Osteoporosis primary/secondary

Osteoporosis is a skeletal disease that is characterized by loss of bone mass as well as microarchitectural deterioration of the bone tissue. This disease is associated with increased bone fragility and susceptibility to fracture. It is a condition that is characterized not by inadequate bone formation but, rather, by a deficiency in the production of well-mineralized bone mass. Whereas no medical cause typically is evident in primary osteoporosis (3), secondary osteoporosis classically stems from medical illness or medication use. There are two types of primary adult osteoporosis, type I, or postmenopausal, and type II, or senile (Table 35.1). In type I osteoporosis, there is an accelerated rate of bone loss via enhanced resorption at the onset of menopause. In this form of the disease, the loss of trabecular bone is threefold greater than the loss of cortical bone. This disproportionate loss of bone mass is the primary cause of the vertebral crush fractures and the wrist and ankle fractures experienced by postmenopausal women. In type II osteoporosis, which is associated with aging, the degree of bone loss is similar in both trabecular and cortical bone (5) and is caused by decreased bone formation by the osteoblasts. 

Osteoporosis can be classified as either primary (no known cause) or secondary (caused by drugs or other diseases). Primary osteoporosis is found most often in postmenopausal women and aging men, but it can occur in other age groups as well. 

This drug class has an enormous potential in the primary and secondary prevention of several types of estrogen-dependent tumors, postmenopausal osteoporosis, and cardiovascular and neurodegenerative diseases. 

Primary osteoporosis is the most common form of the condition. The secondary form of osteoporosis is diagnosed when an illness and/or medications are present with a negative impact on BMD. Examples of common chronic conditions in old people that can cause secondary osteoporosis are seen in Box 5.14. Examples of drugs that can cause secondary osteoporosis are glucocorticoids, too high doses of thyroid hormone, anticonvulsants, and heparin. Especially the use of glucocorticoids has been known to cause severe osteoporosis even within a short period of treatment. Depending on the doses the development of osteoporosis can occur within a few weeks or months. 

Qassification Idiopathic osteoporosis type 1, occurring in postmenopausal females type 11, occurring in senescent males and females (>70 y). Secondary osteoporosis associated with primary disorders such as Cushing s disease, or induced by drugs, e.g chronic therapy with glucocorticoids or heparin. In these forms, the cause can be eliminated. 

Osteoporosis is a metabolic bone disease characterized by low bone mass and micro-architectural deterioration of bone tissue. This will lead to bone fragility and consequent increase in bone fracture risk. Mean bone mineral density (BMD) is measured with dual X-ray absorptiometry (DEXA) and expressed in Tsc (Tscore). WHO standards are a Tsc that is 1 standard deviation (SD) below mean BMD is graded as normal bone, Tsc between 1 and 1.5 SD below mean BMD is graded as osteopenia and a Tsc of more than 2.5 SD below mean BMD is graded as osteoporosis. When the Tsc is below 1.5 SD mean BMD prevention of osteoporosis must be initiated. Primary osteoporosis is caused mainly by hormone deflciency in both women and men. Secondary osteoporosis may result from endocrine, metabolic, nutritional and autoimmune causes or from immobility because of trauma. Also the use of medicaments such as corticosteroids may be contributing. 

Contraindications Primary or secondary hyperparathyroidism, including hypercalci-uria (renal calcium leak), hypomagnesemic states (serum magnesium less than 1.5 mg/dl), bone disease (osteoporosis, osteomalacia, osteitis), hypocalcemic states (e.g., hypoparathyroidism, intestinal malabsorption), normal or low intestinal absorption and renal excretion of calcium, enteric hyperoxaluria, and patients with high fasting urinary calcium or hypophosphatemia. 

Polymorphisms in the VDR gene may be related to bone mineral density and predispose an individual to osteoporosis [337], The use of restriction length fragment polymorphism (RFLP) analysis and other markers of VDR polymorphisms could be an additional early assessment parameter for the future risk of developing osteoporosis. Identification of the defective allele also referred to as BB or bb, depending on the laboratory from which the studies first originated, has been correlated to an increased risk of primary and secondary osteoporosis and primary hyperparathyroidism. But... 

