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Bone‐site‐specific responses to zoledronic acid
Author(s) -
Vermeer JAF,
Renders GAP,
Duin MA,
Jansen IDC,
Bakker LF,
Kroon SA,
Vries TJ,
Everts V
Publication year - 2017
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.12587
Subject(s) - zoledronic acid , osteonecrosis of the jaw , bone resorption , bisphosphonate , diphosphonates , osteoporosis , osteoclast , medicine , bone remodeling , bone density conservation agents , bone marrow , bone mineral , dentistry , endocrinology , receptor
Objectives Bisphosphonates are widely used to treat bone diseases such as osteoporosis. However, they may cause osteonecrosis of the jaw. Here, we investigated whether in vivo exposure to bisphosphonates has a different effect on long bone and jaw osteoclasts, and on the turnover of these different bones. Materials and Methods Zoledronic acid (0.5 mg kg −1 weekly) was administered intraperitoneally to 3‐month‐old female mice for up to 6 months. The effects on the number of osteoclasts, bone mineralization and bone formation were measured in the long bones and in the jaw. Results Long‐term treatment with zoledronic acid reduced the number of jaw bone marrow cells, without affecting the number of long bone marrow cells. Zoledronic acid treatment did not affect the number of osteoclasts in vivo . Yet, the bisphosphonate increased bone volume and mineral density of both long bone and jaw. Interestingly, 6 months of treatment suppressed bone formation in the long bones without affecting the jaw. Unexpectedly, we showed that bisphosphonates can cause molar root resorption, mediated by active osteoclasts. Conclusions Our findings provide more insight into bone‐site‐specific effects of bisphosphonates and into the aetiology of osteonecrosis of the jaw. We demonstrated that bisphosphonates can stimulate osteoclast activity at the molar roots.