- Haematoma formation – immediately after fracture occurs. Fills the fracture gap. This provides a fibrin mesh.
- Inflammation via degranulation of platelets and migration of inflammatory cells eg Neutrophils–> release of PDGF, TGF B which activate osteoprogenitor cells in periosteum and medullary cavity. –> osteoclastic and osteoblastic activity.
- Haematoma Organising by end of first week – Macrophages
- Procallus – provides anchorage between the ends but offers no structural integrity for weight bearing.
- Callus formation – subperiosteal deposition of trabecular woven bone. Maximal girth at week 2-3.
- Endochondral calcification.
- Tissue remodelling after weight bearing. Excesses are resorbed
- Inflammation of bone and marrow. Virtually always infectious.
- Haematogenous, extension from contiguous site, direct innoculation
- Long bones or vertebral bodies in healthy people.
- Staph aureus 80-90%
- Those with IVDU or genitourinary tract infections –> E Coli, Klebsiella, Pseudomonas.
- Neonates – GBS and haemophilus influenzae. Metaphysis, epiphysis or both.
- Childeren – metaphysis
- Adult – ephiphyses and subchondral regions.
- Sickle cell – Salmonella
- Direct innoculation or contiguous spread – mixed organisms.
- 50% of time no organism identified.
- Once infection localised –> inflammatory response –> cell death in 1st 48hrs–> after 1st week chronic inflamation cell infiltrate –> osteoclastic bone resorption–> ingrowth of fibrous tissue–> deposition of reactive bone in periphery (involucrum).
- Children – subperiosteal abscess may form. Lifting the periosteum further.
- Supparative and ischaemic bone injury –> segmental bone necrosis =sequestrum.
- 5-25% become chronic infection.
- Degenerative joint disease characterised by progressive erosion of articular cartilage. Ageing phenomenon. Can be secondary to joint trauma, haemochromatosis etc.
- Normal cartilage has type 2 collagen and proteoglycans.
- Causes – mechanical workload, genetics,
- Characteristics – early – more water and less proteoglycans, less t2 collagen, rise in IL1 and TNF a. Granular articular surface, softer than normal.
- Chondrocytes in deeper layer proliferate
- Subchondral bone exposed –> bone eburnation–> sclerosis of underlying bone.
- Bone cysts from leakage of synovial fluid via small fracture gaps in subchondral bone.
- Osteophyte formation.
- Clinical pic – deep achy pain worse with mobilisation, crepitus, stiffness, limit ROM, vertebral osteophytes –> neurological sx.
Rheumatoid Arthritis RA.
- Chronic systemic inflammatory disorder affecting joints, skin, blood vessels, heart and muscles
- Nonsupparative proliferative and inflammatory synovitis–> destruction of articular cartilage and ankylosis of joints.
- 1% of world affected. Women more.
- Joint synovium – oedema, thickened, and hyperplastic. Perivascular inflammatory cells, B ells, CD4, plasma cells and macrophages. Increased vascularity. Aggregation of fibrin and neutrophils in synovial fluid.
- Osteoclastic activity –> juxta-articular erosions, subchondral cysts and osteoporosis.
- Pannus formation.
- Rh nodules – ulnar aspect of forearm – firm and nontender – central fibrinoid necrosis and surrounding epitheloid histiocytes, lymphocytes and plasma cells.
- Autoimmune disease triggered by exposure of a genetically susceptible host to an unkown antigen.
- Proximal small joints, symmetrical. PIP, MCP, MTP, wrist. Stiffness. Better with activity. Deformity.
- Radiology – juxta-articular osteopenia, bone erosions, narrowing of joint space, destruction of tendons etc.
- Haematogenous, contiguous spread, direct innoculation
- Rapid joint destruction and deformity. Systemically unwell. Pain!
- Gonnococcus(late adolescence and young adults, sexually active women), staphylococcus aureus(main one in older kids and adults), streptococcus, haemophilus influenzae(children under2), GNB. Salmonella(sickle cell)
- Usually knee followed by hip, shoulder, elbow. IVDU – axial joints. Gonoccocal – multiple joints.
Gout and Pseudogout
|Urate crystal deposits in synovium and cause inflammation via C3, C5, neutrophils, macrophages, chemokines, fibroblasts,||Calcium pyrophosphate crystal|
|Negative refringent||Positive refringent|
|Chronic – tophi, joint deformity, urate nephropathy||Sporadic, hereditary (most severe) and secondary.|
|Usually all primary – unkown genetic defects affecting urate metabolism. Secondary can be due to increased cell turnover eg leukaemia, chronic renal impairment.|
|Alcohol predisposes to attacks, as does obesity, genetics, drugs eg thiazides|
- T cell response to unknown antigen
- Ankylosing spondylitis
- Axial joints esp sacroiliac, men more than women, 90% HLAB27 positive,
- Chronic synovitis, destruction of articular cartilage, bony ankylosis, inflammation of tendinoligaments –> calcification.
- Cx – fracure of spine, uveitis, aortitis, amyloidosis.
- Reactive arthritis/Reiters syn
- Episode of noninfective arthritis of appendicular skeleton within 1mo of primary infection elsewhere.
- Usually genitourinary origin or GI – chlamydia, shigella, salmonella, yersinia, campylobacter.
- Triad – arthritis, nongonnococcal urethritis or cervicitis, conjunctivitis.
- 80% HLA B27 positive.
- 50% have recurrent arthritis, tendinitis, fasciitis etc
- Psoriatic arthritis
- 10% of patients with psoraisis
- Distal IP joints of hand and feet first affected, asymmetric,
- Sausage finger from inflam of digital tendon sheaths.
- Conjunctivitis, iritis. Joint destruction les frequent, remission more frequent.
- IBD associated.
Avascular Necrosis – AVN
- All form of bone necrosis result from ischaemia.
- Mechanical vascular interruption eg fracture
- Thrombosis and embolism
- Vessel injury due to radiation etc
- Increased intraosseous pressure with vascular compression
- Venous hypertension
- Medullary infarcts. Cortex usually unaffected due to collateral supply. Usually clinically silent.
- Subchondral infarct – wedge shaped with apex at epiphysis. Causes chronic pain and secondary OA.