Clinical Flashcards
Osteoporosis
bone becomes brittle and fragile from loss of tissue and reduced mineralisation due to increased resorption rates compared to formation
• Clinically determined by a reduced bone mineral density using a DXA scan of the hip of more than -2.5 SD compared to young adult reference group (T-score)
Osteopenia
when the protein and mineral content of bone tissue is reduced
• Less severe than osteoporosis
• Bone does not break easily on contact- reduction in BMD of >-1 SD but <-2.5
• Occurrence in children= ricket’s,
Osteomalacia
softening of the bones that happens when mineralisation doesn’t happen properly due to a deficiency in vitamin D or calcium
Microscopic difference between normal and osteoporotic bone
Histologic examination of osteoporotic bone may reveal generalised thinning of trabeculae and irregular perforation of trabeculae, reflecting unbalanced osteoclast-mediated bone resorption.
The normal bone shows a pattern of strong interconnected plates of bone. Much of this bone is lost in osteoporosis and the remaining bone has a weaker rod-like structure. Moreover some of the rods are completely disconnected.
Steps involved in bone fracture healing
Haematoma formation
Bone generation- fibrocartilaginous callus
Bony callus
Bone remodelling
Steps involved in bone fracture healing - haematoma formation
blood vessels in the broken bone tear and haemorrhage resulting in clotted blood at the break site
• Severed blood vessels are sealed by the clotting process
• Bone cells deprived of nutrients begin to die— osteocytes
Steps involved in bone fracture healing - fibrocartilaginous callus
fibrocartilaginous callus is converted into a bony callus
• This spongy bone takes around 2 months to firmly join together
• Non-union if healing does not occur with 26 weeks
Steps involved in bone fracture healing - bony callus
fibrocartilaginous callus is converted into a bony callus
• This spongy bone takes around 2 months to firmly join together
• Non-union if healing does not occur with 26 weeks
Steps involved in bone fracture healing - bone remodelling
the bony callus is then remodelled by osteoclasts and osteoblasts, going from a simple woven structure to lamellar
• Excess natural material on the exterior of the bone is removed
• Compact bone is added to create bony tissue
• Remodelling can take months and bone can remain uneven for years
Benefits of exercise for bone health
Regular physical exercise is essential for maintenance of optimal bone health in many ways. Other than growth and strength of both muscles and bones, the stress produced by exercise on bones benefits bones by increasing calcium deposition; accordingly, bones become denser and stronger. In contrast, physical inactivity results in a decrease of bone mass. These strains result in the activation of special osteocytes, embedded within the bone, that function as mechanosensitive cells and have the unique property of mechanotransduction and can detect and respond to mechanical strain. These osteocytes, in turn, and via a sequence of molecular signals activate osteoblasts and osteoclasts and in such a way, the osteocytes control both bone formation and resorption (via the differentiation of both the osteoblasts and osteoclasts). The resulting osteogenic response represents the bone adaptation to the strain put by the physical activity and its causative muscular contraction on the bone. It is notable that the response to the strain will obviously be in the predominant loading direction of the contracting muscle and at the site of strain and deformation.
The bone adaptation responses to exercise described above serve the important physiological goal of improving bone mineral density (BMD), bone architecture, and strength and also prevent bone injuries. This effect is particularly significant in high-impact sports, such as tennis.
Actions of AdCal D3
The principal biological function of vitamin D is the maintenance of normal levels of serum calcium and phosphorus in the bloodstream by enhancing the efficacy of the small intestine to absorb these minerals from the diet
Actions of risedronate
Risedronatic acid binds to bone hydroxyapatite. Bone resorption causes local acidification, releasing risedronic acid which is that taken into osteoclasts by fluid-phase endocytosis. Endocytic vesicles are acidified, releasing risedronic acid to the cytosol of osteoclasts where they induce apoptosis through inhbition of farnesyl pyrophosphate synthase. Inhibition of osteoclasts results in decreased bone resorption. Bisphosphonates are adsorbed onto hydroxyapatite crystals in bone, slowing both their rate of growth and dissolution, and therefore reducing the rate of bone turnover.
