Background Rheumatoid arthritis (RA) is an inflammatory autoimmune disease of unknown etiology, affecting the joint and also other tissues [Altindag, 2007]. RA patients usually present weakness and muscle atrophy, non-articular manifestation of the disease [Mirό, 1996]. Although causing great impact, the development of muscle atrophy and mechanisms involved is still very limited.

Objectives To evaluate the development of muscle atrophy in skeletal muscle of murine model of arthritis.

Methods We used the experimental murine model of collagen induced arthritis (CIA) conform Brand et al [2007]. Experimental animals were randomly divided into three groups (n=79): control (CO), sham arthritis (SA) and arthritis (CIA), analyzed in different time-points: 25, 35 and 45 days after induction of the arthritis. The arthritis development was followed by clinical scores three times a week and weight was evaluated weekly. Cytokine analysis was evaluated by CBA in serum collected before the death of the animals. Cross-sectional area of the myofiberof skeletal muscle (tibialis anterior - TA, gastrocnemius - GA) was measured. Significance was considered p<0.05.

Results Disease scores of arthritis groups were always different from their controls in all times, also in 45 days CIA group was different from other times and SA was different from CO (Table 1). There were no differences in myofiber cross-sectional area among groups in 25 and 35 days, however in 45 days CIA had reduced myofiber area (Table 1). Myofiber area did not differed among times on all experimental groups. There was no correlation between myofiber area and disease score when analyzing paws separately (left and right), however using a paw mean, this correlation was significant and inverse in 45 days (TA: -0.68 p=0.029 and GA: -0.71 p=0.021). CBA analysis showed IL-6 significantly inhanced in CIA.

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Conclusions Disease score is inversely correlated with myofiber area in 45 days, demonstrating that muscle atrophy was clearly presented when arthritis is established. Furthermore, this correlation is not symmetric. These observations are relevant to understand the development of muscle loss, as well as for the design of future studies trying to understand the mechanisms involved. As far as we concern, this is the first study to evaluate the relation between disease score and muscle atrophy in a model of arthritis.

Disclosure of Interest None Declared