The osteoclast then induces an infolding of its cell membrane and secretes collagenase and other enzymes important in the resorption process.

High levels of calcium, magnesium, phosphate and products of collagen will be released into the extracellular fluid as the osteoclasts tunnel into the mineralized bone.

[5] Bone resorption rates are much higher in post-menopausal older women due to estrogen deficiency related with menopause.

Bisphosphonates, RANKL inhibitors, SERMs—selective oestrogen receptor modulators, hormone replacement therapy and calcitonin are some of the common treatments.

[9] Bone resorption is highly stimulated or inhibited by signals from other parts of the body, depending on the demand for calcium.

[4] Calcitonin has a greater effect in young children than in adults, and plays a smaller role in bone remodeling than PTH.

[14] The effects of alcohol on bone mineral density (BMD) are well-known and well-studied in animal and human populations.

Through direct and indirect pathways, prolonged ethanol exposure increases fracture risk by decreasing bone mineral density and promoting osteoporosis.

Indirect effects of excessive alcohol use occur via growth hormone, sex steroids, and oxidative stress.

[15] Chronic alcoholism decreases the levels of IGF1, which suppresses the ability of GH to increase bone mineral density.

[15] Increasing alcohol consumption is linked with decreasing testosterone and serum estradiol levels, which in turn lead to the activation of RANK (a TNF receptor) protein that promote osteoclast formation.

Stimulation of osteocyte apoptosis by alcohol exposure may explain decreased bone mineral density in chronic drinkers.

[25] These processes make a child’s skeleton grow and extend, while childhood is characterized by bone tissue growth rather than its resorption.