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Osteoarthritis (OA) Or

Degenerative Joint Disease


DEFINATION
Osteo : Related to bone system
Arthritis : Arthro + itis
↓ ↓
Joint Inflammation
Condition in which one/ more joints are inflamed

So OA is a condition in which one or more joints are inflamed


involving the loss of cartilage
It is progressive disorder of joints which is caused by gradual loss
of cartilage
resulting in development of bony spurs and crysts at the margins
of the joints.

In addition to damage and loss of articular cartilage, there is


remodelling of subarticular bone, osteophyte formation,
ligamentous laxity, weakening of periarticular muscles, and, in
some cases, synovial inflammation

These changes may occur as a result of an imbalance in the


equilibrium between the breakdown and repair of joint tissue
The most common joints involved

• Distal Interphalangeal joints


• Proximal Interphalangeal joints
• Carpometacarpal joints of thumb
• Weight Bearing joints (Hip, knee)
• Metatarsophalangeal joints of the foot
• Cervicle and lumbar vartebrae
The articular cartilage is
slippery tissue that covers the
end of the bones in the joints

Healthy cartilage
allows bones to glid over
each other
&
helps to absorb shock of
movement
In OA the top layer of cartilage
breaks down and wear away

Rubbing of bones under the cartilage

Due to which there is
Pain
Swelling
Loss of motion of
joints

Over the time joint may lose its
normal shape and also there is
growth of bony spurs on the edge of
the joint

Bits of bones/cartilage can break off
and float inside the joint space

Which cause more pain and damage
So in OA there is progressive distruction of articular cartilage and
also there is involvement of
• Diarthrodial joint
• Synovium
• Capsule
• Subchondral bone
• Surrounding ligaments
• Muscles

Changes in structure and function of this tissues leads to clinical


Osteoarthritis
Which is characterized by
• Joint pain
• Tenderness
• Decrease range of motion
• Weakness
• Joint instability
• Disability
Classification
↙ ↘
Primary OA Secondary OA
(idiopathic) (Due to some other disease)
A. Localised i) Congenital and developmental
Hands disorders, bone dysplasias
Hip
Knee ii) Post-surgery / injury – meniscectomy
Spine
B. Generalised iii) Endocrine –acromegaly,
Small joints
Large joints iv) Metabolic –hemachromatosis,
Mixed ochronosis, Marfan syndrome, Ehler-Danlos
C. Erosive osteoarthritis syndrome, Paget disease, gout, pseudogout,
Wilson’s disease, Hurler disease, Gaucher
disease

v) Rheumatologic– rheumatoid arthritis

vi) Neurological– Charcot joints.


Epidemiology
OA is one of the core reason for disability
Nearly everyone who lives long is affected by OA at any point of
life, most probably after the age of 55 to 60.

Approximately 15% of population is affected by OA


↙ ↘
↙ ↘
50 % of those 85% of those
over 65 age over 75 age

OA is most widely assessed in studies using the Kellgren


and Lawrence (K&L) score.

The overall grades of severity are determined from 0 to 4


and are related to the presumed sequential appearance of
osteophytes, joint space loss, sclerosis and cysts
The World Health Organization (WHO) adopted these criteria as
the standard for epidemiological studies on OA

Prevalence of osteoarthritis varies with


I. Age
II. Gender
III. Genetics
IV. Ethic Group
V. Specific Joint Involved
VI. Method For Diagnosis
AGE
With increasing age the prevalence OA also increases

Generally for person age 25 – 75,prevalence is estimated


12%
and for those with age over 70, it is 60 – 70% affectet

Hip OA ← ← AGE → → Hand OA


↙ ↘ ↓ ↙ ↘
Age : 30 – 40 Age : >70 Knee OA Age : 40 Age : 80
Pre : 1.6 % Pre : 14% ↙ ↘ Pre: 5% Pre :
65%
Age : >25 Age : 55
Pre : 5% Pre : 12%
Gender
↙ ↘
Age > 50 Age >60
Men are more affacted Women are more
affacted(26%)
Due to higher rate of sports and Due to repeated use of
Injuries weight bearing joints

Genetics
↙ ↘
Pre : 9% Pre : 4%
White population Black & Asian population

Prevalence of OA is 22% to 39% in India


Etiology
The etiology of OA is multifactorial

Many patients have more than one risk factor for developing the
OA.

The most common risk factor for the development of OA includes


• Obesity
• Occupation
• Participation in certain sports (Often)
• History of joint trauma
• Genetic
• Age
• Sex
• Bone density
• Joint location
Obesity
Increased body weight is strongly associated with hip, knee, and
hand OA
Obesity often precedes OA and contributes to its development,
rather than occurring as a result of inactivity from joint pain

In a three-decade Framingham Study, the highest quintile of body


mass was associated with a higher relative risk of knee OA
(relative risk of 1.5 to 1.9 for men and 2.1 to 3.2 for women).

The risk of developing OA increases by about 10% with each


additional kilogram of weight, and in obese persons without OA,
weight loss of even 5 kg decreases the risk of future knee OA by
one-half.
Recent data suggest that OA is associated with the metabolic
syndrome, suggesting a possible common pathogenic mechanism
involving metabolic abnormalities and systemic Inflammation.

It is also likely that vascular disease may both initiate and hasten
disease progression in OA.

This could be due to venous occlusion, stasis or microembolic


disease leading to episodic reduction in blood flow through small
vessels within the subchondral bone.

Subchondral ischaemia may subsequently reduce nutrient


delivery and gas exchange to articular cartilage in addition to
direct deleterious effects on the bone itself.
Occupation
There is increased risk of OA for those who are in occupation
requiring
Prolong Standing
Kneeling
Squatting
Lifting/Moving Heavy Objects

→Miming
Factory Work
Car paintery
Repetitive motion also contributes to hand OA with dominant hand
usually affected

Risk OA depends on type and intensity of physical activity


Sports
Damage to articular cartilage due to sports greatly increase the
risk of OA

Meniscal damage (common in athlete) also increase the risk of


knee OA

1.Because of loss of proper load bearing and shock absorption


2.Increase focal load on cartilage and subchondral bones

Trauma
AGE AT INJURY DOSE MATTER

As older individuals who damage ligaments tends to develope OA


more rapidly than young people with similar injury

Trauma early in life →Increased risk of OA


Genetic Factors
A number of recent studies discovered the presence of over 80
gene mutations involved in the pathogenesis of OA ,among which
the most relevant one is a single nucleotide polymorphism.

This one, called rs143383 and located in the 3' untranslated region
(3'UTR) of the growth and differentiation factor 5 gene (GDF5), is
responsible for the development, maintenance and repair of
synovial joints

Genes for Vitamin D receptors (VDR) and insulin-like growth


factor 1(IGF-1) also seem to be involved in the patho-physiologic
pathways of OA

It also includes genes related to inflaamation,bone


morphogenetic protiens, protease/ its inhibitors
Pathophysiology
Normal Articular Cartilage

Articular Cartilage Possesses



Viscoelastic Properties
↓Which provides
1. Lubrication With Motion
2. Shock absorbency during rapid movement
3. Load Support

In Synovial joints Articular cartilage is found between synovial


cavity on one side and narrow layer of calcified tissue overlying
subchondral bone on onther side
Charactristics of Articular Cartilage

1.Cartilage is easily compressed lossing up to 40% of its original


hight when load is applied

Compression increase area of contact

Disperse force more evenly to undelying bone,tendon, ligament,
muscles

2.Cartilage is frictionless

Togather with compresibility , this enables smooth movement in


joint and distributes load across joint tissue to prevent damage and
stabilize the joint
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