk of severe bone destruction was observed in individuals carrying the FcgammaRIIIa-VV genotype (OR = 5.3; 95% CI 1.4-26.2). FcgammaRIIIb is in linkage disequilibrium with FcgammaRIIIa. Hence it is also related to periodontal disease. There is no indication of an association between the polymorphism of FcgammaRIIa and periodontitis. The results are evidence that the FcgammaRIIIa genotype coding for the high affinity receptor imposes an additional risk of bone loss as does the FcgammaRIIIb genotype coding for the low affinity receptor.