Download Osteoarthritis Osteoarthritis is the most common type of joint disease

Osteoarthritis
Osteoarthritis is the most common type of joint disease. It is a
degenerative disorder arising from the biochemical breakdown of
articular (hyaline) cartilage in the synovial joints. It is characterized by
loss of articular (the joint) cartilage as well as an abnormal growth of new
bone (bone spur). Osteoarthritis involves not only the articular cartilage
but also the entire joint organ, including the subchondral bone and
synovium. Joints can be classified in functional or structural terms.
Functional classifications, based on movement are synarthroses
(immovable), amphiarthroses (slightly moveable) and diarthroses (freely
A moveable). A structural classification categorizes joints as synovial,
fibrous and cartilaginous. Normal synovial joints allow a significant
amount of motion along their extremely smooth articular surface. These
joints are composed of an articular cartilage, subchondral bone, synovial
membrane, synovial fluid and joint capsule. The normal articular surface
of synovial joints consists of articular cartilage (composed of
chondrocytes) enclosed by an extracellular matrix that includes various
macromolecules, most importantly proteoglycans and collagen.
The cartilage enables joint function, protecting the underlying A
subchondral bone by distributing large loads, maintaining low contact
stresses, as well as reducing friction at the joint.
Synovial fluid is formed through a serum ultrafiltration process
by cells forming the synovial membrane (synoviocytes). Hyaluronic
acid (HA, known also as hyaluronate) is also produced by the synovial
cells, a glycosaminoglycan that is the major non‐cellular component
of synovial fluid. Synovial fluid brings nutrients to the avascular
articular cartilage, as well as providing the viscosity required to
1
absorb shock from slow movements, as well as the elasticity needed
to absorb shock as a result of rapid movements.
Pathophysiology
This degenerative disease affects the whole joint, any joint can be
affected. However, osteoarthritis most commonly affects the knees, hips,
hands, neck and low back. It usually affects multiple joints but it can be
isolated to one joint. It can lead to significant problems
with mobility as well as having socioeconomic and psychosocial
ramifications.
There are a number of risk factors for osteoarthritis and these
include increasing age, obesity, trauma, family history (genetics),
decreased levels of sex hormones, myalgia, repetitive use, infection,
crystal deposition, acromegaly, previous inflammatory
arthritis, heritable metabolic causes, haemoglobinopathies, neuropathic
disorders, disorders of bone, previous surgical procedures
(e.g. meniscectomy).
Pathologically in osteoarthritis, there are focal areas of damage
to load‐bearing articular cartilage, new bone formation at the
joint margins (osteophytosis), alteration in the subchondral bone
(A sclerosis), inflammation of the synovium (synovitis) and thickening
of the joint capsule. Osteoarthritis can be seen as a continuum
of the normal repair process that occurs in all joint tissues as a
result of joint trauma. In some people, however, it may be due to
severe trauma or problems with the repair process; there is continued
tissue damage with the result of symptomatic osteoarthritis.
Conventionally, osteoarthritis was believed to affect primarily
the articular cartilage of synovial joints; however, pathophysiological
2
evidence now demonstrates changes occurring in the synovial fluid,
as well as in the underlying (subchondral) bone, the overlying joint
capsule and other joint tissues.
Osteoarthritis has been classified as a non‐inflammatory arthritis,
yet increasing evidence demonstrates that inflammation occurs
as cytokines and metalloproteinases are released into the joint.
These agents are involved in the excessive matrix degradation that
characterizes cartilage degeneration in osteoarthritis.
In early osteoarthritis, swelling of the cartilage frequently
occurs, reflecting an effort by the chondrocytes to repair cartilage
damage. This may last for years or decades and is depicted by
hypertrophic repair of the articular cartilage.
As the condition develops, the levels of proteoglycans finally
drop to very low levels, causing the cartilage to soften, with a loss
of elasticity compromising joint surface integrity further.
Microscopically, flaking and fibrillations (vertical clefts) develop
along the usually smooth articular cartilage on the surface of an
osteoarthritic joint. Loss of cartilage results in loss of joint space as
time progresses.
Erosion of damaged cartilage in an osteoarthritic joint progresses
until there is exposure of underlying cartilage and the protective
cartilage continues to articulate with the opposing surface.
The damaged subchondral bone can also undergo cystic degeneration.
Osteoarthritic cysts are also referred to as subchondral
cysts, pseudocysts, or geodes. Fragmentation of these osteophytes
or of the articular cartilage itself results in the presence of intraarticular
loose bodies.
3
Signs and symptoms
The progression of osteoarthritis is typically slow, occurring over
several years or decades. The patient can become less and less
active, and more susceptible to morbidities related to decreasing
physical activity. Structural changes can often occur, with no
accompanying symptoms, but joints may appear normal.
Pain is often the first source of morbidity, described as being
deep, achy joint pain exacerbated by extensive use; there may be a
reduced range of movement and crepitus. Stiffness during rest can
develop, along with morning joint stiffness. In the beginning pain
can be relieved by rest and responds to simple analgesia. Pain may
become more evident even during rest and not respond to medications.
There may be joint swelling/synovitis, periarticular tenderness,
bony swelling and deformity, and muscle weakness/wasting
around the affected joint.
Investigations
Diagnosis is typically based on clinical examination. When disease
is advanced it can be seen on plain X‐rays. MRI may be useful to
distinguish other causes of joint pain. For swollen joints joint aspiration
may be considered.
Management
The goals of treatment include alleviation of pain and improvement
of functional status. Patients should receive a combination of
non‐pharmacological and pharmacological treatment. National
guidelines are available.
