Osteoarthritis is caused by a loss of articular cartilage, and results from a degeneration of synovial
fluid [
Buckwalter2006]. The onset of this degeneration may be triggered by an acute injury that negatively
impacts the structural integrity of the joint, such as a sprain of the anterior cruciate ligament,
a tear of a meniscus, or patellar dislocation; in addition, repetitive microtrauma such as found in
distance runners may be the trigger. Since obesity increases load on weight-bearing joints, it may also be
a contributing factor [
ACE2009, pp 377-379];
healthy articular cartilage can tolerate impact forces approximately seven times a normal person's
body weight before damage to the articular surface occurs [
Repo1977].
The chronic pain associated with osteoarthritis arises from pain sensors in the subchondral bone
rather than from the articular cartilage itself, which has no pain sensors [ACE2009, pg 380].
Damage to the articular cartilage causes chemical synovitis, which arises when chemicals inside the
damaged articular cartilage are released into the synovial fluid and irritate the type A synovial cells in the
inner lining of the joint capsule, which in turn increase production of synovial fluid, leading to swelling
of the joint capsule over the subsequent 12 hours and further pain due to the edema
[ACE2009, pg 381].
Specific factors leading to increased risk of osteoarthritis include [ACE2009, pg 383]
weak quadriceps [Bennell2005], [Mikesky2006],
valgus or varus knee alignment, weak hip abductors, and obesity [Issa2006].
Dr. Starr has suggested a correlation between osteoarthritis and
type-II hypothyroidism.