Animal models of cortical porosity

Increased cortical porosity (Ct.Po) has been observed as a consequence of aging, disease (hyperparathyroidism, osteoporosis), and pharmacologic intervention (thyroid hormone, fluoride, parathyroid hormone, prostaglandins). Whether this is permanent or transient in humans has not been established nor has the impact of Ct.Po on bone strength or fracture incidence been determined. There is a need to understand the causes and consequences of increased Ct.Po and how it relates to disease states and osteoporosis therapies. The mechanism of increased Ct.Po is thought to be an increased activation of Haversian remodeling systems accompanied by increased Haversian canal diameter. Increased activation at the endocortical surface and subsequent trabecularization may also contribute to loss of cortical bone. Ct.Po has been observed in several animal models which can be used to further study the phenomenon. Ct.Po is seen in normal dogs and is increased by treatment with PTH and prostaglandins. In the dog it has also been shown that increased Ct.Po is reversible after anabolic therapy is discontinued. Furthermore, in dogs an antiresorptive agent (risedronate) will block PTH-induced increases in Ct.Po (control 1.6% +/- 0.7; PTH 3.0% +/- 1.1, PTH plus risedronate 1.8% +/- 1.2) without interfering with anabolic effects. In rats, increased Ct.Po occurs following treatment with anabolic agents such as PTH, prostaglandin, and insulin-like growth factor 1 (IGF-1). For instance, with IGF-1, Ct.Po increased from 0.4% +/- 0.4 to 5.4% +/- 1.8. Other species in which Ct.Po is observed include primates and ferrets.(ABSTRACT TRUNCATED AT 250 WORDS)