Osteoporosis is a disease characterized by low bone mass and by architectural deterioration of bone tissue. Both are related to abnormalities of bone turnover. Biochemical markers of bone turnover reflect the degree of increase in overall bone turnover, and, so far, there are no data indicating that levels of markers of bone formation and resorption can be combined to assess remodelling imbalance. The rate of bone formation or degradation can be assessed either by measuring an enzymatic activity of the osteoblastic or osteoclastic cells – such as alkaline and acid phosphatase activity – or by measuring components of the bone matrix released into the circulation during formation or resorption, such as osteocalcin and pyridinoline crosslinks (Table 12.1). In osteoporosis, bone turnover markers have been suggested to predict the rate of postmenopausal bone loss, to predict the occurrence of osteoporotic fractures and to monitor the efficacy of treatment, especially antiresorptive therapy (hormone replacement therapy [HRT], bisphosphonates and calcitonin). It has also been suggested that the measurement of bone turnover before treatment might be useful in selecting the type of therapy (antiresorptive or bone-stimulating agent) and in predicting the amplitude of the response to oestrogen and bisphosphonate treatment; however, there is little solid evidence for these two concepts. In this chapter, we will briefly review the clinical use of biochemical markers of bone turnover in predicting fracture risk and in monitoring treatment efficacy.