Bone Pathology

Bone Pathology

• The cells• Anatomy of bone• Bone growth• Types of fractures• Fracture healing• Fat emboli• Osteoporosis• Osteomalacia/Rickets• Compartment syndrome

The Cells

• Osteoblasts

• Osteoclasts

• Fibroblasts

• Chondroblasts

Anatomy of Bone

• Spongy bone

• Compact bone

Spongy Bone

• Trabeculae

• Spaces filled with red marrow

• Haematopoiesis

Compact Bone

• Osteon

• Central Haversian canal surrounded with lamellae of hard bone

• Perforating (Volkmann) canals

• Osteocytes

• Lacunae

• Canaliculi

Osteogenesis

• Intramembranous

• Endochondral

Bone Growth

• Length

• Appositional

• Remodelling

• Hormonal regulation

Types of Fractures

Fracture Healing

1 Haematoma

2 Fibrocartilaginous callous

3 Bony callous

4 Remodelling

Haematoma

• Local shock (minutes to 1/2 hour)

• Static blood at fracture site

• Bone cells lack oxygen and die

Fibrocartilaginous Callous

• 6 - 10 days• Capillaries grow into haematoma• Phagocytes clean up debris• Fibroblasts and osteoblasts migrate • Fibroblasts produce collagen• Osteoblasts form spongy bone• Chondroblasts secrete cartilage matrix• Bone is “splinted”

Bony Callous

• 3 - 10 weeks

• Osteoblasts migrate inwards and multiply to form callous of spongy bone

Remodeling

• Months

• Excess callous shrinks

• Compact bone laid down

• Final structure is a response to the mechanical stress experienced by the bone

Factors Affecting Healing

• nature of injury

• amount of bone loss

• type of bone injured

• degree of immobilization

• infection

• circulation

Fat Emboli

• may appear in lung or peripheral capillaries• Fat Embolism Syndrome

– dyspnoea– confusion– tachycardia– fever– rash– fat globules in sputum and urine

Osteoarthritis

• Wearing out of the joint

• Obesity, marathon runners, gymnasts

• Health of chondrocytes determines joint integrity

• Changes in both composition and mechanical properties of cartilage

• Cracks appear in cartilage

• Subchondral bone becomes exposed

Osteoarthritis

• Fragments of cartilage and bone become free floating “joint mice”

• Osteophytes or spurs form at joint margins

• Non specific inflammation of the synovium

Mechanical injury

Chondrocyte response

Release of Cytokines

(e.g. TNF, IL-1)

Production, releaseof protease enzymes

Destruction ofjoint structures

Development ofsurface cracks

Loss of smoothcartilage surface

Destruction of Subchondral bone

Osteophyteformation

Disc degeneration

• Disc narrowing producing low back pain and disc degeneration are related to increasing BMI.

Osteoporosis

• A gradual decrease in bone mass

• risk of fractures

• bone resorption is greater than bone formation

• bone loss involves matrix and minerals

• exercise and good nutrition may prevent or delay osteoporosis

Postmenopausal osteoporosis

• due to decrease in oestrogen levels

• oestrogen stimulates osteoblasts to form bone and inhibits osteoclasts

• fractures tend to be in vertebrae & distal radius due to loss of trabeculae

Prevention

• changes are reversed during oestrogen therapy (but what else?)

• Calcium: RDA = 1000mg/day; RDA(post-menopause) = 1200mg/day

• weight bearing exercise increases bone mass

Model for the Effects of Physical Activity on Bone

Mass

AGE

BMD(g/cm2)

“Fracture Threshold”

Increased BMD

growth

adulthoodmenopause

Osteomalacia/Rickets

• abnormal levels of minerals in bone

• due to low levels of Vit D

• caused by:– diet deficiency (Vit D or calcium) – low sun exposure– chronic renal failure– liver disease

Compartment Syndrome

Compartment Syndrome

• collagenous fascia doesn’t stretch

• haemorrhage is contained

• pressure may increase compromising blood flow and nervous function distally

• fasciotomy may be required