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39 Cards in this Set

  • Front
  • Back
Functions of Bone
Framework for muscle movement
Protect internal organs and marrow
Adapt to changing physical stress
Reservoir for Calcium and Phosphate (also contains magnesium and sodium)
Mechanical Strength of Bone due to
light weight
High tensile strength
Rigid but not brittle (slightly deformable)
Accomplished by mineralization of collagen matrix
Increase in tissue mass
Trophic Growth
= nourishment - size of cells
Plastic Growth
to form - number of cells (mitotic)
Differentiation growth
acquisition of distinct characters (phenotype)
Sequential Differential Gene Expression in Growth Processes
Sequential Differential Gene Expression in Growth Processes
Progenitor (committed to a particular line of differentiation)
Clonal Expansion (mitotic increase in differentiated cell number)
Directive Hormone Actions
-Directive action elicits a specific physiological response
-Transduction activates or inhibits a particular pathway that controls the response
Permissive Hormone Actions
Permissive action makes a target tissue responsive to a different hormone

Does not elicit a specific physiological response by itself

Controls synthesis of receptors or response elements in target
Growth Hormone (GH or STH)
stimulates hepatic Insulin-like Growth Factors (IGF) and has a direct influence on substrate mobilization (permissive)
Insulin-like Growth Factors (IGF)
directive to bone growth
metabolic substrates for growth (permissive)
Fibroblast Growth Factor (FGF)
fibroblasts collagen deposition, extracellular matrix
Platelet-derived Growth Factor (PDGF) -
vascular smooth muscle proliferation
Promote osteoblast differentiation
Prostaglandin E2
– Local regulation, inhibition of osteoclasts, response to mechanical force
Cortical (compact) bone
dense outer layer provides tensile strength
Trabecular (cancellous) bone
arbors of bone provide strength against compression and lower bone density (weight)
Metabolic responses (calcium balance)
occur mainly on the trabecular bone surfaces and inner (endosteal) surface of the cortical bone
Membranous bone formation(skull, long bone periosteum)
– mesenchymal cells differentiate into osteoblasts around cartilage “prototype”
Endochondral bone (long bone shaft)
epiphyseal cartilage growth plates form mineralized extracellular matrix followed by surface osteoblast deposition of new bone (primary spongiosa) and replacement of deep spicules (secondary spongiosa)
Dynamics of Bone Metabolism
Bone is constantly undergoing remodeling

Local structural modifications respond to mechanical force

Systemic endocrine regulation of osteoblasts and osteoclasts maintains serum calcium concentration
bone forming cells, deposit calcium and phosphate as hydroxyapetite on collagen and osteocalcin matrix
bone “breaking” cells, dissolve hydroxyapetite with lysosomal enzymes to release calcium and phosphate
Mature bone cell trapped within the bone matrix
Phagocytic cells that assist in matrix digestion and local hormone production
To Raise plasma [Ca2+]
Increase absorption by GI tract

Increase net movement out of bone

Increase renal reabsorption of Ca2+

Decrease renal reabsorption of PO43-
To Lower plasma [Ca2+]
Increase net movement into bone

Increase transport out of body
1,25 Dihydroxycholecalciferol Vitamin D3
Nuclear-acting steroid hormone
Promotes Ca2+ mobilization to serum
Synthesis stimulated by PTH (low Ca2+)
Stimulates intestinal and renal Calcium Binding Protein synthesis (CBP)
Promotes bone growth (osteoblasts)
Promotes clastogenesis (osteoclasts)
Inhibits parathyroid PTH (neg. feedback)
Parathyroid Hormone PTH
Preprohormone (protein) produced by Parathyroid Chief Cells
115 aa  90 aa  84 aa PTH
aa1-34 active + aa35-84 inactive
Direct response to low Ca2+ (inhibition lost)
Short Half-life T1/2 = 3-4 minutes

****Raises serum Ca2+ by indirect stimulation of osteoclasts via induction of IL-6 secretion from osteoblasts
Calcitonin CT
Prohormone (protein) produced by Thyroid Parafollicular C-cells (Clear cells)
Variable sequences yield 32aa CT
Direct response to high Ca2+ via cAMP
****Inhibit bone demineralization by osteoclasts
Lowers serum Ca2+
CT Transduction
CT Receptor is homologous to PTH receptor
Uses opposite G-proteins (Gs or Gi)
Counter-regulation of same pathways controlled by PTH
Indicators of Bone Activity
Serum Alkaline Phosphatase originates from bone (osteoblasts) and liver (isoform)
Serum osteocalcin (osteoblasts)
Urinary hydroxyproline from collagen turnover (60% of body collagen is in bone)
Osteomalacia (Ricketts in children
autosomal recessive, 1 alpha hydroxylase deficiency yields low Vit D3 or defective Vit D3receptor, bone not mineralized
X-linked (children) autoimmune (adult), no PTH, Vit D3 deficiency, hypocalcemia
PTH receptor defect, hypocalcemia
unknown cause, adult, hyperplasia, excess PTH, periosteal demineralization, hyperalcemia
Paget’s Disease
autosomal dominant, excessive osteoclast differentiation, bone demineralization, hypercalcemia
post-menopausal, decrease in PTH, VitD3, and sex steroids, loss of E2 -and DHT-mediated osteoblast apoptosis suppression and osteoclast apoptosis promotion, trabecular demineralization in cancellous bone, extranuclear transduction pathway