Musculoskeletal system disorders

Osteomyelitis

Infection of the bone and bone marrow by bacteria, virus, fungus, or parasite

Pathophysiology of osteomyelitis

1. 
   Invading Pathogen: An infective agent (typically bacteria, but can also be virus, fungus, or parasite) enters the body.

2. Inflammatory Response: The pathogen provokes an inflammatory response, causing vascular engorgement and increased vascular permeability, leading to edema.

3. Leukocyte Arrival: Leukocytes arrive at the site, secreting inflammatory chemicals and phagocytosing bacteria.

4. Abscess Formation: Abscesses form, and the exudate seals the bone's canaliculi (spongy bone).

5. Exudate Extension: Inflammatory exudate extends through the metaphysis, marrow cavity, and small openings into the cortex.

6. Ischemia and fractures

Osteosarcoma

Malignant bone tumour. Develops in the metaphysis of long bones, characterised by uncontrollable formation of bone. rapid growth causes destruction of bone cortex.

Multiple myeloma

Bone marrow malignancy. Involves the neoplastic proliferation of a single clone of plasma cell. Causes osteolytic lesions that erode and reduces structural integrity

Osteoporosis

Metabolic bone disease characterised by normal bone mineralisation but reduced mass/density. Leads to decreased structural integrity of trabecular bone and thinner, more porous corticol bone

Calcitriol (activated vitamin D)

Stimulates intestinal calcium absorption, promotes urinary reabsorption of Ca2+, and promotes osteoclast activity, increasing blood calcium.

Calcitonin

Secreted by the thyroid gland when plasma Ca2+ is high. Reduces osteoclast activity and promotes osteoblast activity, promoting calcium deposition in bone.

Parathyroid hormone

Secreted by the parathyroid glands when plasma Ca2+ is low. Stimulates osteoclast activity, inhibits osteoblast activity, promotes renal calcium re-absorption, and promotes calcitriol synthesis, increasing blood calcium.

Rheumatoid arthritis

Inflammatory autoimmune disease when the synovium is infiltrated by the innate and adaptive immune system

Pathophysiology of rheumatoid arthritis

Autoantibodies (serum RF and anti-CCP) appear long before condition becomes clinical. These autoantibodies are produced by plasma cells in the synovium, and then the synovium is infiltrated by monocytes, dendritic, mast (innate), B cells, and plasma cells (adaptive)

Rheumatoid arthritis inflammation

Haemorrhage, coagulation, and fibrin deposition in joint tissues leading to pannus formation (granulation tissue). Can spread across articular cartilage, capsule, and soft tissue

Seronegative arthritis/ seronegative spondyloarthropathies

Inflammatory arthritis where blood test shows negative for rheumatoid arthritis (serum RF and anti-CCP). Tends to affect axial structures

Ankylosing spondylitis

Chronic inflammatory joint disease that stiffens and fusion of the spine and SIJ.

Pathophysiology of ankylosing spondylitis

Antigen presenting cells (APCs) typically express the HLA molecule. These APCs interact with bacterial or environmental factors, which can cause a cross reaction with self antigens found on joint tissues. This makes inflammatory cells infiltrate axial joints.

Gout

Common complex form of arthritis caused by defects in

uric acid metabolism and characterised by inflammation

and pain of joints

Pathophysiology of gout

uric acid is a breakdown product of purine nucleotides (dietary). Can be caused by increased rate of purine production, increased rate of breakdown of purine nucleotides, and decreased renal excretion

Tophi

In gout, collection/deposition of crystals under the skin. Appears in cartilage, synovial membranes, tendons, soft tissue

Osteoarthritis

Degenerative joint disease characterised by incremental cartilage damage with inflammatory features

Pathophysiology of osteoarthritis

Interplay of risk factors, mechanical stress, and abnormal joint mechanics. Can lead to pro-inflammatory markers and proteases.

1. Collagen matrix is damaged

2. Chondrocytes proliferate and form ‘clusters’

3. Hypertrophic chondrocytes cause outgrows that ossify and becomes osteophytes.

4. As collagen matrix becomes more damaged, chondrocytes undergo apoptosis

5. Improperly mineralised chondrocytes causes sclerotic bone.

Chondrocytes

Cells found in cartilage. Produces and maintains the tissues extracellular matrix composed of collagen and proteoglycans

Sprain

Ligament (bone to bone) injury, can cause avulsion fracture. Tearing of dense collagen

Strain

Muscle (movement via tendons) or tendon (skeletal muscle to bone) overstretch or tearing of collagen.

Dislocation

temporary displacement of one of more bones in a joint where opposing bone surfaces lose contact

entirely

Subluxation

contact is only partially lost, often moves back ‘into place’

Compartment syndrome

Oedeme within one area of the compartment of a limb that is between layers of dense connective tissue (fascia). Ischemia or infarction of tissue can occur due to compression of arterial blood supply.

Muscle ischemia and damage releases myoglobin, acid and potassium into the blood, causing renal failure, circulatory dysfunction like shock and cardiac arrhythmia

Pannus

Thickened layer of synovial tissue in rheumatoid arthritis