JOURNAL READING

Osteoarthritis

I Haq, E Murphy, J Dacre

Name : Syalara Fatharani

NIM : 201373108
PRECEPTOR: dr. Hj. Ihsanil Husna, Sp.PD

MEDICAL PROFESSION PROGRAMME DEPARTMENT OF INTERNAL MEDICINE

JAKARTA ISLAMIC HOSPITAL CEMPAKA PUTIH
FACULTY OF MEDICINE UNIVERSITY OF MUHAMMADIYAH JAKARTA
2018
BACKGROUND
• Osteoarthritis is a chronic, degenerative disorder of unknown cause
characterised by gradual loss of articular cartilage. It is the most
prevalent disease in our society, with a worldwide distribution.
• In England and Wales, between 1.3 and 1.75 million people have
symptomatic osteoarthritis.
• Data from the Arthritis Research Campaign show that up to 550
000 people in the UK have severe knee osteoarthritis and two
million people visited their general practitioner in the past year
because of osteoarthritis
 CLINICAL FEATURES
• Patients are usually over the age of 50 and complain of pain
and stiffness in the affected joint(s)
• which is exacerbated with activity and relieved by rest
• Joint tenderness and crepitus on movement
• Swelling may be due to bony deformity such as osteophyte
formation,or due to an effusion caused by synovial fluid
accumulation.
• The presence of fever, weight loss, anorexia, or abnormal
blood tests should alert the physician to other disease
processes such as infection or malignancy.
 PATHOGENESIS
• Cartilage is made of water (70%) and a type II collagen
framework with proteoglycans and glycosaminoglycans
produced by chondrocytes.
• Chondrocytes receive nutrition from the synovium by
diffusion and the synovial fluid is circulated by joint
movement.It has been postulated that if the joint stops
moving and chondrocytes lose their source of nutrition,
they go into shock and cartilage repair ceases.
• Catalyse collagen and proteoglycan degradation. The
synovium has been shown to be variably inflamed in
osteoarthritis producing increased levels of interleukin-1(IL-
1)and tumour necrosis factor-alpha(TNF-α),cytokines that
induce nitric oxide and metalloproteinase production.
Interleukin-6 (IL-6)
 PATHOLOGICAL FINDINGS
• Macroscopically, the osteoarthritic process results in cystic
degeneration of the bone surrounding the joint, with loss of
cartilage and irregular,abnormal bone formation at the
edges of the joint and narrowing of the joint space.
• Microscopically, there is flaking and fibrillation of the
articular cartilage surface and destruction of the cartilage
microarchitecture with formation of holes within it,as well
as bony cysts
FACTOR RISK
Age
The Framingham Study found that 27% of those aged
63 to 70 had radiographic evidence of knee
osteoarthritis, increasing to 44% in the over 80 age
group.
Other studies have found that 80% of people over the
age of 65 have some radiographic evidence of
osteoarthritis (although this may be asymptomatic).
Incidence and prevalence of symptomatic
osteoarthritis levelled off or declined in men and
women at around 80 years of age.
FACTOR RISK
Trauma
Cruciate,collateralligamentandmeniscaltearsaswellasj
oint fracture lead to increased risk of osteoarthritis.
The Framingham Study found men with a history of
knee injury were at a 5–6-fold increased risk of
developing osteoarthritis.
Meniscectomy after a knee injury resulted in an
increased risk of developing tibiofemoral
osteoarthritis.
FACTOR RISK
Occupation
Osteoarthritis is commoner in those performing
heavy
physicalwork,especiallyifthisinvolveskneebending,squ
atting,or kneeling.
There is a significant relationship between
occupational kneeling12 or repetitive use of joints
during work and osteoarthritis
FACTOR RISK
Exercisse
Elite athletes who take part in high impact sports do
have an increased risk of knee osteoarthritis.
Primary quadriceps
weaknessisariskfactorforitsdevelopmentbydecreasing
the stability of the joint and reducing the shock
absorbing properties of the muscle.
FACTOR RISK
Exercisse
Elite athletes who take part in high impact sports do
have an increased risk of knee osteoarthritis.
Primary quadriceps
weaknessisariskfactorforitsdevelopmentbydecreasing
the stability of the joint and reducing the shock
absorbing properties of the muscle.
Gender and ethnicity
Under the age of 50, men have a higher
prevalence and incidence than
women.However,once over 50,women have a
higher overall prevalence and incidence than
men.
Osteoarthritis of the hip is more common in
Europeans (7%–25%) than in Chinese, Africans
from Nigeria and Liberia, and Jamaicans (1%–
4%).
Genetics
There is increased concordance for osteoarthritis
in monozygotic twins compared with dizygotic
twins,indicating there is a genetic susceptibility to
the disease.
Families have been found with rare autosomal
dominant patterns of inheritance of
osteoarthritis.
