Objective. To analyze enzymes involved in joint damage by simultaneous investigation of glycosidases and matrix metalloproteinases (MMPs) in patients with various joint diseases. In joint diseases, the major clinical symptoms and disability of patients are caused by an irreversible destruction of hyaline cartilage. Enzymes capable of degrading extracellular matrix components (collagen and aggrecan) and concomitantly exposing chondrocytes to a variety of cytotoxic and/or apoptosis-inducing factors are considered to be the major effector molecules in cartilage degradation. Methods. Activities of glycosidases (␤-DRecently, significant advances have been made in our understanding of joint destruction and the mechanism of proteolytic cleavage of cartilage. Active proteases are currently implicated in the destructive processes and include matrix metalloproteinases (MMPs), the ADAM family (1), the ADAM-TS family (2), and serine proteases (elastase, cathepsins, and granzymes) (3-5). Of the 4 groups of MMPs, collagenase (MMP-1 in particular) appears to be responsible for the degradation of interstitial collagens. The gelatinases (including MMP-2 and MMP-9) degrade the denatured form of collagens, thus acting in synergy with MMP-1. The stromelysins (including MMP-3) have a broader substrate specificity for non-connective tissue components.

• ▶ body composition • ▶ Cushing ' s syndrome • ▶ rheumatoid arthritis • ▶ glucocorticoids Body Composition After Endogenous (Cushing ' s Syndrome) and Exogenous (Rheumatoid Arthritis) Exposure to Glucocorticoids abolition of the normal male to female diff erence in visceral fat [5]. It has been assumed that resolution of hypercortisolism is followed by normalization of body composition; a decrease in fat mass has been reported in the early recovery after successful treatment of CS [6, 7]. However, patients who have suff ered from CS, often complain of central obesity, despite successful treatment, which may even have rendered them adrenal insuffi cient. Persistence of increased cardiovascular risk and carotid atherosclerosis has been reported in patients with CS after fi ve years of cure [8]. Moreover, there could be a relationship between cortisol and fasting glucose [9]. Rheumatoid arthritis (RA) is a chronic, systemic infl ammatory disorder that may aff ect many tissues and organs, but principally attacks the joints producing an infl ammatory synovitis that often progresses to destruction of the articular carti