Osteoarthritis
In Global Burden of Disease (GBD) studies, OA is consistently ranked among the leading
contributors to global Years Lived with Disability (YLDs). Osteoarthritis (OA) is the most
common form of arthritis.
It is characterized by thinning and fibrillation of the cartilage with loss of joint space,
osteophyte formation, subchondral bony sclerosis, subchondral cysts and deformity. The
pathophysiology of OA involves not only cartilage degradation, but also changes in the
subchondral bone, synovium, ligaments, tendons, meniscus, muscle and nerve tissues.
Recently, OA has been relabeled as a whole organ disease because pathological
abnormalities such as periarticular muscle weakness, lax ligaments, low-grade synovitis,
meniscal degeneration and neurosensory system alteration are often present in these
patients.
It can be described pathologically, radiographically or clinically. Clinical OA is usually
defined by abnormalities on physical examination consistent with OA, such as Heberden or
Bouchard nodes in the hand, or limited and painful range of RoM on internal rotation of the
hip. Symptomatic OA is usually defined as pain, aching, or stiffness in a joint with
radiographic OA.
Epidemiology
Incidence of knee (350/100.000), hand (80/100.000), other sites (43/100.000) and hip
(19/100.000). The incidence of OA increases with age and is higher in females compared
with males. In Greece, prevalence= 13%.
One estimate of the lifetime risk of developing symptomatic knee OA was 47% in ♀
and 40% in ♂, with similar estimates for hand OA (25% ♂, 47% ♀). The risk of symptomatic
hand OA was greater in individuals with obesity than those without obesity. Similarly, the
lifetime risk of developing symptomatic hip OA has been estimated at 25%. 1
Prevalence: globally, 528 x106 people are affected by OA. This rate is destined to
increase as the population ages and obesity rates increase.
Mortality: OA-associated mortality is largely driven by cardiovascular death. Possible
explanations for the excess mortality of OA include reduced levels of physical activity among
persons with OA due to involvement of lower limb joints and presence of comorbid
conditions, as well as adverse effects of medications used to treat symptomatic OA (NSAIDs),
in addition to mortality associated with complications of joint replacement surgery.
Risk factors
Systemic risk factors
-Age: OA occurs primarily as people get older. Cartilage gets thinner with age. This
may increase the laxity of the joint, making it more vulnerable to injury and it increases
cartilage susceptibility to shear stress at the basal levels where cartilage attaches to bone.
With age, chondrocytes, which do not replicate throughout life, become senescent and
become less responsive to regulatory growth factors in the cartilage matrix environment and
the cartilage matrix itself changes in ways that make it more vulnerable to injury.
-Female sex: women after menopause
-Obesity: the relationship is stronger for women. Obese persons have more severe
pain than non-obese persons with the same level of radiographic disease and they also tend
to be more functionally limited. Increased load on the joint, decreased muscle strength and
altered biomechanics. In addition to these physical factors, obesity is characterized by a low-
grade inflammatory state, which exerts effects on the joint tissue including cartilage,
synovium and bone. Individuals with a BMI >30 were 6.8x more likely to develop knee OA
than normal-weight controls. A five-unit increase in BMI was associated with a 35%
, increased risk of knee OA. Weight loss in OA can impart clinically significant improvements in
pain and delay progression of joint structural damage, in a dose-dependent manner. The
relationship between obesity and OA is stronger for knee than hip (first cause of hip OA is
anatomical dysfunction). There is evidence that demonstrates a positive association
between increased BMI and the risk of hand OA. As hands are a non-weight bearing joints,
this association between obesity and hand OA suggests a role for metabolic or inflammatory
processes.
-Genetics: 30% of the risk of OA is thought to be genetically related, with genetic
factors being typically stronger for hand and hip OA compared with knee OA. Another
emerging area of interest in OA pathophysiology is the study of miRNA that is expressed
differently in OA cartilage compared with non-OA cartilage, that regulate chondrogenesis
and chondrocyte function.
-Nutritional deficiencies (vit. D, vit. K).
Local joint environment
-Malalignment.
