Synovial joints, arthritides, osteoarthritis, rheumatoid arthritis, osteoblastic & osteolytic lesions
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What is pathologic synovial disease?
- Inflammatory - Infectious - Degenerative - Traumatic - Haemorrhogic - Neoplastic => Leading to irreversible joint destruction |
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What are arthritides? Inflammation of joints due to infectious, metabolic, or constitutional causes
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⏺ Physiology/ function in abnormal states → specifically the functional changes that accompany a particular syndrome or disease
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⏺ It's about disordered function, i.e. there's function but it's abnormal
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⏺ When you wish to find/define the pathophysiology of a condition it's helpful to ask: What's not functioning well?
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⏺ Determined by the pathophysiology, i.e. disordered function
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⏺ They're the defects in systems, organs, cellular & molecules that constitute the triggers of specific diseases
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⏺ They originate & explain the clinical signs & symptoms
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⏺ When you wish to find/define the mechanism of disease, it's helpful to ask: How is the specific pathophysiology leading to occurrence of these specific signs & symptoms?
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Signs & symptoms:
- Acute form: painful, warm & swollen joint - Chronic tophaceous form: top in tendons, bursae & cartilages |
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Pathophysiology:
- Hyperuricaemia & a ↓ in urinary excretion of uric acid → both lead to deposition & crystallisation of uric acid in joints → followed by an inflammatory response with release of enzymes in joint space |
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Mechanism:
- Deposition & crystallisation occurs in previously traumatised or "cooler" joints. Neutrophil disruption leads to enzyme release & inflammatory cascade |
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Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- Yes - Hyperuricaemia leads to deposition of uric acid - Previous trauma & location favours crystallisation - Crystal deposition triggers immune response - Damage to neutrophils produces the release of enzymes which irritate joints & cause an inflammation, i.e. arthritis |
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Do the mechanism explain the clinical signs & symptoms, how?
- Yes - Inflammation causes painful, warm, swollen joints in the acute form - In chronic tophaceous form: long term deposition of uric acid crystals in avascular tissues cause tophi in tendons, bursae & cartilages |
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Signs & symptoms:
- Poly-articular joint pain, swelling & stiffness - Most commonly affecting the small joints (wrists, metacarpal-phalangeals) - Joint involvement is bilaterally symmetrical - Extra-articular manifestations are often seen |
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Pathophysiology:
- Autoimmune activation & proliferation of T-cells → leading to production of inflammatory cytokines & B-cells differentiation into plasma cells → there's an inflammatory response which is systemic & damage of cartilage tissue in joints |
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Mechanism:
- The joint damage recruits more immune cells into joint spaces - Immune cells infiltrate synovial membrane causing it to proliferate & forming new blood vessels - Swollen & blood rich synovial (pannus) invades & enzymatically destroys joint tissue - Severe RA will affect the entire body |
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Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- Yes - The autoimmune activation of T- & B- cells with consequent inflammation & cartilage damage stimulate nerve endings in subchondraln bone & synovial membrane - Inflammation of synovial leads to its enlargement with formation of palpable lumps in the affected joints - Neovascularisation & synovial enlargement cause physical narrowing of joint space & a decrease joint mobility - Neovascularisation & synovial enlargement erode cartilage & subchondral bone which may cause joint mal-alignment, subluxation or collapse |
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Does the mechanism explain the clinical signs & symptoms, how?
- Yes - Stimulation of nerve endings in subchondraln bone & synovial membrane, causes joint pain - Inflammation of synovial leads to its enlargement with formation of palpable lumps in the affected joints - Physical narrowing of joint space & ↓ in joint mobility causes joint stiffness & a ↓ in the range of movement - Cartilage & subchondraln bone erosion causes joint mal-alignment, subluxation or collapse, explaining the various types of joint deformities - The systemic inflammation explains the various extra-articular signs of the disease |
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Signs & symptoms:
- Pain in Lx & gluteal regions - ↓ in Lx spine flexion - ↓ in Lx lordosis - ↑ in Tx kyphosis - Asymmetric arthritis & enthesitis |
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Pathophysiology & mechanism:
- Autoimmunity causes inflammation of axial joints, peripheral joints & entheses |
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Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- Yes - Axial joint arthritis (sacroiliac & vertebral column) causes release of inflammatory substances that stimulate nociceptors - Inflammation leads to osteoclast activation & erosion of bone, which in turn causes osteoblast activation with new bone formation - Leads to an ↑ in spinal rigidity - In peripheral joints, the arthritis causes release of inflammatory substances that stimulate nociceptors - There's infiltration of the synovium by inflammatory cells & inflammation of the entheses (places of tendon insertions in bone) |
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Do the mechanism explain the clinical signs & symptoms, how?
- Yes - Stimulation of nociceptors causes pain in axial & peripheral joints - ↑ in spinal rigidity causes a ↓ in Lx spine flexion, ↓ in Lx lordosis & ↑ in Tx kyphosis - Late complications include spinal ankylosis & fractures - In peripheral joints, stimulation of nociceptors causes pain of lower limb joints & knees - Enthesitis causes pain in achilles tendon, plantar fascia & tibial tuberosity* |
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Signs & symptoms:
- Joint pain with loading & motion - Palpable bone hypertrophy - ↓ in ROM - Crepitus (popping/crackling sound) - Joint effusion |
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Pathophysiology & mechanism:
- Joint cartilage destruction with inflammation |
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Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- Yes - Cartilage inflammation in weight bearing joints (knee,hip) & smaller joints stimulates nociceptors - Joint cartilage loss causes wear of exposed subchondral bone, which induces defective new bone formation leading to the appearance of osteophytes & subchondral bone sclerosis leading to changes in joint architecture - During movement osteophytes & subchondral sclerosis are firmly pressed against normal joint structures - Cartilage loss brings joint bones into direct contact between themselves with reduction in joint movement & stimulation of nociceptors - Joint inflammation leads to chemical changes within the joint causing a ↓ in synovial fluid viscosity & an ↑ in joint fluid production |
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Do the mechanism explain the clinical signs & symptoms, how?
- Yes - Stimulation of joint nociceptors causes joint pain whether upon loading or during motion - Change in joint architecture consists of the appearance of palpable bone hypertrophy, i.e. Bouchard's nodes - Osteophytic & subchondral sclerosis impaction against normal joint structures causes pain & ↓ joint ROM - Joint bones into direct contact causes friction & crepitus, pain & further ↓ in ROM - ↓ in synovial fluid viscosity & an ↑ in joint production produce joint effusions |
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Signs & symptoms:
- Morning stiffness - Aching of pectoral & pelvic girdle muscle structures - Malaise - Weight loss |
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Pathophysiology & mechanism:
- Aging combined with systemic (auto) immunologic/inflammatory process targeting structures in the walls of arteries with activation of macrophages |
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Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- More challenging to connect pathophysiology & mechanism - The inflammation of arteries may lead to their obstruction potentially causing hypoxia, ischemia & necrosis of affected tissues - This include muscles in the shoulder girdle & pelvic girdle |
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Do the mechanism explain the clinical signs & symptoms, how?
- Yes but challenging - It's plausible that the arteritis & consequent hypoxia & ischemia of affected muscles together with the systemic inflammation lead to stiffness, aching, malaise & weight loss* |
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