Purpose: A 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 methods: BRONJ+ 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. Results: The 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. Conclusion: The present matched case–control study suggests that vitamin D deficiency is not a risk factor for BRONJ.
Bedogni A., Bettini G., Bedogni G., Basso D., Gatti D., Valisena S., et al. (2019). Is vitamin D deficiency a risk factor for osteonecrosis of the jaw in patients with cancer? A matched case–control study. JOURNAL OF CRANIO-MAXILLOFACIAL SURGERY, 47(8), 1203-1208 [10.1016/j.jcms.2019.03.007].
Is vitamin D deficiency a risk factor for osteonecrosis of the jaw in patients with cancer? A matched case–control study
Bedogni G.;
2019
Abstract
Purpose: A 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 methods: BRONJ+ 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. Results: The 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. Conclusion: The present matched case–control study suggests that vitamin D deficiency is not a risk factor for BRONJ.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.