- ONCOLOGY Vol 24 No 8
- Volume 24
- Issue 8
Bone Complications of Cancer Treatment in the Elderly
Osteopenia and osteoporosis are increasingly common in cancer patients, owing to the aging of the population and to new forms of cancer treatment. Androgen and estrogen deprivation, as well as some forms of cytotoxic chemotherapy, may lead to osteopenia and osteoporosis. Patients at risk for osteoporosis include those treated with aromatase inhibitors and with androgen deprivation for more than 1 year. In addition, all patients 65 years of age and older are at risk of osteoporosis when treated with cytotoxic agents, and so should be screened for bone loss. Several treatments have been effective in the prevention and management of osteoporosis. In patients at risk for this complication, it is recommended to obtain a bone density evaluation and to start appropriate treatment. This may include calcium and vitamin D supplementation for mild forms of osteopenia, and bisphosphonate therapy or denosumab (Prolia) for more advanced osteopenia and osteoporosis.
Osteopenia and osteoporosis are increasingly common in cancer patients, owing to the aging of the population and to new forms of cancer treatment. Androgen and estrogen deprivation, as well as some forms of cytotoxic chemotherapy, may lead to osteopenia and osteoporosis. Patients at risk for osteoporosis include those treated with aromatase inhibitors and with androgen deprivation for more than 1 year. In addition, all patients 65 years of age and older are at risk of osteoporosis when treated with cytotoxic agents, and so should be screened for bone loss. Several treatments have been effective in the prevention and management of osteoporosis. In patients at risk for this complication, it is recommended to obtain a bone density evaluation and to start appropriate treatment. This may include calcium and vitamin D supplementation for mild forms of osteopenia, and bisphosphonate therapy or denosumab (Prolia) for more advanced osteopenia and osteoporosis.
With the aging of the population, osteopenia and osteoporosis are becoming an increasingly common cause of morbidity, mortality, and health care costs.[1-3]
Given the increased survival of cancer patients, cancer treatment has become a major contributing factor to osteoporosis.[4-5] This long-term complication of cancer treatment is particularly relevant, as the majority of cancers occur in individuals 65 years of age and older who are already at risk for osteoporosis.[6] After a review of the pathogenesis of osteoporosis, this article examines the effects of common cancer treatments on the bones and explores a research agenda in this important field.
Osteoporosis and Osteopenia: Definition and Pathogenesis
Osteoporosis involves increased bone fragility resulting from decreased bone mass and microarchitectural distortion.[7-8] The diagnosis of osteopenia and osteoporosis is based on assessment of bone density by dual energy x-ray absorptiometry (DEXA) scan. According to the World Health Organization, one can identify four different situations with regard to bone stability:
• Normal bone, with a T-score higher than or equal to −1 SD;
• Osteopenia, indicated by a T-score between −1 and −2.5 SD;
• Osteoporosis, defined as a T-score lower than −2.5 SD; and
• Severe osteoporosis that involves one or more fragility fractures, in addition to a low T-score.
Fragility fractures are those occurring in the absence of recognizable trauma or as the result of a trauma that would not cause fractures of normal bones.
Central to the pathogenesis of osteoporosis is bone remodeling, a lifelong process that involves the reabsorption of old bone and the formation of new bone.[3,9] This takes place in the so-called bone remodeling centers (BRC),[9] which include the basic multicellular unit (BMU), the canopy of bone cells, and the blood vessels. The BMU consists of osteocytes, osteoblasts, and osteoclasts. Osteocytes are mechanosensors and trigger remodeling to adapt the bone to incoming and ongoing mechanical strains. The remodeling appears to start with the bone-lining cells that recruit osteoclasts to reabsorb the old bone, and these in turn stimulate a wave of new bone formation by the osteoblasts. Contrary to what was previously believed, the process of bone remodeling is essentially the same for the cancellous bone (the bone in contact with the marrow) and for the solid bone in the diaphysis of long bones. Osteoclasts originate from the pluripotent hematopoietic progenitors, and osteoblasts originate from mesenchymal cells. Osteocytes represent the final osteoblastic differentiation.
TABLE 1
Factors That Influence Bone Remodeling