See also non-immune cells (for discussion of osteoblasts and osteoclasts)

Osteoporosis:

Osteoprosis is characterised by a progressive loss of bone mass and microarchitecture which leads to incrased fracture risk. The World Helath Organization (wHO) defines osteoporsis as a systemic skeletal disease characterised by low bone mass and microarhitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture. with the ageing of the population, the complications of osteoporsis, fractures, represent a growing medical and socio-economic threat in industrialised countires. Switzerland belogs to the countries with the highest and still fastest growing life expectancy at birth worldwide (84.6 years for women and 80.2 for men in 2010). As the incidence of osteoporotic fractures increases exponentially with age, the implementation of meassures aimed at reducing fracture risk is needed to preserve quality of life and to ensure adqueate control of health care costs. “Kurt Lippuner, “the future of osteoporsis treatment –a research update” Current opinion, July 2012). 

Types of Osteoporsis:

The goal of steoporsis treatment is to reduce fractures . this can be acheived either by decreasing bone resorption and/or by increasing bone formation. 

–Primary Osteoporsis: is linked to the normal aging process. There is a link between two hormones, estrogen and progesteron and teh rate at hwih bone is lost. Estrogen regulates osteoclasts that break down bone and progesterone controls osteoblasts, which help in making new bone. Other hromones are also important. Primary osteoporsis can be divided into “primary type I and “primary type II” osteoporsis.

—-Primary Type I osteoporsis: is generally referred to as postmenopausal osteoporsis, as it is seen in women six times more frequently who have gone through menopause, resulting in a drop in levels of estrogen. It occurs in women about 10-15 years after menopause, usually between age 50 and 70. The loss of bone structure because of the increase in bone resorption is connected to estrogen deficiency in women and the lack of testosterone in men. People who suffer from primary type I osteoporosis are at high risk of spinal and wrist factures. 

—-Primary Type II osteoporosis: is caused by a long term calcium deficiency. Women are twice as more likely than men to suffer form Type II osteoporosis. It resutls in loss of outer bone structure and also the inner trabecular bone to wear down and become thin. Studies have linked deficiency in dietary calcium and vitam D decle due to age, or the hyper activity of the parathyroid glands (secondary hyperparathyroidism). It is also called low-turnover osteoporsis becasue the rate of bone turnover is much lower in this type of osteoporsis. 

Secondary Osteoporisis: develop swhen certain medical conditions and medications incrase bone remodeling leading to disruption of bone reformation. The loss of bone mass occurs due to the imbalance beween the production of new bone and the loss of old bone, leading to lower bone turnover rate. An imbalance in hormones from the increased activity of the parathyroid glands or hyperparathyroidism can result in secondary osteoporsis. Hormonal imbalance can also occur form hyperthyroidism, which is an excessive secretion from thyroid glands. Seondary osteoporsis is common amon patients fufering form diabetwes, which can often lead to hyperglycemia or increasing level sof glycosuria. The long term use of oral corticosteroids can cause hypercotisolisms, which increases the chance of developing secondary osteoporsis. 

Treatments:

–Antibodies against endogenous inhibitors of bone formation scelerostin, dickkkofp-1, PTH and PTHrp analogues.

–inhibitors of bone resorption: This includes cathepsin K inhibitors: which may suppress osteoclase function without impairing osteoclast viability and thus maintain bone formation by preserving the osteoclast-osteoblast corsstalk.

—-Bisphophonates: are today’s mainstay of osteoporosis treatment. They act as inhibitors of bone resorption with a high affinity for bone and were shwon to increase BMD and reduce fracture risk in patients with postmenopausal, male, and glucocorticosteroid-induced osteoporsis. Due to their long half-life in bone, they can be adminsitered either orally or intravenously.

–antibody against RNAKL: such as denosumab which inhibits osteoclast formation, function and survival.