2. Outlines
• Histologic features of bone
• Bone injury and Repair
• Conditions of bone
mineralization, bone mineral
density and bone viability
3. A. types Of bOne
1.Lamellar:
Collagen fibers parallel and osteocyte between
them
•Cortical (compact bone)
-Constitutes 80% of the skeleton
-consist of tightly packed osteon or haversian
system.
-Interstitial lamellae( between osteons)
-Characterrized by slow turnover ,higher youngs
modulus of elasticity ,more stiffness
-like femoral shaft
4. • Cancellous bone (spongy or
trabecular)(honey comb app)
• less dense and more remodelling
according to lines of stress (Wolffs
law)
• Characterized by high turnover rate
, smaller yaoungs modulus and
more elacsticity
• like distal femoral metaphysis
5. 2.Woven
-immature
which is non stress oriented ,like
embryonic skeleton and fracture callus
-pathologic
Rondom organization ,increased
turnover
,weak and flexible
Like fibrous dysplasia , Osteogenic
6.
7. b.CellulAr biOlOgy
1.Osteoblast :
-Derived from undifferentiated mesenchymal
stem cells (more ER ,golgi apparatus and
Mitiochondia )
-Osteoblast differentiation in vivo effected by
Interleukin ,PDGF and IDGF
9. Osteoblast produce the
following
• ALP ase
• Osteocalcin
• Type 1 collagen
• Bone sialoprotein
• Receptor activator of nuclear factor B
ligand RANK
10. • Osteoblast activity stimulated by
intermittent (pulsatile) exposure to
parathyroid hormone
• Inhibited by TNF- alpha
11. • Certain antiseptics toxic to cultured
osteoblasts
1.Hydrogen peroxide
2.Povidone-iodine(betadine)
3.Bacitracin ( believed to be less toxic)
12. 2.Osteocyte
• Maintain bone
• Constitute 90% of the cells in the mature
skeleton
• Less active in matrix production than are
osteoblast
• Important in control of EC Ca and Ph conc.
• Participate in bone resorption (osteocytic
osteolysis)
• Directly stimulated by Calcitonin
• Inhibited by PTH
13. 3.Osteoclast
• Reasorb bone
• Acts normally and pathologically
• Derived from hematopoietic cells in
macrophage linage
• Possess ruffled border
• Have receptor for calcitonin which
inhibit osteoclastic resorption
14. • IL-1 potent of osteoclast diff.and bone
resorption
• IL-10 suppresses osteoclast
• Biphosphonates : inhibit osteoclastic
bone resorption , which has 2 subtype
1.Nitrogen conatianing
2.Absence nitrogen
15. 4.Osteoprogenitor Cells
• Originate from mesenchymal stem cells
• Become osteoblasts under conditions of
low strain and increased oxygen
tension
• Become cartillage under conditions of
intermediate strain and low O2 tension
• Become fibrous tissue under high strain
17. C.MAtriX
1.Organic (40% of dry wt of bone)
A.Collagen:
90% of organic componenet
primarily type 1 (Bone)
B.Protoglycans
18. C.matrix protein
(noncollagenous)
-osteocalcin most abundant
- inhibited by PTH
-stimulated by1,25 dihydroxyvit D3
- can be measured in serum and urine
as marker of bone turnover
D.Growth factor and cytokines
like BMP
21. e.bOne CirCulAtiOn
• Anatomy
-5%-10% of cardiac output
- sources for long bones
a.nutreint artry system
b.Metaphyseal-epiphyseal system
c.periosteal system
22.
23.
24. 2.physiology
-direction of flow
-fluid compartment of bone
65% extravascular
6% haversian
6% lacunar
3% RBC
20% others
-Physiologic states
hypoxia,hypercapnia and sympathectomy
25. • 3.fracture Healing
-Blood flow
-Nutrient
-Decrease blood flow
-Increase blood flow
4.Regulation of bone
blood flow
29. Appositional ossification
– Osteoblasts align on the existing bone
surface and lay down new bone
– Periosteal bone enlargement
– Bone formation phase of bone remodeling
30. Bone injury and repair
–Fracture repair
1.A continum from inflammation to repair
2.Blood supply
3.Stages of fracture repair
-inflammation
-Repair
-Remodelling
34. 7.head injury
8.Nicotine (smoking)
9.NSAIDs
10.Quinolone Antibiotics
11.Ultrasonography and fracture healing
12.Effect of radiation on bone
13.Diet and fracture healing
14.Electricity and fracture healing
15.Pathalogic fracture
36. Normal Bone metabolism
1.Calcium
-Imp in Muscle, nerve and clotting
-99% in bone
-1% in plasma in free and bound
-400mg released from bone daily
-Absorbed in duodenum actively and
passively in jejunum
-Kidney reabsorb 98% in proximal tubule
37. – Primary homeostatic regulator of serum Ca
are PTH and 1,25(OH)2-vit D3.
