12 Şubat 2014 Çarşamba

BASIC PATHOPHYSIOLOGY WİTH OSTEPOROSSİS

Bone mass in older adults equals the peak bone mass achieved by age 18-25 years minus the
amount of bone subsequently lost. Peak bone mass is determined largely by genetic factors,
with contributions from nutrition, endocrine status, physical activity and health during growth.7


The process of bone remodeling that maintains a healthy skeleton may be considered a
preventive maintenance program, continually removing older bone and replacing it with new
bone. Bone loss occurs when this balance is altered, resulting in greater bone removal than
replacement. The imbalance occurs with menopause and advancing age. With the onset of
menopause, the rate of bone remodeling increases, magnifying the impact of the remodeling
imbalance. The loss of bone tissue leads to disordered skeletal architecture and an increase in
fracture risk.

Figure 1 shows the changes within cancellous bone as a consequence of bone loss. Individual
trabecular plates of bone are lost, leaving an architecturally weakened structure with
significantly reduced mass. Increasing evidence suggests that rapid bone remodeling (as
measured by biochemical markers of bone resorption or formation) increases bone fragility and
fracture risk.

FIGURE 1. Micrographs of Normal vs. Osteoporotic Bone8















Bone loss leads to an increased risk of fracture that is magnified by other aging-associated
declines in functioning. Figure 2 shows the factors associated with an increased risk of
osteoporosis-related fractures. These include general factors that relate to aging and sex
steroid deficiency, as well as specific risk factors, such as use of glucocorticoids, which cause
decreased bone formation and bone loss, reduced bone quality and disruption of
microarchitectural integrity. Fractures result when weakened bone is overloaded, often by falls
or certain activities of daily living.

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