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DEFINITION- joint failure, a disease in which all structures of the joint have undergone
pathologic change, often in concert. The pathologic sine qua non of disease is HYALINE
ARTICULAR CARTILAGE LOSS present in a focal and, initially, nonuniform manner. This is
accompanied by increasing thickness and sclerosis of the subchondral bony plate, by outgrowth
of osteophytes at the joint margin, by stretching of the articular capsule, by mild synovitis in
many affected joints, and by weakness of muscles bridging the joint. In knees, meniscal
degeneration is part of the disease. There are numerous pathways that lead to joint failure, but the
initial step is often joint injury in the setting of a failure of protective mechanisms.
-the most common type of arthritis. Its high prevalence, especially in elderly, and the high rate of
disability related to disease make it a leading cause of disability in the elderly.
-OA affects certain joints, yet spares others. Commonly affected joints include the cervical and
lumbosacral spine hip, knee and first metatarsal phalangeal joint (MTP).
- In the hands, the DISTAL and PROXIMAL INTERPHALANGAL JOINTS and the BASE of
the THUMB are often affected.
PATHOGENESIS:
The lesions of OA stem from degeberation of the articuolar cartilage and its disordered repair.
The articular cartilage contributes to the virtually frictionless movement of the joint while
providing resistance to tension and compression, from type II collagen and proteoglycans,
respectively both synthesized by chondrocytes.
The chondrocytes can be divided into 3 phases:
1. Chondrocyte injury, reated to genetic and biochemical factors
2. Early OA, in which chondrocytes proliferate and secret inflammatory mediators,
collagens, proteoglycans, and proteases, which act together to remodel the cartilaginous
matrix and initiate secondary inflammatory changes in the synoviu and subchondral bone
3. Late OA, in which repetitive injury and chronic inflammation lead to chondrocyte drop
out, marked loss of cartilage, and exyensive subchonral bone changes.
CLINICAL FEATURES:
Joint pain from OA is activity-related. Pain comes on either during or just after joint use and then
gradually resolves.
***early in disease, pain is episodic, triggered often by a day or two of overactive use of a
diseased joint. As disease progresses, the pain becomes continuous and even begins to be
bothersome at night. Stiffness of the affected joint may be prominent, but morning stiffness is
usu. Brief (<30 min).
DIAGNOSTIC TEST
Joint aspiration
X-ray
MRI
TREATMENT:
Goal: to alleviate pain and minimize loss of physical function.
NONPHARMACOTHERAPY:
Avoiding activities that overload the joint
Improving the strength and conditioning of muscles that bridge the joint
Unloading the joint, either by redistributing load within the joint with a brace or a splint
EXERCISE
Correction of malalignment
Pharmacotherapy:
Acetaminophen, NSAIDs, and COX-2 Inhibitors
Intraarticular injections: glucocorticoids and hyaluronic acid
SURGERY
Tibial osteotomy
Total knee or hip replacement
Cartilage regeneration
Genisa A. Gumansing