School of Health & Social Care

Division of Physiotherapy

Musculoskeletal Management 1

Level 2

Osteoarthritis

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OSTEOARTHRITIS

INTRODUCTION

Osteoarthritis (OA) is a common progressive disorder of synovial joints which is characterised by

joint destruction with cartilage loss. The rate of degeneration and destruction of the cartilage
exceeds its rate of repair and replacement.

Osteoarthritis may also be referred to as degenerative joint disease or osteoarthrosis. These

terms are preferred by those who maintain that the condition exhibits few or none of the features
of inflammation and differs from inflammatory conditions such as Rheumatoid Arthritis. There is,
however, considerable clinical and pathological evidence of an inflammatory component in the
disease and many authors continue to call it osteoarthritis.

The tissues involved are articular cartilage and bone. It is not known in which of these tissues the
changes occur first. Some authorities support changes occurring in cartilage followed by changes
in bone and other authorities support the opposite, What is important to you is that you
understand the changes occurring and how these affect your patients.

Patients with OA comprise a major part of the workload of the physiotherapist and therefore the
condition warrants careful study. There are many relevant textbooks and journal articles in the
library and you are strongly advised to read around the subject from more than one source.

INCIDENCE

Osteoarthritis is considered to be the most common joint disease among white populations.
Prevalence is based on the presence of symptomatic and non symptomatic radiographic (Xray)
degenerative changes. About 30% of people with radiographic evidence of degenerative joint
changes complain of pain at those sites. In any population group of 35 years and over one or two
out of every three individuals will show radiographic evidence of O.A.

In Britain in 1974 2.3% of men and 1.3% of women in the working population had to retire
because of O.A.and as a result 4.7 million working days were lost. 5% of the 55-64 age group
are absent from work for 3 or more months because of peripheral O.A.

In the U.S.A. in 1973 O.A. was the second leading cause of permanent incapacity in people over
50 years.

O.A. of the hip affects 5% of the over 55 year population and about half will require hip surgery.
The hands are affected in 29% of people aged 59-69 years. This increases to 69% in the over 75
and over age group. Females over 55 are likely to have several joints involved.
O.A. is seen earliest in the first metatarsophalangeal joint in people over 25 years. From 35 years
on the disease begins to appear in the wrist and spine. In the 45 year old and over the distal
interphalangeal joints are likely to be involved followed by other small joints of the hand - first
carpometacarpal, metacarpophalangeal and proximal interphalangeal joints. The knees, especially
in females, are involved in later life and the hip is affected latest of all joints.

AETIOLOGY/RISK FACTORS

O.A. is usually classified as primary when there is no known underlying predisposing factor or
secondary when there is a known underlying factor.

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Although the aetiology of the condition is unknown, patients with primary O.A. share some
common characteristics.

• Gender
O.A. is less common in the under 45 age group than the over 45 age group but is likely to affect
males slightly more so than females. Between 45 and 55 the sexes are affected equally. In the
over 55 years females are affected more so than males. The ratio of female to male is 2:1.

• Race
There is a striking uniformity in the geographic prevalence of O.A. However O.A. is less prevalent
in the hip amongst Chinese and there is a low prevalence of involvement in the first
metatarsophalangeal joint of black South Africans.

• Heredity
A pattern of heredity for Heberden's nodes (bony enlargement of the distal interphalangeal
joints) has been noted.

Some known predisposing factors resulting in secondary O.A. are listed below:

• Trauma - acute, chronic (occupational, sports, obesity)

• Avascular necrosis
• Infection
• Systemic metabolic disease
• Endocrine disorders
• Neuropathic disorders

PATHOPHYSIOLOGY

Changes in Articular Cartilage

In synovial joints, articular cartilage serves as a wear-resistant, smooth, nearly frictionless, load-
bearing surface. These characteristics are due to the mechanical behaviour of normal articular
cartilage which is as a result of the structure of the extracellular matrix and is composed of
collagen, proteoglycans and water.

When the structure alters so will the mechanical behaviour and also the characteristics. Gross
changes occur to the articular cartilage when it begins to fibrillate. Fibrillation occurs when
vertical tears develop in the cartilage. For a tear to occur a tensile stress needs to be applied to
pull the structure apart. This occurs when joint articular surfaces come into contact and a load is
applied. Where the articular surfaces meet there is compression of the articular cartilage but the
cartilage immediately adjacent is pulled i.e. is subjected to a tensile stress. When the tensile
stress applied is greater than the tensile strength of the cartilage vertical tears will result. The
depth of the vertical tears increases because of cavitation between the superficial layers of
collagen bundles. This destruction of cartilage occurs in non-weightbearing areas.

High tensile stresses occur in the cartilage under compression when there are small changes in
the relative stiffness of the underlying bony bed. Fibrillations can be initiated in this instance
where there is a sudden change in stiffness in the subchondral bone. In this situation the
fibrillations which develop are horizontal. Once this occurs the cartilage is no longer able to
survive and parts flake off into the synovial cavity of the joint where, as a foriegn body, they
trigger an inflammatory response in the synovial membrane. In this situation cartilage loss occurs

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in weight-bearing areas. Cartilage continues to be lost through flaking and fibrillation and
eventually the subchondral bone is exposed.

