Non Inflammatory
Pathology of Bone &Joints
By
Dr . Atif Ali
MSK system
Bone
Joints
Muscles
Soft tissues
1-Metabolic
2- Infections
3- Tumors
4Congenital
1- Bone
Pathology
The Normal
© Dr. Atif 2010
Canaleculae
Normal bone
Trabeculae
Types of bones
Compact
Lamellar
Bones
Cancellous
Woven
Bone turn over (physiology)
1-Metabolic Bone Diseases
Due to imbalance in bone turn over:-
Defect
Disease
Formation + Resoption Osteoporosis
Mineralization
Resoption
Osteomalacia &
rickets
PTH
Formation + Resorption Paget's disease
Investigations in Bone Disorders
Radiological
Biochemical
: X-ray, bone scan,….
 Calcium
 Phosphates
 PTH
 Vit D3
 Alkaline phosphatase.
Biopsy.
Others
1- Osteoporosis
Definition :
Skeletal disorder chr by ↓↓bone mass with
↑ fragility and ↑ tendency to fracture
Pathogenesis and Causes
Bone atrophy due to↓ formation and ↑ resoption
Primary:
Postmenopausal
Senile
Secondary:
Hormonal : DM, Cushing,
estrogen,..
Immobilization.
Nutritional.
Other bone pathology.
Genetic factors: Vit D
receptors,..
Pathogenesis ( 1 ry)
Estrogen
Cytokines
RANK, RANKL
Pathology
Normal bone
◙↓ bone mass ( osteopenia)
Normal mineralization.
◙Thin trabiculae and wide canaliculae.
 Collapse of vertebrae ( code fish #)Osteoporosis
◙Pathological fractures.
Clinical Features
in elderly females.
Early : asymptomatic.
Bone pain.
Pathological factures.
Diagnosis
 Radiological : osteopenia and pathological
#
 Biochemical :
 All bone profile normal.
 Routine and hormonal studies .
 Bone biopsy:
Osteomalacia and Rickets
Defective mineralization of bone matrix
resulting in excessive osteoid formation and
bone softening.
Causes
 Vit D3 deficiency.
  Diet
 Malabsorption.
 ↓ sun exposure
 Vit D3 abnormal metabolism.
 Liver , renal ( Vit D dependent rickets type I)
 Normal level Vit D3.
  PO4.
End organ resistance (type II)
Toxins
Hypophosphatesia.
Pathology
↓
bone mineralization.
 ↑Osteoid
↑
formation.
Cartilage formation.
Clinical Features
Adults
Children
 ↓ Growth
Long bone deformity
Pigeon breast
Rickets rosary
Bone pain
Proximal
muscles weakness
Pathological
fractures.
Diagnosis
Clinical
Treatment
??
Radiological.
Biochemical
Ca
PO4
Vit D3
PTH
ALP
Radiological findings
Deformity
Green stick
fracture
Wide
epiphysial
plate
1ry Hyperparathyroidism
↑↑ PTH due to primary PT gland disorder.
Causes : adenoma , adenocarinoma.
Effects ↑bone resorption , ↑Ca ,↓ PO4.
Clinically:
 Of hypercalcaemia: bone, GIT, CNS,
Kidney.
 Bone :pain and pathological fractures.
 Bone pathology:
Bone inflammation, fibrosis and cysts
formation ( Osteitis fibrosa cystica)
Brown tumor: deposition of hemosedren.
Osteoporosis.
 Diagnosis: Bone profile:Ca
PO4
Vit D3
N
PTH
ALP
N
Renal Osteodystrophy
In CRF: low Vit D3 and low Ca.
Lead to 2ry ↑PTH.
Lead to bone ↑resoption : pathological #
Paget's disease
 ↑↑ bone turnover → disorganized bone
structure , fibrosis and thickening.
 Both osteoclast and osteoblasts are active.
 Causes : unknown( viral infections?)
 Pathology:
 Fibrosis ( bone mosaic)
 Bone vasculature.
 Thickening and deformity.
 Clinically:
 Bone deformity (local or general)
 Common site : skull & pelvic
 Complications:
Pathological fracture.
Nerves compression.
Congestive heart failure.
Late : malignancy.
Diagnosis:
 Clinical
 Radiological
 biochemical
Ca
PO4
N
N
Vit D3
N
PTH
N
ALP
Question ?
Congenital Bone Diseases
A chondroplasia
Ostegenesis imperfecta
Osteopetrosis
Others
1-Osteopetrosis
 Called marble bone disease (AR)
 Due to congenital ↓ in osteoclastic activity
↓resoption  large fragile bone
Complications
 Pathological #
 BM compression  Anemia, LEP
 Nerve compression
Osteopetrosis
2- Ostognesis imperfcta
 Rare inherited disease (1/8000)
 AD
 Mutations of gene for type I collagen
– COL 1A1 gene on chromosome 17
– COL 1A2 gene on chromosome 7
 Abnormal osteoid production – osteopenia
 Clinically :pathological #, blue sclera, ....
3- A chondroplasia
 Congenital defect in cartilage formation
 Premature closure of epiphysis
 Short stature ( what ∆ ∆ ?)