Vitamin D Deficiency: The Missing Etiological Factor in the Development of Juvenile Osteochondrosis Dissecans?

BACKGROUND: Vitamin D deficiency can result in rickets and hypocalcemia during infant and childhood growth. There is an increasing interest in the role of vitamin D with regards to childhood bone health. Osteochondrosis dissecans (OD) is a common disease affecting different joints. To date, the exact etiology of OD still remains unclear. The aim of this study was to evaluate a possible association of vitamin D deficiency and juvenile OD. METHODS: A retrospective chart review of the years 2010 to 2015 of all orthopaedic patients with an initial diagnosis of juvenile OD admitted to undergo operative treatment of the OD was performed. Patient demographics, medical history, information on sports activity (if available) and serum vitamin D (25-OH-D) level on admission date were obtained. For statistical comparison, we measured baseline prevalence of vitamin D insufficiency in age-matched orthopaedic patients presenting at the department of pediatric orthopaedics. RESULTS: A total of 80 patients were included in this study. Overall, 97.5% (n=78) of tested patients in the OD group had serum vitamin D levels below the recommended threshold of 30 ng/mL (mean value of 10.1 ng/mL (±6.7 ng/mL)). Over 60% (n=49) were vitamin D deficient, 29 patients (37%) showed serum levels below 10 ng/mL corresponding to a severe vitamin D deficiency. Of note, only 2 patients (2.5%) reached serum vitamin D levels above the recommended threshold of 30 ng/mL. No statistical difference was found in respect to sports activity level before onset of the symptoms (P=0.09). Statistical analysis found a significant difference in vitamin D levels between patients with OD and patients without an OD (P=0.026). CONCLUSIONS: We found an unexpected high prevalence of vitamin D deficiency in juveniles diagnosed with OD presenting with significant lower mean 25-OH-D level compared with a control group. These results suggest that vitamin D deficiency is potentially associated with the development of OD. Thus, vitamin D deficiency might be an important cofactor in the multifactorial development of juvenile OD. For this reason, supplementation of vitamin D might not only be a potential additional therapy but also be a possible preventative factor in patients with juvenile OD. However, future prospective studies are needed to confirm this preliminary data. LEVEL OF EVIDENCE: Level III-this is a case-control study.

Biomarkers of joint tissue metabolism in canine osteoarthritic and arthritic joint disorders.

OBJECTIVE: To explore the levels of matrix metalloprotease-3 (MMP-3), tissue inhibitor of metalloproteases-1 (TIMP-1), 5D4 keratan sulfate, and two 3B3 chondroitin-sulfate epitopes in several canine osteoarthritic and inflammatory arthropathies. METHODS: Blood and synovial fluid were obtained from 103 dogs with rupture of the anterior cruciate ligament (ACLR), osteochondritis dissecans (OCD), fragmented coronoid process (FPC), patella luxation (PL), hip dysplasia (HD) or infectious arthritis. Dogs with non-musculosceletal disorders were used as controls. The biomarkers were measured by immunoassays. RESULTS: Median levels of synovial MMP-3, TIMP-1 and molar ratios of MMP/TIMP-1 were significantly higher in the arthritis than in the control group. The release of 5D4 keratan sulfate epitope and serum 3B3 neoepitope was reduced in arthritis patients. Increases in synovial TIMP-1 in OA were less pronounced and the molar ratio of MMP-3/TIMP-1 remained far below 1.0, demonstrating a surplus of the protease inhibitor. In osteoarthritic patients median levels of synovial 5D4 keratan sulfate were up-regulated after ACLR and PL and were inversely correlated with increasing duration of lameness. Serum TIMP-1 levels were significantly reduced in the joint disorder group when compared with the control group. CONCLUSION: Our observations present the TIMP-1 serum level as a potential marker for the detection of degenerative changes in cartilage and also indicate that in canine OA, the MMP-3 mediated matrix destruction is not of major importance. However MMP-3 seems to be a sensitive marker for the local inflammation in canine arthritis.