-Previous joint injury (post-traumatic OA)(ACL and meniscal tears), graft surgeries to
repair the ACL or reconstitute the ACL do not decrease the risk of later knee OA, in part
because the grafts probably do not reestablish normal knee biomechanics and knees that
have undergone these partial meniscectomies are at high risk of later knee OA. The risk of
developing OA after an ACL tear is the same whether the ligament is repaired or not, this
suggests that either the mechanics of the joint are not completely restored after ACL
reconstruction or that the acute inflammation that occurs with the tear puts the OA process
in motion and it is not stopped by reconstruction of the ligament.
-Bridging muscles: in theory, a person whose muscles bridging the joint are strong
should have less risk of developing knee OA and a lower risk of progression if disease is
present. Quadriceps weakness may predispose to structural disease in the patellofemoral
joint more than it does in the tibiofemoral articulation.
-Abnormalities of joint shape: when one of the bones is misshapen, either due to a
developmental abnormality or as a result of injury, this can introduce increased levels of
focal load (stress) across the joint (ex. femoroacetabular impingement [FAI] and acetabular
dysplasia). Abnormal bone shape likely accounts for a large percentage of hip OA in the
community. The weaker relationship of obesity with hip OA than with knee OA may be
because hip OA is often caused by hip shape abnormalities and weight therefore may play a
lesser role in hip disease.
-Work: repetitive knee bending etc.
Clinical
OA is no longer considered a “degenerative” or “wear and tear” arthritis but rather involves
dynamic biomechanical, biochemical and cellular processes. OA is currently viewed as a
disease of the entire joint and therefore, the failure of the joint as an organ. Although the
lesions of OA are almost always bilateral, there is a tendency for one side to be more
symptomatic than the other.
-Pain
The pain of OA changes during the day and has been demonstrated to vary by 20% within a
given week and from week to week. Often described as poorly localized and is often referred
distally. Increasing pain and stiffness to changes in weather. It is usage-related and relieved
by rest. Pain is generally worse in the late afternoon and early evening but can also be worse
in the morning soon after waking up (but <30min). There may also be night pain in severe
OA that can interfere with sleep. In some people, the pain has a burning (neuropathic)
quality, is widespread around the joint and is associated with paresthesia.
In Global Burden of Disease (GBD) studies, OA is consistently ranked among the leading
contributors to global Years Lived with Disability (YLDs). Osteoarthritis (OA) is the most
common form of arthritis.
It is characterized by thinning and fibrillation of the cartilage with loss of joint space,
osteophyte formation, subchondral bony sclerosis, subchondral cysts and deformity. The
pathophysiology of OA involves not only cartilage degradation, but also changes in the
subchondral bone, synovium, ligaments, tendons, meniscus, muscle and nerve tissues.
Recently, OA has been relabeled as a whole organ disease because pathological
abnormalities such as periarticular muscle weakness, lax ligaments, low-grade synovitis,
meniscal degeneration and neurosensory system alteration are often present in these
patients.
It can be described pathologically, radiographically or clinically. Clinical OA is usually
defined by abnormalities on physical examination consistent with OA, such as Heberden or
Bouchard nodes in the hand, or limited and painful range of RoM on internal rotation of the
hip. Symptomatic OA is usually defined as pain, aching, or stiffness in a joint with
radiographic OA.
Epidemiology
Incidence of knee (350/100.000), hand (80/100.000), other sites (43/100.000) and hip
(19/100.000). The incidence of OA increases with age and is higher in females compared
with males. In Greece, prevalence= 13%.
One estimate of the lifetime risk of developing symptomatic knee OA was 47% in ♀
and 40% in ♂, with similar estimates for hand OA (25% ♂, 47% ♀). The risk of symptomatic
hand OA was greater in individuals with obesity than those without obesity. Similarly, the
lifetime risk of developing symptomatic hip OA has been estimated at 25%. 1
Prevalence: globally, 528 x106 people are affected by OA. This rate is destined to
increase as the population ages and obesity rates increase.
Mortality: OA-associated mortality is largely driven by cardiovascular death. Possible
explanations for the excess mortality of OA include reduced levels of physical activity among
persons with OA due to involvement of lower limb joints and presence of comorbid
conditions, as well as adverse effects of medications used to treat symptomatic OA (NSAIDs),
in addition to mortality associated with complications of joint replacement surgery.
