Cortical bone comprises 80% of the adult skeleton. Yet in recent years it has received less attention from bone researchers than cancellous bone. Cortical bone undergoes both modeling (resorption and formation occurring independently of each other at different sites) and remodeling (coupled and sequential resorption and formation occurring at the same site). Modeling and remodeling occur on both the endocortical and periosteal surfaces of the cortex, whereas within the cortex only remodeling referred to as Haversian remodeling takes place. Bone modeling plays a key role during growth and determines the size and shape of the adult bone. This process is largely under genetic control. Disruptions in the modeling process during growth results in deformed bones, the classic case of which is the Erlenmeyer flask deformity. Modeling also occurs in adults, primarily in response to changes in mechanical loading. For example, modeling is responsible for the increase in mass and strength of the forearm bones in the dominant arm of experienced tennis players. Remodeling of the cortex, occurs, throughout life and is influenced by a variety of endocrine, mechanical and local factors. After skeletal maturity, remodeling increases with age and particularly after menopause. On the endocortical surface net resorption exceeds formation leading to expansion of the medullary cavity, thinning and trabecularization of the cortex. On the periosteum, net formation exceeds resorption leading to a gradual increase in the diameter of the bone, but the rate of periosteal expansion is less than that of the endocortex and so cortical thickness declines. Resorption also exceeds formation in the intracortical envelope leading to an increase in the diameter of the Haversian canals and evolving Haversian systems can fuse to form giant canals. The net result of these age- and menopause- related changes is loss of cortical, mass, structure and strength leading to skeletal fragility.