Bone Pathology Flashcards
What are the different ways to classify fractures?
- by orientation of fracture line
- open vs closed
- comminuted (more than two pieces)
- stress (repeated low force injury to a normal bone)
- pathological (abnormal bone)
What are the 3 stages of fracture healing?
- Inflammatory phase
- bleeding and haematoma formation
- vascular granulation tissue - Reparative phase
- soft callus
- hard callus (made of new woven bone) - Remodelling phase
Describe the inflammatory phase of fracture healing
Haematoma formation
- fibrin mesh creates a framework and the damaged matrix releases trapped growth factors and cytokines
- stem cells are activated to start repair
- granulation tissue formed
- hours to days
Describe the first part of the reparative phase of fracture healing
Soft callus
- cartilage formation (holds the fractured ends together but no structural rigidity)
- periosteum repairs itself on the outside
- days to weeks
Describe the second part of the reparative phase of fracture healing
Hard callus
- osteoid formation and ossification
- a thickened area of woven bone (rigid, but not as strong as it was)
- weeks to months
Describe the remodelling phase of fracture healing
Woven bone –> lamellar bone, along lines of stress
- result is complete reconstitution
- takes months to years
What is the clinical management of a fracture?
Goal = union How? - minimise the gap - minimise the strain or movement - minimise any other factors that slow healing
What are some complications of fracture healing?
- non-union
- delayed union
- mal-union
- infection
- osteonecrosis/AVN
What is osteoporosis?
Reduction in bone mass more than 2.5 SD below the norm for healthy 30yr old women
- loss of both cells and matrix
- loss of trabeculae and thinning of what remains
In women rapid decline in bone density following menopause
What is osteopaenia?
Reduction in bone mass 1-2.5 SD below the norm for healthy 30yr old women
What are the different classifications of osteomyelitis?
- haematogenous
- non-haematogenous (direct inoculation)
- non-haematogenous (local invasion)
Describe the pathogenesis of haematogenous osteomyelitis
- slow flow through looped capillaries and venous sinusoids
- bacteria seed metaphyseal-epiphyseal junction
- protected from the immune response
- pressure from pus further limits blood supply
- infection spreads to subperiosteal space, lifts the periosteum and invades the shaft
- growth plate is a barrier to the infection
What are the most common microbiological causes of bone and joint infections?
Staphlococcus aureus (95% and more) - then streptococcus pyogenes
What are the clinical features of bone and joint infections?
Fever, pain and tenderness, warmth, swelling
- history preceding trauma 1/3 cases
What are some differential diagnoses for bone and joint infections?
- septic arthritis (often coexistent)
- malignancy
- cellulitis
What is the common treatment of bone and joint infections?
Flucloxacillin given IV for 3-5 days, then complete a 3 week course with oral antibiotics, provided uncomplicated and demonstrated response to Rx
What are the signs and symptoms of osteoarthritis?
- joint pain, worse at the end of the day
- insidious onset with no systemic symptoms
- reduced ROM, crepitus, osteophytes
What are the risk factors for osteoarthritis?
- age
- obesity
- previous injury/abnormality of joint
- repeated heavy use of joint
- genetics
What is the pathophysiology of osteoarthritis?
- damage stimulates chondrocyte hypertrophy, proliferation and enzyme/cytokine secretion
- unravelling of cartilage matrix
- thickening and microfractures in bone
- shedding of cartilage “fibrillation”, erosions
What is the morphology of osteoarthritis?
- non-uniform loss of cartilage
- subchondral thickening
- osteophytes
What are osteophytes?
- cartilage growths that have become bone
- increases the joint stability
What are the signs and symptoms of rheumatoid arthritis?
- systemic symptoms (fever, weight loss, anaemia)
- symmetric polyarthritis
- morning stiffness
- warm, swollen “rubbery” joints
- rheumatoid nodules
- eventual destruction and deformity of joints
What are the risk factors for rheumatoid arthritis?
- genetic
- female gender
- increased age
- smoking
What is the pathophysiology of rheumatoid arthritis?
- self-reactive T-helper cells are activated
- secrete cytokines (IL-1,6,17, TNF-alpha)
- induce fibroblasts, macrophages, osteoclasts, B cells, T cells, plasma cells
- “granulation tissue” like synovium, collagenases and MMPs, breakdown of cartilage and bone