At the same time as the mechanical changes are taking place there are also changes occurring in
the extracellular matrix and the chondrocytes.

In the early stages of O.A. there is an increase in the turnover of proteoglycans and collagen. As
the proteoglycans are hydrophilic there is an increase in the water content of the cartilage.
Because of this and disruption of the restraining collagen bundles the cartilage is slightly thicker
than normal. As fibrillation continues there is loss of proteoglycans, the cartilage becomes thinner
and mechanically is weaker than normal cartilage in both tension and compression.

Type II collagen which is characteristic of normal adult articular cartilage is replaced partially by
type I collagen usually found in skin and fibrous tissue.

Chondrocytes are responsible for producing all the constituents of the matrix. The proteoglycans
and collagen synthesised, being more typical of immature cartilage than adult cartilage, can
provide neither the strength nor stiffness required. As cartilage is avascular chondrocyte mitosis
is very limited. It only occurs in the early stages of O.A. after which there is a progressive overall
loss of cells.

Changes in Bone

Changes in periarticular bone occur at the same time as the fibrillation and flaking of the articular
cartilage. Subchondral bone underlying fibrillated cartilage becomes sclerotic (more dense) and
stiffer than normal subchondral bone. Cartilage is lost from the articular surface of the joint and
exposes the smooth, white (ivory-like) sclerotic bone which is referred to as eburnated. In areas
of eburnation there is proliferation of osteoblasts and formation of new bone which occur both on
the surfaces of existing intact trabeculae and as a result of microfractures.

Subarticular cysts are common, especially in the hip and digits, and are present only in areas
denuded of cartilage. It is thought that they are the result of transmission of inter-articular
pressure through defects in the articulating bony surface into the marrow spaces of the
subchondral bone. The cysts increase in size until the pressure within them is equal to the intra-
articular pressure. The cysts are areas of complete bone loss and are filled with gelatinous
material. Cyst formation may reflect avascular necrosis (focal pressure necrosis) secondary to
raised interosseous pressures (increased local stress).

Bone at the margins of the joint remodels.In some areas there is osteophyte formation and in
other areas bone is resorbed. This remodelling of bone is in accordance with Wolff's law - bone
remodels to resist applied stress, stress which was previously decreased and distributed by the
articular cartilage and subchondral bone. Osteophytes may protrude into a joint space or may
extend into the adjacent ligaments, tendons and periosteum. The shape of the osteophyte
usually follows the existing joint contours and the articulating surface is often covered with a
hyaline-like cartilage or fibrocartilage.

Although the main tissue changes associated with O.A. occur in cartilage and bone, as a result of
these changes other tissues are affected such as synovial membrane, joint capsule, capsular
ligaments muscle and nerve. These are considered below.

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Synovial Membrane

Flakes of cartilage circulate within the synovial fluid of the joint and when they come into contact
with the synovial membrane can provoke the inflammatory response. As a result, in the later
stages of O.A. the membrane thickens by the addition of several cell layers and becomes more
vascular. Changes in the synovial membrane are accompanied by increased production of
synovial fluid which results in effusion of the joint.

Joint Capsule

Gross thickening of the capsule may occur reflecting the chronically recurring low-grade
inflammatory response which takes place when the joint destruction is well underway.

As a result of joint effusion there will be distension of the joint capsule in some regions which will
encourage osteophyte formation where the capsule attaches to the articular bone as a result of
increased stress. In other regions there will be laxity of the capsule initially but over time
contractures will occur due to the patient being unwilling to move a painful swollen joint.

Capsular Ligaments

Because of bone remodelling, alterations to the capsule and synovial membrane the mechanics of
the joint also alter. This can result in ligament(s) on one side of the joint being stressed, leading
to further osteophyte formation, and ligament(s) on the opposite side of the joint being lax.

Lacerations and repair by scar tissue are both evident in the capsule and capsular ligaments of
joints with O.A. Currently it is unknown when these occur in relation to the bony and
cartilaginous changes.

Muscle

There is a decrease in the number and cross-sectional diameter of type II muscle fibres in
patients with O.A. This may be as a result of disuse atrophy. However in muscles of an
immobilised limb it is type I muscle fibres which are lost.

Some of the muscle weakness may be due to neurogenic reflex inhibition of the motoneuron
pool. Both inhibition and facilitation of specific motor activation patterns have been shown by
activation of periarticular receptors.

Nerve

Chemical by-products of the inflammatory response stimulate nociceptors in the inflammed and
adjacent structures i.e. capsule, ligaments,periosteum,fascia and blood vessels to produce
chemical pain. Mechanical pain is the result of stimulation of the nociceptors through joint
effusion causing distension of the capsule.

Joint proprioception becomes impaired with the development of O.A.

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CLINICAL FEATURES

In the space provided list the clinical features of O.A. During the tutorial you will describe the
pathophysiology which results in these features.