Osteoporosis is a condition in which bone mass, and therefore bone strength, is decreased. This results in a greatly increased risk of fracture. Primary osteoporosis is osteoporosis which occurs due to normal, predictable changes within the body during the aging process. Secondary osteoporosis occurs as a result of some other specific disease process which produces osteoporosis as one of its symptoms. 

Treatment of secondary osteoporosis varies depending on the actual disease process which has produced the osteoporosis, and may include adjustments to thyroid medication, dietary supplementation with calcium or vitamin D (which is involved in the ability of the intestine to absorb calcium in the diet), or other treatment of the primary disease. 

In a prospective study, 64 patients with a recent history of at least one vertebral fracture caused by primary and secondary osteoporosis were recruited from six osteoporosis centers in Germany between December 1999 and April 2001 (63). Transdermal fentanyl 25 pg/hour was the recommended starting dose, with incremental steps of 25 pg/hour if there was insufficient analgesia. Treatment was stopped after less than 28 days in 15 patients (23%). In 10 of these, fentanyl was stopped because of nausea and/or vomiting and/or dizziness. In 49 patients, pain at rest (55% reduction) and on motion (47% reduction) abated significantly from baseline. The starting dose of 25 pg/hour of fentanyl was sufficient in most patients (70%). 

Osteoporosis is of two forms- primary i.e. idiopathic and secondary. Primary osteoporosis is classified into type I and type II osteoporosis. Type I is referred to post menopausal osteoporosis which is the main type affecting women, characterized by rapid bone loss and affects women after the menopause, mainly in trabecular bone and is associated with vertebrae and distal radio fractures whereas type II also termed as senile osteoporosis occurs due to chronic deficiency of calcium, increase in parathormone activity and decrease in bone formation and is associated with aging. On the other hand secondary type results from inflammatory processes, endocrine changes, multiple myeloma, sedentariness and the use of drugs such as heparin, corticoid and alcohol [3]. Prevention is the main treatment of osteoporosis, for which bone mass peak and the prevention of postmenopausal reabsorption are critical elements. The common treatment of osteoporosis includes calcium consumption as calcium salts, vitamin D supplements, and hormone reposition [4], the use of calcitonin to modulate serum levels of calcium and phosphorous [5], the use of bisphosphonate, mainly alendronates [6], use of ipriflavone and sodium fluoride [7], besides physical activity to strengthen muscles, stimulate osteoblasts formation and prevent reabsorption. 

Elevated concentrations of telopeptides and DPD have been reported in osteoporosis, Paget s disease, metastatic bone disease, primary and secondary hyperparathyroidism, hyperthyroidism, and other diseases with increased bone... 

Biochemical tests cannot be used to iliagnose primary osteoporosis or monitor accelerated bone loss becau.se the results of the common bihealthy subjects and patients with the disorder. Biochemical tests are of value in the diagnosis of hyperthyroidism. gonadal failure or Cushing s syndrome which cause secondary osteoporosis. 

Osteoporosis can be categorized as primary (idiopathic) or secondary to a systemic illness or medication such as glucocorticoids or phenytoin. A major factor in the former category is the decline in estrogen levels, and the resulting sharp decrease in bone mass that accompanies menopause in women. 

Those who believe in strong control of error rates will point out that one could nominate a man of straw endpoint that was almost certain to yield significance and then regard oneself as entitled to look at anything one liked. For example, in a trial of osteoporosis in which it was important to show an improvement in fracture rates one could nominate the much weaker endpoint of bone mineral density as the primary one and then have a host of different fracture measures (overall, vertebral, wrist, hip and so forth) as secondary endpoints, claiming a therapeutically demonstrated success if at least one of these was significant. This type of criticism is discussed further in connection with the problem of comparing many treatments in section 10.2.9. 

Some herbs are used in bone fracture treatment as well as osteoporosis. The studies of Sun et al. 2002 and Jeong et al. 2005 [4, 5] showed that Gu-Sui-Bu has potential effects on primary and secondary bone cells culture. The herbal extract enhanced proliferation and differentiation of bone cell in the studies. On the other hand, the crude extract has been proven possessing inhibition effect on osteoclast obtained from fetal mouse long bone [6]. 

Kruse, H. P. and Kuhlencordt, F. (1975) On an attempt to treat primary and secondary osteoporosis with human growth hormone. Hormone metabol. Res., 7, 488. 

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