4
Osteoporosis
Osteoporosis is a chronic, progressive disease of multifactorial aetiology.
The condition is a systemic skeletal disease depicted by low bone mass
and micro‐architectural deterioration of bone tissue; this then leads to an
increase in bone fragility. It is not until a fracture occurs that the disease
becomes clinically apparent. Many people experience pain, disability and
diminished quality of life as a result of having this condition. Because
this condition is so often clinically silent before manifesting in the form
of fracture, the adverse effects of osteoporosis are in part often
overlooked and undertreated. Failing to identify those people at risk, to
educate them and to put in place preventive
measures can lead to tragic consequences.
Although it is a preventable disease, osteoporosis can result in
devastating physical, psychosocial and economic consequences.
Prevention and recognition of the secondary causes of osteoporosis
are first‐line measures to lessen the impact of the condition.
The World Health Organization’s definition of osteoporosis is
based on bone mineral density (BMD) measurements in white
women. The definition applies to post‐menopausal women and
men aged 50 years or older.
Initially bone formation exceeds bone resorption, but by the
time the person reaches 30 years of age this has reversed, resulting
in a net loss of bone mass, leading to increased bone fragility and
susceptibility to fracture.
5
Osteoporotic (fragility) fractures result from mechanical forces
that would not normally result in fracture. Osteoporotic fractures
are defined as fractures associated with low BMD; they include
spine, wrist, hip and shoulder fractures.
Pathophysiology
There are multiple pathological factors that interact in the development
of osteoporosis, some are discussed here.
There is an imbalance in remodelling in osteoporosis, with a
relative increase in resorption that has not been matched to the
related increase in bone formation. The bone matrix is mineralized
as is usual but there is less bone. Bone remodelling is controlled by
a number of cytokines, including interleukins, colony stimulating
factors and calcitrophic hormones, such as parathyroid hormone
(PTH), 1,25‐dihydroxyvitamin D, calcitonin and oestrogen. This
imbalance in bone remodelling causes lower bone density and
bone quality, resulting in bone fracture.
Whilst age is a factor in the development of osteoporosis, other
circumstances are also indicated, for example when there is
reduced mechanical loading as occurs when a person is immobilized
or confined to bed rest, the menopause (when there is a
reduction in sex hormone concentration) and if there is an excess
of corticosteroids.
Common sites of fracture after minor trauma, due to osteoporosis,
include the spine, wrist, hip or pelvis; however, any bone can
be affected.
There are several risk factors associated with osteoporosis (see
6
Table
55.1).
Oestrogen
deficiency
accelerates
bone
loss
postmenopausal
women and plays a role in bone loss in men. This can
lead to excessive bone resorption, accompanied by inadequate
bone formation. Osteoblasts, osteocytes and osteoclasts all express
oestrogen receptors. In addition, oestrogen affects bones indirectly
through cytokines and local growth factors. An oestrogen‐replete
state may enhance osteoclast apoptosis via increased production of
transforming growth factor beta.
Bone loss that accompanies ageing, in contrast to post‐‫�آ‬
menopausal bone loss, which is associated with excessive osteoclast
activity, is associated with a progressive decline in the amount of
osteoblasts in proportion to the demand. This demand is determined
by the frequency with which new multicellular units are created
and new cycles of remodeling are commenced.
Calcium, vitamin D and PTH assist in the maintenance of
bone homeostasis. Inadequate dietary calcium or reduced intestinal
absorption of calcium caused by ageing or disease may lead to
secondary hyperparathyroidism. PTH is secreted in response to
low serum calcium levels, increasing calcium resorption from
bone, decreasing renal calcium excretion and increasing renal
production of 1,25‐dihydroxyvitamin D that enhances calcium
and phosphorus absorption, and inhibits PTH synthesis and bone
resorption.
Vitamin D deficiency can result in secondary hyperparathyroidism
via decreased intestinal calcium absorption.
7
in
Signs and symptoms
The process that leads to established osteoporosis is asymptomatic
as the condition typically presents only after fracture. The clinician
should remember that osteoporosis occurs in many people who
have no symptoms, or just a few risk factors.
Investigations
Diagnosis of osteoporosis centres on the assessment of BMD using
dual‐energy X‐ray absorptiometry (DEXA). The following screening
blood tests should be considered, in those people with osteoporosis,
to identify treatable underlying causes: full blood count, urea
and electrolytes, liver and thyroid function tests, serum calcium,
alkaline phosphatase, serum immunoglobulins and paraproteins,
urinary Bence‐Jones’ proteins. In men testosterone/gonadotrophins
should be screened.
Treatment is aimed at fracture prevention and includes modification
of general lifestyle factors, such as increasing weightbearing
and muscle‐strengthening exercise and ensuring optimum
calcium and vitamin D intake as an adjunct to active anti‐fracture
therapy.
Currently, no treatment can completely reverse established osteoporosis.
Pharmacological measures include the administration of
adequate calcium, vitamin D and anti‐osteoporotic medication
such as bisphosphonates, PTH, raloxifene and oestrogen. In addition,
potentially treatable underlying causes of osteoporosis such as
hyperparathyroidism and hyperthyroidism should be ruled out or
treated if detected.
Surgical care includes vertebroplasty and kyphoplasty; these are
8
minimally invasive spine procedures used for the management of
painful osteoporotic vertebral compression fractures.
The first goal is to control pain if a fracture has occurred. Oral
analgesics on a regular basis can be implemented. Moist hot packs
and transcutaneous electrical nerve stimulation should also be
considered.
A comfortable mechanical support for the spine and in some
cases, a thoracic orthosis may need to be prescribed (this helps to
limit motion in the spine); hip protectors can also be used.
9