ICL 8.8: Osteoarthritis & Cristal Induced Arthritis Flashcards
what is osteoarthritis?
the most common form of arthritis
it’s a degenerative joint disease, occurring primarily in older individuals, characterized by erosion of the articular cartilage, hypertrophy of bone at the margins (i.e., osteophytes), subchondral sclerosis, and a range of biochemical and morphologic alterations of the synovial membrane and joint capsule
it is strongly associated with aging and typically affects the knee, hip, spine, great toe, and hands
what parts of the body are more likely to be effected by osteoarthritis in african americans?
blacks more likely to have knee osteoarthritis but less likely to have hand osteoarthritis compared with whites
what part of the body is most often effected by osteoarthritis?
- knee
- hip
- hand
how does osteoarthritis increase mortality?
mortality is increased in individuals with osteoarthritis compared with the general population
higher mortality was associated with increasing age, male sex, walking disability, and self-reported comorbidities (diabetes, cancer, cardiovascular disease)
increased mortality risk appears to be primarily due to cardiovascular and gastrointestinal causes.
what components of the joints are effected by osteoarthritis?
all the components of the joint
- Bone
- Cartilage
- Synovium
- Capsule
- Meniscus
what factors effect OA?
- Age
- Joint location
- Obesity
- Genetic predisposition
- Joint malalignment
- Trauma
- Gender
what is the genetic effect on OA?
twin pair and family risk studies have indicated that the heritable component may be on the order of 50% to 65%
family, twin, and population studies have indicated differences among genetic influences that determine the site of OA (hip, spinal, knee, hand)
genetic studies have identified multiple gene variations associated with an increased risk of OA [ Collegen 2,4,5,6, Vit D , IGF-1 ETC]
how do biomechanics factors effect OA?
mechanical loading that is either below or in excess of the physiologic range causes cartilage degeneration
for this reason, abnormalities of mechanical loading are central to the development of OA
OA arises when there is an imbalance between the mechanical forces within a joint and the ability of the cartilage to withstand these forces
this arises in two situations: either normal articular cartilage is exposed to abnormal mechanical loads or the articular cartilage is fundamentally defective with biomaterial properties that are insufficient to withstand normal load bearing
what are the different types of loading modes?
- tensile loading = pulling apart
- compressive loading = squishing
- shear loading = ripping in half
what are the two types of lubrication in the joints of the body?
- boundary lubrication
2. fluid film lubrication
what is boundary lubrication?
boundary lubrication is achieved by a macromolecular monolayer attached to each articular surface
looks like a fluid pocket
these layers carry loads and are effective in reducing friction
what is a diarthrodial joint?
a joint in which the opposing bony surfaces are covered with a layer of hyaline cartilage or fibrocartilage within a joint cavity that contains synovial fluid, lined with synovial membrane and reinforced by a fibrous capsule and ligaments; and there is some degree of free movement possible
what kind of lubrication do diarthrodial joints have?
a mixed mode of lubrication occurs
the joint surface loads being sustained by fluid film pressures in areas of noncontact and by boundary lubrication in areas of contact
what are the early changes you see in cartilage in an OA patient?
- swelling of articular cartilage
- loosening of collagen framework
- chondrocytes increase proteoglycan synthesis but also release more degradative enzymes
- increased cartilage water content
what are the late changes you see in cartilage in an OA patient?
- degradative enzymes break down proteoglycan faster than it can be produced by chondrocytes, resulting in diminished proteoglycan content in cartilage
- articular cartilage thins and softens (joint space narrowing on radiographs will be seen eventually)
- fissuring and cracking of cartilage. Repair is attempted but inadequate
- underlying bone is exposed, allowing synovial fluid to be forced by the pressure of weight into the bone
what happens when the extracellular matrix of cartilage breaksdown in OA?
- loss of compressive stiffness and elasticity, resulting in greater mechanical stress on chondrocytes
- an increase in hydraulic permeability, resulting in loss of interstitial fluid during compression and increased diffusion of solutes through the matrix (including the movement of degradative enzymes and their inhibitors)
what changes in bone are seen during OA?
osteophytes
these are bony proliferations at the joint margins and in the floor of cartilage lesions—are in part responsible for the pain and restriction of joint movement in OA
osteophytes may result from penetration of blood vessels into the basal layers of degenerating cartilage or as a result of abnormal healing of stress fractures in the subchondral trabecular near the joint margins
what is subchondral bone sclerosis?
increased remodeling and hardening of subchondral bone is evident early in osteoarthritis and can sometimes be detected before loss of cartilage thickness is evident radiologically
what are bone marrow lesions a sign of?
OA
studies suggest that they contribute to the pain felt by OA patients
how do you diagnose OA?
the diagnosis of OA is a clinical one
the purpose of additional diagnostic testing in OA is primarily to exclude potentially treatable underlying conditions such as metabolic or inflammatory arthropathies
what is the clinical presentation of OA?
- pain in involved joints
- pain is worse with activity but better with rest
- morning stiffness; less than 30 minutes
- stiffness after periods of immobility = gelling
- bony joint enlargement
- joint instability
- limitation of joint mobility
- periarticular muscle atrophy
- crepitus
how do you treat OA?
no treatment available for structural damage
only symptomatic treatment available
how can you supportively treat knee OA?
- weight loss
- exercises
- adjustment in daily activity
- orthotics and brace
- cane walking aid
- psychosocial Intervention
how can you supportively treat hip OA?
- Weight loss
- Exercises
- Adjustment in daily activity
- Physical therapy
- Psychosocial
- Intervention
how can you surgically manage OA?
indications for surgery include pain that is refractory to the previously discussed interventions and significant impairment of the patient’s daily life
joint replacement surgery (joint arthroplasty) is effective in providing pain relief and restoring function in many patients with OA
hip and knee joint replacements are most common
how is obesity a risk factor for OA?
it’s a strong risk factor especially for your knees which causes mechanical loading and Inflammation
activated adipose tissue increases the synthesis of proinflammatory cytokines [ leptin, adiponectin, resistin, interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF), IL-10 are decreased]
what lab features are seen in OA?
- erythrocyte sedimentation rate (ESR) typically within normal limits
- rheumatoid factor (RF) is negative
- antinuclear antibodies (ANAs) are not present
- synovial fluid is normal; normal viscosity with good string sign, color is clear, no crystals, negative cultures