-Dietary requirement of Ca
-600mg/day for children
-1300 mg/day for adolescent and young
adults(10-25 yrs)
-750 mg/day for adults( 25-65 yrs)
-1500 mg/day for pregnant
- 2000 mg/day for lactating women
- 1500 mg/day post menopausal women and for
patient with a healing fracture in along bone
38. • Calcium balance is +ve in the 1st
three
decades of life and –ve after the fourth
decade.
39. 2.Phosphate
• 85% of body phosphate in the bone
• Plasma phosphate mostly unbound
• Imp in enzyme and molecular interaction
• Dietary intake usually adequate
daily req. 1000-1500mg
40. 3.PTH
• PTH is 84-amino acid peptide
• Synthesized and secreted in chief cells
of four parathyroid gland
• PTH regulate plasma calcium
Decreased Ca level in the ECF stimulate
B2 receptors to release PTH which acts
at the intestines, kidney and bones
43. 5.Calcitonin
32-amino acid peptide hormone
Produced by parafollicles of the thyroid gland
Has limited role in calcium regulation
Increase ECF Ca level cause secretion of
calcitonin
Controlled by B2 rec.
Inhibit osteoclastic bone resorption
1.Osteoclasts have Calcitonin rec
2.Calcitonin decrease osteoclast No. and activity
3.Decrease Ca serum level
44. 6.Other hormones affecting metabolism
A.Estrogen
Inhibit bone loss by inhibiting bone resorption
Decrease in urinary pyridinoline cross links
Because bone formation and resorption is a
couple mechanism that is why estrogen also
decrease bone formation
Supplemantaion
45. B.Corticosteroid
Increase bone loss
Decrease gut absorption of Ca by decreasing
binding protein
Decrease bone formation (cancellous more
than cortical) by inhibiting collagen synthesis
and osteoblast productivity
Do not affect mineralization
Alternate day therapy may reduce effects
46. C. Thyroid hormone
Affect bone resorption more than
formation
Thyroxin can lead to osteoporosis
Regulate skeletal growth at physis ,
stimulate chondrocyte growth , type X
collagen syn. & ALP activity
47. D. Growth Hormone
cause positive Ca balance
-increase gut absorption of calcium more
than it increases urinary excretion
insulin and somatostatin participate in
this effect
48. E. Grwoth Factor
TGF-B ,PDGF , monokines & lymphokines
Have roles in bone and cartillage repair
49. 7.Bone Aging
Peak bone mass between 16-25 yrs
After peak bone loss occurs at a rate 0.3%
to 0.5% per year
Rate of bone loss 2-3% per year in
untreated women during ten year after
menopause
Affect trabecular more than cortical bone
50. Cortical bone becomes thinner &
intracortical porosities increase
Cortical bone becomes more brittle , less
strong and less stiff.
Long bones have increased inner and
outer diameter
63. Rickets (osteomalacia in
adult)
• Is failure of mineralization , leading to
changes in the physis in the zone of
provisional calcification ( increase width
and disoreintation ) and bone ( thinning
and bowing)
68. C. Phosphate –deficiency
rickets• May be due to renal tubular disease
• Ca serum level normal
• There is no any sign of
hyperparathyroidism
69. 2.Heriditory Vit –D dependent
rickets
Less common and same like nutritional and
more severe , may have total baldness
1.Type 1: 25(OH)-vit D 1 alpha hydroxylase
2.Type 2:defect in intracellular 1,25(OH) vit
D3
70. 3.Familial Hypophosphatemic
rickets
• Most common type encountered
• X-linked dominant
• Imp. Renal tubular ph reabsorption
• Normal GFR with an impaired vit D3
response
• Treatment
-phosphate replacement (1-3 g daily)
- high dose vit D3
71. Hypophosphatasia
• Autosomal reciessive
• Error in isoenzyme of ALK
• Similar to rickets
• Increased urinary phosphoethanolamine
diagnostic
• Treatment may include phosphate
72.
