The definition of osteoporosis includes a quantitative aspect (the decrease in bone mass measurable with densitometry), and a qualitative aspect (the alteration of the microarchitecture and bone resistance). Both, separately or together, predispose to fractures.
The treatment of osteoporosis is far from satisfactory. There are two circumstances that contribute to this:
-The treatments aimed at delaying bone resorption are much more effective than those aimed at promoting remineralization. This means that the treatments must be preventive and start before the destruction of the bone structure is irreversible.
-The difficulty of identifying risk factors.
They delay demineralization. The mechanism is not well understood, but it is thought to be a direct reaction on the bone because estrogen receptors have been discovered in osteoblasts (they are bone cells responsible for synthesizing the bone matrix, so they are involved in the development and growth of bones). The estrogen replacement therapy is the most experienced of osteoporosis treatments and the one with the highest efficacy tests.
Calcitonin delays demineralization. It is a hormone that intervenes in the natural regulation of bone calcium metabolism and its main action is the inhibition of osteoclasts (they are cells that degrade, reabsorb and remodel bones).
The efficacy of calcitonin in the conservation of bone mass is similar to that of estrogen and the long-term undesirable effects are minor.
It delays demineralization, probably because the increase in blood calcium inhibits the secretion of parathyroid hormone. After the initial postmenopausal period, the data indicate that the regular supply of calcium significantly delays the rate of decalcification.
They delay demineralization. Alendronate is a bisphosphonate of more recent introduction and specifically selected for having suitable properties for the treatment of osteoporosis.
It induces the increase of bone mineral density, possibly by stimulation of osteoblasts.