Metabolic Bone Disease Flashcards
Osteoporosis
Clinical disease to reduce bone mass
Osteopenia
reduced bone mass without clinical disease
Causes of osteoporosis
humans–estrogen loss at menopause
animals–protein calorie malnutrition; low calcium with normal phosphorus diets (usually experiemental in mammals); localized due to disuse
Pathogenesis of osteoporosis–post menopausal
increased resorption due to loss of protective effect of estrogen; formation is normal or decreased
Ovariectomy and osteopenia
ovariectomy induces osteopenia mostly in animals with monthly estrous cycles–so does NOT affect ovariectomized dogs and cats
Pathogenesis protein calorie malnutrition
decreased formation due to overall anti-antibolic effects of malnutrition; normal resorption
Pathogenesis localized disuse
Increased resorption and decreased formation.
Osteocytes sense mechanical use and signal osteoblasts concerning what bone mass they think is appropriately needed
Structural Changes
- *Less bone: thin, less connected and fewer trabeculae (in long appendicular bones of adults) –trabecular bone should span from epiphysis to metaphysis–increased porosity of cortices and thin cortices in advanced stages
- *Increased microcracks
- *pathologic fractures
Clinical Consequences of Osteoporosis/osteopenia
- -Pathologic fractures=force to fracture was not as high as is necessary to fracture normal bone
- -bone pain
What is Osteomalacia/Rickets
Failure of mineralization in adults=osteomalacia
Failure of mineralization of bone and growth plate in young=rickets
Causes of Osteomalacia/rickets
Vitamin D deficiency
phosphorus deficiency
xenobiotics that inhibit mineralization
Pathogenesis of osteomalacia/rickets
Inadequate calcium/ phosphorus product at the mineralization site
vitamin D metabolites needed at mineralization site or just for calcium absorption from intestine??
Inhibition of mineralization process by drugs
Structural changes with osteomalacia/rickets
accumulation of osteoid (young/adult)
retention of chondrocytes in the growth plate due to failure of mineralization
deformity due to bone softness
accumulation of microcracks secondary to reduced ability to remodel bone because unmineralized surfaces are resistant to osteoclasis
pathologic fracture
Retention of chondrocytes in growth plate (osteomalacia/rickets)
causing flaring of the metaphysis due to the thickened growth plate and failure of osteoclasts to taper the bone at the cut back zone OSTEOCLASTS CAN ONLY BIND TO AND RESORB MINERALIZED BONE MATRIX
Clinical consequences of osteomalacia/rickets
1) deformity
2) pathologic fracture
3) Bone Pain