Children of parents with early onset
osteoarthritis are at higher risk of developing it
themselves compared with families where this is
not the case
Obesity
This is the strongest modifiable risk factor.
 The Chingford Study showed that for every two unit
increase in body mass index (approximately 5 kg), the
odds ratio for developing radiographic knee
osteoarthritis increased by 1.36.
Being overweight at an average age of 36–37 is a risk
factor for developing knee osteoarthritis in later life
(>70 years of age).
 Losing 5 kg of weight reduced the risk of
symptomatic knee osteoarthritis in women of average
height by 50%
Diet
People in the lower tertile of vitamin C and vitamin D
blood levels had a threefold risk of progression of knee
Vitamin D intake and status had no effect on
development of knee osteoarthritis but those with low
intake and low serum levels had anincrease drisk of
osteoarthritis knee progression.
Bone density There is an inverse relationship between
bone density and osteoarthritis. Increasing
subchondral bone density may lead to increased
loading through weightbearing joint cartilage.
Bone density
There is an inverse relationship between bone density
and osteoarthritis.
NATURAL HISTORY
• The presence of osteophytes had a very strong
association with knee pain, whereas the absence or
presence of joint space narrowing was not
associated.25 Knee pain severity was a more
important determinant of functional impairment than
radiographic severity of osteoarthritis.
NATURAL HISTORY
Magnetic resonance imaging
• This is already well established for use in assessing
ligament and meniscal tears in the knee. It has no
place in routine clinical assessment of
osteoarthritis,but may be a specific and sensitive way
of quantifying cartilageloss.
NATURAL HISTORY
Other imaging techniques Computed tomography is
thought to have little advantage
• studies have found that retention of technetium
labelled diphosphonate in the knee predicts
subsequent cartilage loss in patients with advanced
osteoarthritis
• Ultrasound is good for assessing cartilage integrity and
destruction,but in most weight bearing joints,cartilage
is not easily accessible.
NATURAL HISTORY
Biochemical markers in osteoarthritis
• Molecular markers may theoretically be able to detect
osteoarthritic changes at an early stage. Ideally these
markers would be sensitive to change,reliable,and
quantitative
• Cartilage oligomeric matrix protein (COMP) may be a
marker of cartilage destruction. C-reactive protein,
hyaluronan, YKL-40, and metalloproteases are markers
of synovial inflammation.Pyridinoline and bone
sialoprotein are markers of bone turnover
Osteoarthritis is a common disease with high morbidity.
• The aetiology is multifactorial.
• Biochemical markers of disease activity are not yet
available for routine clinical care.
• Plain radiographs are the current most common way
of assessing progression of osteoarthritis, although
there are problems with standardisation of joint
positioning with respect to the knee.
• Any assessment of effect of a therapy should include a
measure of health status in addition to radiological
assessments.
MANAGEMENT OF OSTEOARTHRITIS IN CLINICAL
PRACTICE
The aims of management of patients with osteoarthritis are:
• Patient education.
• Pain control.
• Improve function.
• Alter the disease process.
Management interventions in osteoarthritis include:
• Education.
• Exercise.
• Weight loss.
• Physiotherapy.
• Appliances.
• Drugs.
• Surgery.
Non-drug therapy
Education and community support
• Formal education by any member of the
multidisciplinary team should be an initial part of
management.
Exercise
• This is the single most important intervention.
Inactivity due to the pain of osteoarthritis leads to
reduction of muscle bulk surrounding the joint,thus
destabilising it.
• Aerobic capacity is also reduced, and the risk of
obesity is increased
• Warm up: 5 min. Exercises
• Isometric strength training: daily.
• Isotonic strength training: 2–3 times/week.
• Flexibility training: daily.
• Aerobic training (endurance): 3–5 times/week. Cool
down: 5 min. Many patients need to concentrate on
strength and flexibility training first before considering
aerobic training. The exercise programme should be
adapted to the patient’s age and functional ability.
Weight loss
• A study of 21 obese elderly men and women with knee
osteoarthritis randomised to either a diet and exercise
group or diet alone group found that the former group
lost more weight but both groups had similar
improvements in self reported disability, knee pain
intensity, and frequency after six months.
Mechanical aids
• The occupational therapist can provide assessment for
walking aids, for example, sticks and for providing a
