SLR - January 2020 - Toby Ishizuka
Reference: Maier G, Lazovic D, Maus U, Roth K, Horas K, Seeger J. Vitamin D Deficiency: The Missing Etiological Factor in the Development of Juvenile Osteochondrosis Dissecans? Journal of Pediatric Orthopaedics. 2019 January; 39(1), 51-54.Scientific Literature Review
Reviewed By: Toby Ishizuka, DPM
Residency Program: Kaiser SF Bay Area Foot and Ankle Surgery – Oakland, CA
Podiatric Relevance: While it is well understood that Vitamin D deficiency in the pediatric population can lead to rickets and hypocalcemia, its role in osteochondral defects are unknown. Pediatric osteochondrosis dissecans (OD) is not well understood as some authors theorize it can be related to genetics, endogenous, vascular, mechanical and infectious aspects. Juvenile OD is more common in active kids who experience repetitive trauma. There is no consensus on Juvenile OD treatment algorithms. Previous authors have proposed that vitamin D3 deficiency may contribute and play a role in the initiation and progression of OD. This study aims to correlate Vitamin D deficiency and juvenile OD.
Methods: A retrospective case control study was performed of pediatric patients from 2010 to 2015 who underwent operative treatment for Juvenile OD. Conservative treatment of OD was excluded. OD diagnosis was confirmed on MRI. Operative treatment was determined from the OD lesions with a MRI demonstrating instability (cartilage breach) or conservative treatment failure. OD lesions were classified by the International Cartilage Research Society (ICRS) classification. Serum Vitamin D (25-OH-D) on admission were obtained. A pediatric orthopedic age-matched control group was created with surgical pediatric scoliosis patients which correlated seasonal Vitamin D levels. Sufficient serum Vitamin D (25-OH-D) levels were above 30 ng/mL, insufficiency was 20-30 ng/mL, deficiency was under 20 ng/mL, and severe deficiency was 10 ng/mL. Statistical analysis performed with two tailed, Mann Whitney U test.
Results: A total of 80 pediatric surgical OD were identified, with 61 percent (49 patients) with talus OD lesions. Overall, 97.5 percent of patients were not Vitamin D sufficient (mean 10.1ng/mL) with 49 patients (60 percent) who were Vitamin D deficient and 29 patients (37 percent) were severe Vitamin D deficient. There was a statistical significance between Vitamin D levels of OD group compared non-OD control group (10.1 ng/mL vs 26.4ng/dl; p=0.026). No significant difference of ICRS OD lesion type and Vitamin D levels. No OD patients had metabolic bone disorders. No demographic differences. No patients reported inciting ankle trauma or ankle instability.
Conclusions: There was a high prevalence of Vitamin D deficiency with juvenile OD. Serum levels of Vitamin D were also lower in the surgical OD group compared to the non-OD control group, which suggests vitamin D deficiency is associated with the development of OD. Previous studies demonstrate that juvenile OD is different and adult OD with histologic specimens revealing no osteonecrosis. Juvenile OD have focal accumulation of non-mineralized bone matrix which indicate lack of mineralization, correlated with low serum vitamin D levels. As theorized, osteonecrosis of an OD lesion could be secondary to cartilage detachment rather initiation. Thus, Vitamin D deficiency maybe an important cofactor in a multifactorial development of juvenile OD. Vitamin D supplementation may become a potential preventive treatment target for juvenile OD initiation and progression.