chondroitin-sulfates and Atrophy

Topics: Adult; Anti-Inflammatory Agents; Atrophy; Biopsy; Chondroitin Sulfates; Diagnosis, Differential; Female; Glucocorticoids; Humans; Immunohistochemistry; Japan; Muscular Diseases; Ocular Motility Disorders; Oculomotor Muscles; Pharyngeal Muscles; Prednisone; Respiration Disorders; Treatment Outcome

A 71-year-old man developed severe limb, bulbar, and respiratory weakness over 18 months. A muscle biopsy showed only a moderate degree of type 2 atrophy, but immunocytochemistry showed absence of chondroitin sulfate C glycosaminoglycan in the endomysium. Prednisone produced a marked increase in strength. Diffuse loss of endomysial chondroitin sulfate C was a feature of this treatable myopathy with severe weakness, but few pathologic changes.

Topics: Aged; Amyotrophic Lateral Sclerosis; Atrophy; Biopsy; Chondroitin Sulfates; Diagnosis, Differential; Hand Strength; Humans; Immunohistochemistry; Male; Muscle Fibers, Skeletal; Muscle, Skeletal; Muscular Diseases; Prednisone; Reference Values; Regeneration

The capacity of articular cartilage matrix to recover during 50 weeks of remobilisation after an atrophy caused by 11 weeks of immobilisation of the knee (stifle) joint in 90 degrees flexion starting at the age of 29 weeks, was studied in young beagle dogs.. Proteoglycan concentration (uronic acid) and synthesis ([35S]sulphate incorporation) were determined in six and three knee joint surface locations, respectively. Proteoglycans extracted from the cartilages were characterised by chemical determinations, gel filtration, and western blotting for chondroitin sulphate epitope 3B3.. The proteoglycan concentrations that were reduced in all sample sites immediately after the immobilisation, remained 14-28% lower than controls after 50 weeks of remobilisation in the patella, the summit of medial femoral condyle, and the superior femoropatellar surface. In the contralateral joint, there was a 49% increase of proteoglycans in the inferior femoropatellar surface after remobilisation, while a 34% decrease was simultaneously noticed on the summit of the medial femoral condyle. Total proteoglycan synthesis was not significantly changed after immobilisation or 50 weeks' remobilisation in the treated or contralateral joint, compared with age matched controls. The chondroitin 6- to 4- sulphate ratio was reduced by immobilisation both in the radioactively labelled and the total tissue proteoglycans. In the remobilised joint, this ratio was restored in femur, while in tibia it remained at a level lower than controls. Neither immobilisation nor remobilisation induced epitopes recognised by the monoclonal antibody 3B3 on native (undigested) proteoglycans.. These results show that the depletion of proteoglycans observed after 11 weeks of immobilisation was not completely restored in certain surface sites after 50 weeks of remobilisation. The significant changes that developed in the contralateral joint during the remobilisation period give further support to the idea that a permanent alteration of matrix metabolism results even from a temporary modification of loading pattern in immature joints.

Topics: Animals; Atrophy; Biomechanical Phenomena; Cartilage, Articular; Chondroitin Sulfates; Dogs; Female; Hindlimb; Immobilization; Physical Conditioning, Animal; Proteoglycans; Time Factors; Uronic Acids

Recently, there has been an exponential increase in the use of alpha-hydroxy acids in dermatologic practice. Their inclusion in a myriad of cosmetic preparations underscores their popularity. Among the clinical effects of alpha-hydroxy acids are their ability to prevent the atropy resulting from potent topical corticosteroids, improve the appearance of photoaged skin, and correct disorders of keratinization. Despite this range of desirable effects, very little is known about the specific changes produced by various alpha-hydroxy acid preparations in the epidermis and dermal extracellular matrix. Previous work by others has demonstrated the ability of another alpha-hydroxy acid to increase viable epidermal thickness, and dermal glycosaminoglycans.. In this study, we examined the effect of 20% citric acid lotion, as compared with vehicle alone, on skin thickness, viable epidermal thickness, and dermal glycosaminoglycan content. Biopsy samples were harvested after 3 months of treatment.. Image analysis of biopsy sections revealed increases in viable epidermal thickness and dermal glycosaminoglycans in treated skin.. Topical citric acid produces changes similar to those observed in response to glycolic acid, ammonium lactate, and retinoic acid including increases in epidermal and dermal glycosaminoglycans and viable epidermal thickness. Further studies of citric acid and other alpha-hydroxy acids are warranted to clarify their clinical effects and mechanisms of action.