Risk factors
Systemic risk factors
-Age: OA occurs primarily as people get older. Cartilage gets thinner with age. This
may increase the laxity of the joint, making it more vulnerable to injury and it increases
cartilage susceptibility to shear stress at the basal levels where cartilage attaches to bone.
With age, chondrocytes, which do not replicate throughout life, become senescent and
become less responsive to regulatory growth factors in the cartilage matrix environment and
the cartilage matrix itself changes in ways that make it more vulnerable to injury.
-Female sex: women after menopause
-Obesity: the relationship is stronger for women. Obese persons have more severe
pain than non-obese persons with the same level of radiographic disease and they also tend
to be more functionally limited. Increased load on the joint, decreased muscle strength and
altered biomechanics. In addition to these physical factors, obesity is characterized by a low-
grade inflammatory state, which exerts effects on the joint tissue including cartilage,
synovium and bone. Individuals with a BMI >30 were 6.8x more likely to develop knee OA
than normal-weight controls. A five-unit increase in BMI was associated with a 35%
, increased risk of knee OA. Weight loss in OA can impart clinically significant improvements in
pain and delay progression of joint structural damage, in a dose-dependent manner. The
relationship between obesity and OA is stronger for knee than hip (first cause of hip OA is
anatomical dysfunction). There is evidence that demonstrates a positive association
between increased BMI and the risk of hand OA. As hands are a non-weight bearing joints,
this association between obesity and hand OA suggests a role for metabolic or inflammatory
processes.
-Genetics: 30% of the risk of OA is thought to be genetically related, with genetic
factors being typically stronger for hand and hip OA compared with knee OA. Another
emerging area of interest in OA pathophysiology is the study of miRNA that is expressed
differently in OA cartilage compared with non-OA cartilage, that regulate chondrogenesis
and chondrocyte function.
-Nutritional deficiencies (vit. D, vit. K).
Local joint environment
-Malalignment.
-Previous joint injury (post-traumatic OA)(ACL and meniscal tears), graft surgeries to
repair the ACL or reconstitute the ACL do not decrease the risk of later knee OA, in part
because the grafts probably do not reestablish normal knee biomechanics and knees that
have undergone these partial meniscectomies are at high risk of later knee OA. The risk of
developing OA after an ACL tear is the same whether the ligament is repaired or not, this
suggests that either the mechanics of the joint are not completely restored after ACL
reconstruction or that the acute inflammation that occurs with the tear puts the OA process
in motion and it is not stopped by reconstruction of the ligament.
-Bridging muscles: in theory, a person whose muscles bridging the joint are strong
should have less risk of developing knee OA and a lower risk of progression if disease is
present. Quadriceps weakness may predispose to structural disease in the patellofemoral
joint more than it does in the tibiofemoral articulation.
-Abnormalities of joint shape: when one of the bones is misshapen, either due to a
developmental abnormality or as a result of injury, this can introduce increased levels of
focal load (stress) across the joint (ex. femoroacetabular impingement [FAI] and acetabular
dysplasia). Abnormal bone shape likely accounts for a large percentage of hip OA in the
community. The weaker relationship of obesity with hip OA than with knee OA may be
because hip OA is often caused by hip shape abnormalities and weight therefore may play a
lesser role in hip disease.
-Work: repetitive knee bending etc.
Clinical
OA is no longer considered a “degenerative” or “wear and tear” arthritis but rather involves
dynamic biomechanical, biochemical and cellular processes. OA is currently viewed as a
disease of the entire joint and therefore, the failure of the joint as an organ. Although the
lesions of OA are almost always bilateral, there is a tendency for one side to be more
symptomatic than the other.
-Pain
The pain of OA changes during the day and has been demonstrated to vary by 20% within a
given week and from week to week. Often described as poorly localized and is often referred
distally. Increasing pain and stiffness to changes in weather. It is usage-related and relieved
by rest. Pain is generally worse in the late afternoon and early evening but can also be worse
in the morning soon after waking up (but <30min). There may also be night pain in severe
OA that can interfere with sleep. In some people, the pain has a burning (neuropathic)
quality, is widespread around the joint and is associated with paresthesia.
