BONE IS a vital, metabolically active tissue that may suffer when medications interfere with normal homeostatic processes. Because of the measured pace of bone turnover, clinically significant bone damage becomes a relevant risk for patients who are receiving medications recurrently or on a long-term basis. Drugs that are incorporated directly into bone have persistent effects long after discontinuation of treatment; eg, the elimination half-life for geminal bisphosphonates is approximately one decade.1 In assessing the potential mechanisms for bone damage, dermatologists should use an algorithm based on their knowledge of bone turnover and growth patterns. A precise delineation of a drug's interference with normal bone metabolism can guide both therapeutic and preventative measures.
NORMAL BONE REMODELING AND TURNOVER
Bone turnover occurs continuously within the framework of a tightly integrated process termed the bone multicellular unit.2 Osteoclast activation is the initial triggering event for all bone remodeling and is primarily
Sewell KL. Iatrogenic Osteoporosis. Arch Dermatol. 1995;131(11):1321–1322. doi:10.1001/archderm.1995.01690230101016
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