Senile osteoporosis has been recently recognized as a geriatric syndrome with a particular pathophysiology. There are different classification of osteoporosis: primary, in which bone loss is a result of aging and secondary, in which bone loss occurs from various clinical and lifestyle factors. Primary, or involuntary osteoporosis, can further be classified into Type I or Type II. Type I refers to postmenopausal osteoporosis and is caused by the deficiency of estrogen. While senile osteoporosis is categorized as an involuntary, Type II, and primary osteoporosis, which affects both men and women over the age of 70 years. It is accompanied by vitamin D deficiency, body's failure to absorb calcium, and increased parathyroid hormone. Research over the years has shown that senile osteoporosis is the product of a skeleton in an advanced stage of life and can be caused by a deficiency caused by calcium. However, physicians are also coming to the conclusion that multiple mechanisms in the development stages of the disease interact together resulting in an osteoporotic bone, regardless of age. Still, elderly people make up the fastest growing population in the world. As bone mass declines with age, the risk of fractures increases. Annual incidence of osteoporotic fractures is more than 1.5 million in the US and notably 20% of people die during the first year after a hip fracture. It costs the US health system around $17 billion annually, with the cost projecting to $50 billion by 2040. These costs represent a higher burden compared to other disease states, such as breast cancer, stroke, diabetes, or chronic lung disease. Although there are cost effective and well-tolerated treatments, 23% of the diagnosed are women over 67 have received either bone mineral density (BMD) tests or prescription for treatment after fracture. The clinical and economic burdens indicate there should be more effort in assessment of risk, prevention, and early intervention when it comes to osteoporosis.
Presentation
Complications Because senile osteoporosis is caused by the loss of bone mass due to aging, the bones are more fragile and thus more prone to fractures and fracture-related complications. These complications can include a more than doubled risk increase for future fractures and a lower quality of life resulting from chronic pain or disability, sometimes needing long-term nursing care. Depending on the site, pathologic fractures can also increase relative mortality risk. Hip fractures alone are particularly debilitating and have a nearly 20% higher mortality rate within one year of the fracture. Other fractures are more subtle and can go undetected for some time. For example, vertebral compression fractures in the spine, often noticeable by a loss of vertical height, can occur even during routine motions like twisting, coughing, and reaching. In addition to decreased bone mineral density, there are other factors that contribute to fracture risk such as advanced age, lower body mass index, fracture history, smoking, steroid use, high alcohol intake, and fall history. Studies linking alcohol and fracture risk define high intake as three or more drinks per day. High caffeine intake may also play a role in fracture risk. Many healthcare organizations also utilize a Fracture Risk Assessment Tool (FRAX) that can estimate a 10-year probability of having an osteoporotic fracture based on an individual's health information and the criteria listed above.
Cause Bone remodeling, or the absorption and resorption of bone, is a natural mechanism that occurs to repair and strengthen bones in the body. However, an imbalance between the resorption and formation of bone occurs as people age, contributing to the development of senile osteoporosis. The aging of cortical and trabecular bones in particular cause the decrease in bone density in the elderly population. Although most of the etiologic considerations regarding senile osteoporosis are not very clear for physicians yet, risk factors of osteoporosis have been identified. These factors include gender, age, hormone imbalances, reduced bone quality, and compromised integrity of bone microarchitecture. Based on the current evidence attached to clinical experimentation, there is some evidence that the pathogenesis of the disease is related to a deficiency of zinc. Such deficiency is known to lead to an increment of endogenous heparin, which is most likely caused by mast cell degranulation, and an increase in the bone resorption (calcium discharge in the bones) reaction of prostaglandin E2, which constrain the formation of more bone mass, making bones more fragile. These co-factors are shown to play an important role in the pathogenetic process attached to senile osteoporosis as they enhance the action of the parathyroid hormone. The intake of calcium in elder people is quite low, and this problem is worsened by a reduced capability to ingest it. This, attached to a decrease in the absorption of vitamin D concerning metabolism, are also factors that contributes to a diagnosis of osteoporosis type II.
Risk factors While senile osteoporosis (type II) is mainly attributed to age, other risks include medical, pharmacological, genetic, and environmental factors. Peak bone mass is a major determinant of bone density, which starts in utero and is typically complete by the age 40.
Medical Though secondary osteoporosis is a separate category when it comes to osteoporosis diagnosis, it can still be a contributing factor to primary osteoporosis. Secondary osteoporosis can be present in pre- and post-menopausal women and in men and have found to be factors contributing to osteoporosis in both sexes (50-80% of men and 30% of post-menopausal women). Therefore, when treating people over 70, it is important to exclude secondary causes of osteoporosis which include endocrine disorders (e.g. hyperthyroidism and diabetes mellitus), gastrointestinal, hepatic and nutritional disorders (e.g. celiac disease and inflammatory bowel disease), hematological disorders (e.g. systemic mastocytosis), renal disorders (e.g. chronic kidney disease), and autoimmune disorders (e.g. rheumatoid arthritis and systemic lupus erythematosus).
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