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, release of protease enzymes Loss of smooth cartilage surface Development of surface cracks Destruction of Subchondral bone Destruction of joint structures Osteophyte formation

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 Increased BMD BMD (g/cm2) adulthood menopause growth “Fracture Threshold” AGE

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