Abstract

PurposeA previous case–control histomorphometric study showed higher odds of osteomalacia in patients with bisphosphonate-related osteonecrosis of the jaw (BRONJ). Vitamin D deficiency causes osteomalacia and may therefore be involved in the pathogenesis of BRONJ. The present case–control study aimed at testing such hypothesis. Materials and methodsBRONJ+ and BRONJ− patients treated with bisphosphonates were matched by sex (same) and age (within 5 years). Serum 25-hydroxy-vitamin D (25-OH-D), parathyroid hormone, bone alkaline phosphatase, total procollagen type 1 amino-terminal propeptide, carboxy-terminal collagen crosslinks, Dickkopf WNT signaling pathway inhibitor 1 and sclerostin were measured. ResultsThe main outcome was vitamin D deficiency defined as 25-OH-D < 50 nmol/l. A total of 51 BRONJ+ and 73 BRONJ− patients were studied. The frequency (95% CI) of vitamin D deficiency was 59% (45%–72%) in BRONJ+ and 62% (48%–75%) in BRONJ− patients. This amounts to a difference of −3% (−22%–16%, p = 0.77) for BRONJ+ patients. Serum 25-hydroxy-vitamin D and parathyroid hormone were similar in BRONJ+ and BRONJ− patients. Among the bone metabolism markers, only sclerostin differed between the two groups, being higher in BRONJ+ patients. ConclusionThe present matched case–control study suggests that vitamin D deficiency is not a risk factor for BRONJ.

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