Greater bone formation

Epidemiologic studies have consistently documented that increased potassium intake is associated with greater bone mineral density. In trials, supplemental potassium bicarbonate reduced bone turnover as manifest by less urinary calcium excretion and by biochemical evidence of greater bone formation and reduced bone resorption. However, no trial has tested the effect of increased potassium or diets rich in potassium on bone mineral density or clinical outcomes related to osteoporosis. 

Teriparatide, the recombinant form of PTH 1-34, is approved for treatment of osteoporosis. Teriparatide is given in a dosage of 20 meg subcutaneously daily. Like fluoride, teriparatide stimulates new bone formation, but unlike fluoride, this new bone appears structurally normal and is associated with a substantial reduction in the incidence of fractures. Teriparatide is approved for use for only 2 years. Trials examining the sequential use of teriparatide followed by a bisphosphonate after 1 or 2 years are in progress and look promising. Giving teriparatide with a bisphosphonate has not shown greater efficacy than the bisphosphonate alone. 

Although Al bone disease can occur in any patient intoxicated by Al, the risk is greater in diabetics. This may be related to a lower than normal bone formation rate, an abnormality that has be demonstrated in type 1 diabetics prior to the onset of clinical renal disease [109, 110]. The risk for developing acute Al encephalopathy also seems to be increased in diabetic patients this might be related to a decreased storage capacity of the bones [17]. 

Glucocorticoid treatment for arthritis or other ailments can very quickly produce a form of osteoporosis caused by the inhibition of bone formation [334]. In such cases, the decrease in bone mass may be as much as 10-20%, but examination of trabecular bone reveals a much greater (30-40%) decrease in this component of bone [335]. Combination therapies with vitamin D and bisphosphonates, calcitonin or fluoride can be effective [336]. Therapy employing vitamin D or 1,25-(OH)2D3, the latter being highly calcaemic, should also include serum calcium monitoring and the use of thiazide diuretics as appropriate. 

The analytical and clinical performance of these BAP immunoassays have been characterized in a series of articles. Unfortunately, current immunoassays are not completely specific for BAP and exhibit 7% to 17% cross-reactivity with ALP from liver. It has been difficult to exactly determine cross-reactivity for the liver isoform because of limitations of existing preparations and an incomplete understanding of the exact nature of the circulating isoforms. BAP immimoassays provide greater sensitivity and specificity for bone formation than does the... 

C. Calcitonin Calcitonin, a peptide hormone secreted by the thyroid gland, decreases bone resorption and serum calcium and phosphate (Figure 42-2). Bone formation is not impaired initially, but ultimately it is reduced. The hormone has been used in conditions in which an acute reduction of serum calcium is needed, eg, Paget s disease and hypercalcemia. While calcitonin is approved for treatment of osteoporosis, it is questionable whether long-term use prevents fractures. Although human calcitonin is available, salmon calcitonin is most often selected for clinical use because of its longer half-Ufe and greater potency. Calcitonin is administered by injection or as a nasal spray. 

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. 

When compared to other intrinsically osteoinductive biomaterials reported in the literature, these open HA microspheres have the advantages of ease of fabrication, low cost, and reasonable large-scale production for routine clinical use. However, in common with other intrinsically osteoinductive biomaterials [71, 73], new bone formation is limited to within the micro-concave geometry. Consequently, the effectiveness of these open HA microspheres remains to be improved in order to achieve greater and more significant bone formation. 

The proximal humeral epiphysis arises from two, sometimes three separate ossification centres (Fig. 7.12). The first ossification centre develops medially at about 2 weeks of age and the second ossification centre develops in the greater tuberosity between 6-12 months of age. When the arm is internally rotated, the first appearing medial ossification centre is rotated into a lateral position and can give the false impression of shoulder joint disruption. The rare third centre occurs in the lesser tuberosity in the third year of life, and when visualised on the axillary shoulder view, may be mistaken for a fracture. This ossification centre fuses with the shaft of the humerus at 6-7 years of age. The radiolucent proximal physis of the humerus is tented and in various oblique positions can be mistaken for a fracture (Fig. 7.13). The normal bicipital groove in the proximal humerus may simulate periosteal new bone formation (Fig. 7.14). 

---