title: Is cortical bone hip? What determines cortical bone properties?
abstract: Increased bone turnover may produce a disturbance in bone structure which may result in fracture. In cortical bone, both reduction in turnover and increase in hip bone mineral density (BMD) may be necessary to decrease hip fracture risk and may require relatively greater proportionate changes than for trabecular bone. It should also be noted that increased porosity produces disproportionate reduction in bone strength, and studies have shown that increased cortical porosity and decreased cortical thickness are associated with hip fracture. Continued studies for determining the causes of bone strength and deterioration show distinct promise. Osteocyte viability has been observed to be an indicator of bone strength, with viability as the result of maintaining physiological levels of loading and osteocyte apoptosis as the result of a decrease in loading. Osteocyte apoptosis and decrease are major factors in the bone loss and fracture associated with aging. Both the osteocyte and periosteal cell layer are assuming greater importance in the process of maintaining skeletal integrity as our knowledge of these cells expand, as well being a target for pharmacological agents to reduce fracture especially in cortical bone. The bisphosphonate alendronate has been seen to have a positive effect on cortical bone by allowing customary periosteal growth, while reducing the rate of endocortical bone remodeling and slowing bone loss from the endocortical surface. Risedronate treatment effects were attributed to decrease in bone resorption and thus a decrease in fracture risk. Ibandronate has been seen to increase BMD as the spine and femur as well as a reduced incidence of new vertebral fractures and non vertebral on subset post hoc analysis. And treatment with the anabolic agent PTH(1-34) documented modeling and remodelling of quiescent and active bone surfaces. Receptor activator of nuclear factor kappa B ligand (RANKL) plays a key role in bone destruction, and the human monoclonal antibody denosumab binds to RANKL, inhibiting its action and thus improving BMD significantly.
authors.affiliation: Medicine and Geriatrics, Mount Sinai School of Medicine, New York, USA. bonedocsol@aol.com
authors.forename: Sol
authors.initials: S
authors.lastname: Epstein
mesh_terms: D019386:Alendronate / Q000494:pharmacology / Q000627:therapeutic use; D015519:Bone Density / Q000187:drug effects; D016723:Bone Remodeling / Q000187:drug effects; D001842:Bone and Bones / Q000033:anatomy & histology* / Q000166:cytology / Q000473:pathology; D012968:Etidronic Acid / Q000031:analogs & derivatives / Q000494:pharmacology / Q000627:therapeutic use; D005598:Fractures, Spontaneous / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D006615:Hip / Q000473:pathology; D006620:Hip Fractures / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D006801:Humans; D010024:Osteoporosis / Q000150:complications*; D010446:Peptide Fragments / Q000627:therapeutic use; D053245:RANK Ligand / Q000037:antagonists & inhibitors / Q000378:metabolism; D000068296:Risedronic Acid; D019379:Teriparatide / Q000031:analogs & derivatives / Q000627:therapeutic use
chemical_list: D010446:Peptide Fragments; D053245:RANK Ligand; D019379:Teriparatide; C035748:parathyroid hormone (1-34)amide; D000068296:Risedronic Acid; D012968:Etidronic Acid; D019386:Alendronate