safe and functional environment at home and work.
Drug therapies
Analgesics
• Paracetamol is used first line up to a dose of 1 g four
times a day.
• Paracetamol/opiate combinations such as coproxamol
may be used if paracetamol alone is unhelpful.
Drug therapies
Non-steroidal anti-inflammatory drugs
• NSAIDs have been found to have equal efficacy to
paracetamol in most patients.
• Renal and gastrointestinal side effects are a major
source of mortality and morbidity,especially in the
elderly.
• If a patient is at risk of peptic ulceration,
gastroprotection in the form of H2 antagonists,
misoprostol, or proton pump inhibitors should be
prescribed
Drug therapies
Intra-articular corticosteroids
• There are significant short term benefits of 2–4 weeks
over placebo with injection of triamcinolone
hexacetonide or methylprednisone in knee joints.
• Anecdotal evidence suggests some patients achieve a
sustained improvement in symptoms.
• Side effects include skin atrophy and dermal
depigmentation, especially with long acting
preparations and if the soft tissues are injected,
Infection is an important but rare complication.
Drug therapies
Hyaluronic acid derivatives
• The molecular weight and amount of hyaluronic acid
decrease in osteoarthritis. It was postulated that
supplementation with intra-articular hyaluronic acid
could help to improve synovoial fluid viscoelasticity.
• Several preparations are available, either low (for
example, Hyalgan) or high molecular weight (for
example,Synvisc).
• Symptomatic effect started at week 3–5 and persisted
up to 12 months.
• here is also evidence that hyaluroni \c acid injections
have similar efficacy to NSAIDs for between 3–6
months after injection
Drug therapies
Topical treatments
• Topical capsaicin cream is often used on hands and
knees in patients with moderate pain. There have been
some trials showing the efficacy of capsaicin in
osteoarthritis.
• There is little evidence of efficacy of topical NSAIDs.
Drug therapies
Glucosamine sulphate
• Glucosamine sulphate is a nutrient supplement
available over the counter from pharmacies and health
food shops in Europe and USA, and is used to relieve
musculoskeletal symptoms.
• Glucosamine sulphate has probably an analgesic effect
in mild to moderate knee osteoarthritis.
• There is little evidence for its use in osteoarthritis at
other sites.
Drug therapies
Other possible disease modifying osteoarthritis drugs
• Diacerein is a drug that inhibits production and activity
of metalloproteinases and interleukins and may have
an effectin delaying progression of hip osteoarthritis as
measured by minimum joint space measured visually.
NICE recommendations for the use of COX-2 selective
inhibitors
• Aged over 65 years.
• Using other medicines known to increase the
likelihood of gastrointestinal problems.
• Having serious co-morbidities.
• Requiring long term use of standard NSAIDs at the
maximum dose. These drugs should be prescribed after
discussion with the patient and assessment of the risks
and benefits for each patient.
Surgery
• Surgery is used where medical therapy has reached its
limits.
• Arthroscopic debridement and lavage can improve
symptoms in degenerative meniscal tears, but does
not halt progression.
• Autologous cartilage transplantation, where grafts of
normal cartilage are taken from the edge of the
diseased joint, cultured in vitro and reimplanted into
areas where the cartilage is denuded may be an
effective technique.
• Osteotomy in early osteoarthritis may relieve
symptoms and slow the rate of progression.
Learning points in management of osteoarthritis
• Importance of patient education.
• Early involvement of multidisciplinary team to help with
exerciseadvice,weightlosswhereappropriate,orwalking aids.
• Each patient should have an individual plan made after full
discussion
• Paracetamol is the most appropriate first line drug treatment.
• NSAIDs should be used with caution, especially in at-risk
patients.
• Newer COX-2 selective drugs are of equal analgesic efficacy to
standard NSAIDs.
• Intra-articular injection tends to work better in those with joint
effusions.
• Glucosamine and chondroitin sulphates are safe over the
counter treatments that can be tried.
• Hyaluronic acid derivatives should bereserved for use in severe
disease or if surgery is not possible.
CONCLUSION
• This review has detailed current knowledge about the
epidemiology and best practice in treating
osteoarthritis.
• diagnostic measuresare based on clinical findings and
clumsy radiological methods and none of our
therapeutic interventions are curative.
• Robust outcome measures are needed in order to
assess the efficacy of any disease modifying
osteoarthritis drug in the future.