Consensus and WHO definitions of @entity170 are provided. The pathogenesis of the disorder has genetic, hormonal and environmental influences which affect peak bone mass, @entity14577 and age-dependent @entity604 . Peak bone mass is mainly genetically determined, though dietary factors and physical activity can have positive effects. Peak bone mass is attained at the point when skeletal growth ceases, after which time @entity604 starts. Loss of @entity2931 with the menopause results in accelerated @entity604 . Bone remodelling balance @entity2527 , with osteoblastic bone formation not able to match the level of resorption. @entity9646 replacement therapy can reverse this trend. Proposed mechanisms and the parts played by the different cell populations and factors are discussed. Osteoblasts are particularly sensitive to ageing phenomena--more sensitive than are osteoclasts, so the negative bone balance increases with increasing age. Age-dependent @entity604 is aggravated by reduced @entity460 absorption, a mutation in the collagen gene and polymorphism in TGF-beta and @entity2931 receptor proteins.

The pathogenesis of XXXX .

@entity9646 :: ('MESH:D006728', 'Chemical') :: ['Hormone'] @entity2931 :: ('CHEBI:50114', 'Chemical') :: ['oestrogen'] @entity14577 :: ('MESH:D015663', 'Disease') :: ['perimenopausal bone loss'] @entity604 :: ('MESH:D016301', 'Disease') :: ['bone loss'] @entity170 :: ('MESH:D010024', 'Disease') :: ['osteoporosis'] @entity2527 :: ('MESH:D001862', 'Disease') :: ['tips in favour of osteoclastic bone resorption'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['calcium']
@entity170 :: (MESH:D010024,Disease) :: ['osteoporosis']
