Sclerostin level in rheumatoid arthritis patients and its relationship to disease severity and bone mineral density

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Abstract

Background
Bone loss in rheumatoid arthritis is caused by increased bone resorption without increasing bone formation. The Wnt pathway is important in the control of bone formation through the regulation of osteoblast activity. Sclerostin is an important regulator of the Wnt pathway by blocking Wnt binding to its receptor and thereby, inhibiting bone formation.
Aim Of The Work
was to correlate the relation between level of serum sclerostin and bone mineral density with disease severity in rheumatoid arthritis patients.
Subjects
The study was conducted on 50 subjects divided into two groups: Group I : Thirty patients of rheumatoid arthritis subjects diagnosed according to 2010 ACR / EULAR diagnostic criteria. Group II : Twenty persons as a control group.
Methods
All patients were subjected to; thorough medical history taking, DAS -28, disability Index, complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), RF, antinuclear antibody (ANA), Anti-CCP Antibodies, Human Sclerostin levels using ELISA technique, Plain X- ray on both hands and feets, U/S on both hands, and (DEXA) scan.
Results
There was a statistical significant difference between the two studied groups regarding the age, gender, sclerostin level, and DAS-28 (P>0.05).
Conclusion
Most of patients were under treatment with disease modifying anti-rheumatic drugs (DMARDs) as methotrexate, fracture risk was not assessed, and measurements for renal function were not measured. However, it is possible that circulating sclerostin levels may not reflect changes of sclerostin at a local level. Despite the many questions that remain, pre-clinical studies and clinical trial results would imply that sclerostin antibodies will emerge as a dominant first- line treatment in the management of osteoporosis.

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