Loco PBL 3: Osteoarthritis and Perthes Disease Flashcards
What is Perthes disease?
Where blood supply the head of the femur (epiphysis) because inadequate leading to avascular necrosis of the femoral head (usually due to insufficiency of the acetabular branch of the obturator artery)
What are the signs/symptoms of Perthes disease?
Hip/groin/knee pain, muscle wasting of upper thigh and shortening of the leg with hip stiffness
What are the four stages of Perthes disease?
> Necrosis
Fragmentation (resorption of bone)
Re-ossification (deposition of bone)
Remodelling
What is the pathophysiology of Perthes disease?
Avascular necrosis of the femoral head and over several months the blood vessels re-grow and revascularise the dead bone tissue leading to new bone growth and the moral head regrows and remodels over years
How is Perthes disease diagnosed from x-ray?
Flattened femoral head
How is Perthes disease treated?
Promote the healing process and provide good positioning for healing
What is the prognosis for Perthes disease?
Children <5 = good chance of full recovery
Children/adults >5 = less chance of full recovery without complications
What is osteoarthritis?
Degeneration of joint cartilage and the underlying bone, most common from middle age onward. It causes pain and stiffness, especially in the hip, knee, and thumb joints.
What are the signs and symptoms of osteoarthritis?
Joint pain with use, less than 30 minutes of morning stiffness, loss of function, crepitus, bony enlargements, joint deformity and muscle atrophy
What are the risk factors for osteoarthritis?
Use (obesity, exertion and labour), increasing age, being female, nutrition and previous joint damage alongside genetic factors (HMGB2)
What gene conveys an increased risk of developing osteoarthritis?
HMGB2 - this gene is expressed in the superficial zone of the cartilage and is used to support the chondrocytes and allow differentiation of osteoprogenitor cells. Therefore dysfunction of this one causes superficial zone death and a loss of progenitor cells (which can’t replace damaged tissue)
How may HMGB2 mutations lead to osteoarthritis?
This gene is expressed in the superficial zone of the cartilage and is used to support the chondrocytes and allow differentiation of osteoprogenitor cells. Therefore dysfunction of this one causes superficial zone death and a loss of progenitor cells (which can’t replace damaged tissue)
What are the two main types of cell that are found in articular cartilage synovium?
Type A (macrophage) and Type B (fibroblast)
Explain the pathophysiology of osteoarthritis
A factor leads to increased expression of degradative enzymes by chondrocytes, leading to necrosis of the cartilage and release of inflammatory mediators such as IL-1, IL-6 and TNF. The chondrocytes detect this damage and increase type II collagen production and decrease proteoglycan production leading to swelling and thickening of cartilage. Eventually the chondrocytes become ‘stressed out’ and change type II to type I collagen production leading to softer articular cartilage. Cartilage begins to crack and break off (fibrillation) into the joint space (joint mice) which are engulfed by Type A synoviocytes which attracts lymphocytes and neutrophils until eventually no articular cartilage will remain (eburnation) and the ends will rub which can cause microfractures of the subchondral bone.
Why is a second tidemark formed in osteoarthritis?
When the chondrocytes become exhausted and begin to produce type I instead of type II collagen