73. Conditions of bone mineral
density
Bone mass is regulated by relative rates of
deposition and withdrawal
74.
75. 1.osteoporosis
• Age related decrease in bone mass
• Is quantitative not qualitative defect
• WHO (L2-L4) density is 2.5 or more
standard deviations less than mean peak
bone mass of healthy 25 yrs old (T-score)
• Osteopenia: 1.0 – 2.5 deviatioans
76. • Responsible for more than 1 million
fracture/year
- vertebral # more common
-after initial vertebral # the risk for second
vert. # 20%
• vertebral compression # associated with
increase mortality rate
• More higher incidence in Men than women
• Life time risk of # in white women after 50
yrs of age 75%
• Risk of hip # 15% - 20%
77. Risk factorWhite, female gender, northern European
Sedentary life
Thinner
Smoking
Heavy drinking
Phenytoin
Diet low in Ca and Vit. D
History of breast feeding
Positive family history
Premature menopause
79. Types of Osteoporosis
1. Type 1 :
Primarily affect trabecular bone
Vertebral and distal radius more common
2.Type 2:
In pt more than 75 yrs old
Affect both trabecular and cortical
Relared to poor Ca absorption
Hip and pelvic # more common
80. Diagnosis
• Obtained to role out secondary causes of
low bone mass like hyperthyroidism, vit D
def. , HPTH, cushing syndrome,
haematologis disorder, malignancy
• CBC , serum Ca, Vit D , ALK, creatinine
and total albumin leverl . Results of these
studies usually unremarkable in
osteoporosis
• Plain radiograph not helpful unless bone
loss exceeds 30%
81. Special study
1.Single photon ( appendicular) absorptiometry
2.Double photon (axial) absorptiometry
3.Quantitative computed tomography (CT)
4.Dual-energey X-ray absorptiometry
(DEXA)
85. 2. Idiopathic transient
osteoporosis of the hip
• Uncommon
• Most common during 3rd
trimester
• Groin pain, limited ROM, localized
osteopenia without history of trauma
86. • Self limiting and tend to resolve spontaneously
after 6 – 8 months
• Traetmant : analgesia and limiting wt bearing
• Stress # may occure
87. 3.Osteomalacia
• Qualitative defect
defect of mineralization result in large
amount of unmineralized osteoid
• Causes :
- vit D def.
-GIT dis
-Renal dystrophy
-Drugs
-Alcoholism
94. Histologic feature
• Primary trabeculae replaced with
granulation tissue
• Areas of haemorrhage
• Widening of the zone of provisional
calcification in the physis
97. Lead poisoning
• Result in short stature and reduced bone
density
• Lead alters chondrocyte response to PTH
related protein and to TGF-B
98. 4.Increased Osteodensity
A. Osteopetrosis (marable bone disease)
-due to decrease osteoclast function
- may be due to immune sys
- abnormal osteoclast
- one of them infantile autosommal
recessive dis (malignant)
- Another one AD (tarda) benign (albers –
schonberg dis), typical rugger jersy spine
99.
100. B. Osteopoikilosis
• Spotted bone disease
• Islands of deep cortical bone appear
within the medullary cavity and the
cancellous of the long bone
• Especially in the hands and feet
• No malignancy incidence
101. 5.Pagets disease
-virus inclusion like bodies in osteoclast
-both decrease and oncrease osteodensity
may be present
1.active phase:
lytic
mixed
sclerotic
2. Inactive phase
102. Conditions of viability
1.Osteonecrosis
• death of bony tissue other than infection
•Usually adjacent to a joint surface
•Caused by loss of blood supply
•Like SCFE, perths disease
106. Traetment:
1.Arthroplasty associated with increased
loosening.
2.Non traumatic necrosis of femoral condyle
and proximal humerus may improve spont.
With out surgery
3.Precise role Core decompression is still
unresolved
4.Core decompression is benefit in early hip
disease
107. Osteochondrosis
1.This condition can oocure at traction
apophysis in children
2.It may or not associated with trauma,joint
capsule inflammation, vascular insult or
secondary thrombosis
3.The pathologic process is similar to that of
Osteonecrosis in the adult.
