Osteo-arthrirtits

Question 1

Define Osteo arthritis -

Answer 1

etiology of OA includes joint injury, obesity, aging, and heredity.

results from breakdown of joint cartilage and underlying bone.[5] The most common symptoms are joint pain and stiffness

Initially, symptoms may occur only following exercise, but over time they may become constant.

Other symptoms may include joint swelling, decreased range of motion, and, when the back is affected, weakness or numbness of the arms and legs.

Question 2

describe it’s pathogenesis

Answer 2

During the early stages of OA, the cartilage surface is still intact. The molecular composition and organization of the extracellular matrix is altered first

The loss of articular cartilage has been thought to be the primary change, but a combination of cellular changes and biomechanical stresses causes several secondary changes, including subchondral bone remodeling, the formation of osteophytes, the development of bone marrow lesions, change in the synovium, joint capsule, ligaments and periarticular muscles, and meniscal tears and extrusion.

Osteoarthritis result from failure of chondrocytes to maintain homeostasis between synthesis and degradation of these extracellular matrix components

Question 3

Marec is a 65 year old man who comes to your practice following referral from
his GP with osteoarthritis of the right hip and low lumbar spine.

List and explain four symptoms that Marec might present with indicating
clearly how these symptoms might have been caused.

Answer 3

1. Crepitus - When a joint’s cartilage degenerates, the joint is no longer adequately protected against friction and impacts. In addition, the loss of cartilage can alter the joint’s biomechanics and cause bones to grind against one another. These changes can result in crepitus.
2. Decreased range of motion: - with joint capsular changes (shortening and lengthening) creating limitation in hip joint range of motion (ROM) along with subsequent articular cartilage degeneration

osteophytes or spurs may develop from excessive tensile force on the hip joint capsule or from abnormal pressure on the articular cartilage.

3. Pain -central - . disinhibition of dorsal horn nociceptors results from the death of local inhibitory interneurons, which potentially are replaced by excitatory A-δ̣ fibers that “sprout” from the dorsal horn esp. after inactivity -

peripheral sensitization, -

Nociceptors are located throughout the joint in the capsule, ligaments, menisci, periosteum and subchondral bone

cellular and structural changes within the peripheral joint components may be the sources of heightened nociception within the arthritic joint

biochemical sensitization and may activate nociceptors located on the afferent nerve fibers of either primary lesions in the cartilage or subchondral bone, even though catrilage has no pain sensitivity

synovial fluid, synovium, joint capsular tissues and cartilage from OA patients with severe pain, highly expresses multiple inflammatory cytokines, and neuropeptides (13). These inflammatory cytokines may further increase biological function of pain mediators by stimulating their cognate receptors, contributing to clinically symptomatic pain perception

Under disease conditions, the innervation territories of the various nerve fibers are highly plastic. An example of such plasticity, is the innervation of normally aneural tissues such as cartilage with substance P and calcitonin-gene-related peptide (CGRP) positive nerves in patients with OA

4. Muscle weakness/joint instability - Muscle weakness often develops around a joint with OA, specifically the abductor muscles of the hip (. Infiltration with fat or other non-contractile components, )
   Most significantly, the hip abductor muscles progressively weaken in the later stages of hip OA, which may create a Trendelenberg gait pattern over time. This is due to athrogenic inhibition, where atrophy of certain muscles can occur

Question 4

List and explain two signs that you might expect on examination suggestive of
hip osteo-arthritis.

Answer 4

1. Fixed Flexion Deformity - Caused by

Wasting of quadriceps and Gluteal muscles - Muscle atrophy caused by a term known as arthrogenic muscle inhibition (AMI

the main known molecular pathways leading to muscle wasting are related to reduction of protein syntheses, increased proteolysis and impaired muscle regeneration by satellite-cells

Myostatin is recognized as a negative regulator of muscle mass growth and may promote protein degradation by stimulating the activity of ubiquitin-proteasome system

Question 5

Trauma/degenberative physiology/

Answer 5

trauma causing a microfracture or inflammation causing a slight increase in enzymatic activity may allow the formation of ”wear” particles, which could be then engulfed by resident macrophages

Initial degenerative changes in the articular cartilage lead to cartilage softening, fibrillation zone of the superficial layers, fissuring and diminished cartilage thickness, but these changes become more pronounced with time, when articular cartilage thins to total destruction, eventually leaving the underlying subchondral bone plate completely exposed. All these changes in the articular cartilage are referred to as chondropathy.