Topics: Administration, Cutaneous; Aged; Aged, 80 and over; Anti-Inflammatory Agents; Atrophy; Biopsy; Chondroitin Sulfates; Citric Acid; Dermatologic Agents; Epidermis; Extracellular Matrix; Female; Follow-Up Studies; Glucocorticoids; Glycolates; Glycosaminoglycans; Humans; Hyaluronic Acid; Hydroxy Acids; Image Processing, Computer-Assisted; Keratins; Keratolytic Agents; Lactates; Pharmaceutical Vehicles; Quaternary Ammonium Compounds; Skin; Skin Aging; Tissue Survival; Tretinoin

We report a case of atrophoderma of Pasini and Pierini. We determined the glycosaminoglycan content in the involved skin. Dermatan sulfate content in the involved skin (1.88 micrograms uronic acid/mg dry skin) was greater than that in the uninvolved skin (1.05 micrograms uronic acid/mg dry skin). No significant differences in hyaluronic acid, chondroitin sulfate or heparan sulfate content between involved and uninvolved skin were observed. These results suggest that abnormal metabolism of dermatan sulfate may be involved in the pathogenesis of atrophoderma; this pattern has been observed in systemic or localized scleroderma.

Topics: Adult; Atrophy; Chondroitin Sulfates; Dermatan Sulfate; Glycosaminoglycans; Heparitin Sulfate; Humans; Hyaluronic Acid; Male; Pigmentation Disorders; Scleroderma, Localized; Scleroderma, Systemic; Skin; Uronic Acids

Previous studies have shown the presence of a native chondroitin sulfate epitope in articular cartilage proteoglycans from canine knee joints with experimental early osteoarthritis (OA), but not in normal cartilage. The objective of this study was to quantitate the native epitope recognized by monoclonal antibody 3-B-3 in synovial fluids and articular cartilage of diseased joints.. An immunoassay with monoclonal antibody 3-B-3, which recognizes a native chondroitin-6-sulfate structure, was developed and used to analyze synovial fluid lavage material and extracts of articular cartilage from canine knee joints with early experimental OA or with mild disuse atrophy, and from control animals.. The concentration of epitope in the OA fluids was elevated 33-35-fold, and in the OA articular cartilage extracts it was elevated > 200-fold, compared with samples from the control group. No significant difference was detected in the levels of 3-B-3 epitope in the synovial fluid lavage material or cartilage extracts from the joints of the disuse group versus the control group.. The native 3-B-3 epitope in articular cartilage and synovial fluids may be a specific marker of ongoing anabolic events in early degenerative joint disease.

Topics: Animals; Antibodies, Monoclonal; Atrophy; Cartilage, Articular; Chondroitin Sulfates; Dogs; Epitopes; Immunoassay; Osteoarthritis; Synovial Fluid

Canine experimental models of osteoarthritis (OA) and disuse atrophy were used to study cartilage metabolism. The synovial fluids from the OA joints showed elevated levels of keratan sulfate (KS) epitope and link protein, indicating increased catabolism. Analysis of fluids from joints with disuse atrophy showed high levels of KS epitope, but no increase in link protein. Quantitation of a novel chondroitin sulfate (3B3) epitope showed it to be present only in the synovial fluids and articular cartilage of the OA joints. The results indicate that these may be important indicators, or markers, of degenerative joint disease.

Topics: Animals; Atrophy; Cartilage, Articular; Chondroitin Sulfates; Disease Models, Animal; Dogs; Keratan Sulfate; Osteoarthritis; Proteoglycans; Synovial Fluid