Download Philippine Orthopaedic Association, Inc.

Osteoarthritis
Philippine Orthopaedic Association, Inc.
W2106B, PSE Building, Exchange Road, Barangay San Antonio,
Ortigas Center, Pasig City
Tel. Nos.: 667-3926; 667-3946 Fax No.: 637-9842
E-mail: [email protected]
Website: www.philortho.org
Board of Trustees 2008
President
Vice President
Secretary
Treasurer
Board of Trustees
Trustee (Ex-Officio)
Francisco P. Altarejos, MD, FPOA
Jose S. Pujalte, Jr., MD, FPOA
Lauro R. Bonifacio, MD, FPOA
Albert U. Dy, Jr., MD, FPOA
Emiliano B. Tablante, MD, FPOA
Geoffrey R. Battad, MD, FPOA
Adrien R. Quidlat, MD, FPOA
Julyn A. Aguilar, MD, FPOA
Paul Ruel C. Camiña , MD, FPOA (Luzon)
Jose Antonio G. San Juan, MD, FPOA (Visayas)
Manuel Z. Sison, MD, FPOA (Mindanao)
Edward A. Sarrosa, MD, FPOA
173
Osteoarthritis
Algorithm for the Management of Osteoarthritis
1
Osteoarthritis

2
With pain, swell­ing,
joint stiffness, loss
of motion/function
deformity
4
• Narrowed
joint space
• increased density
(sclerosis) of
subchondral bone
• osteophyte formations
or spurs
• subchondral
cysts

3
X-ray (+) ?
Y

N
Y

Severe
symptoms
and with
deformities
N
Mild to
moderate
symptoms
Mild
symptoms
•Pharmaceuticals:
- analgesics e.g. paracetamol
- NSAIDs e.g. aceclofenac, diclofenac, naproxen
- COX2-inbitors e.g. celecoxib, etoricoxib
- steroids – oral, injectable
(intra-articular)
- supplements – glucosamine, chondroitin
- viscosupplementation - hyaluronic acid,
•Non-Pharmaceuticals
- physical therapy
- braces, walking aids
•Lifestyle modification
•Weight reduction management
•Psychological counseling
9


8

7

6
5
•Surgical options:
- Arthroscopy - debridement
- Cartilage restoration
– mosaic plasty
- Joint realignment procedure
– osteotomy
- Arthrodesis or fusion of joints
- Joint replacements
FIGURE 1
175
Osteoarthritis
Guidelines for the Management of
Osteoarthritis
Introduction
Osteoarthritis is one of the well-known arthritides or
affectations of joint and is otherwise also known as
degenerative joint disease. As the term suggests, it is
of degenerative nature as a consequence of “wear and
tear” of a joint in constant motion. Pain, stiffness and loss
of mobility characterize osteoarthritis. The result­ant pain
and loss of function not only diminishes the quality of life
but also has significant economic burden to society. The
cost of medical care such as physician visits, diagnostic
procedures, prescription and even non-prescription medications, physical therapy and surgery are tremendous.
These, if combined with difficult to measure costs such
as home care, lost wages, decreased employment opportunities, the costs of which are staggering and impose
a big economic burden not only to the individual but also
to the health care system and the national economy.
The condition referred to as osteoarthritis, degenerative
arthritis, osteoarthrosis, or hypertrophic arthritis refers
to a joint condition characterized by a progressive loss
of articular cartilage that is accompanied by inadequate
repair of articular cartilage and remodeling of subchondral
bone and in its place there is the formation of osteophytes.
This condition may affect one or many joints not necessarily at the same time. This condition affects mostly the
synovial joints but often the hips, knees, spine, foot and
of the hands. A strong association exists between joint
degeneration, age and obesity.
The cause of osteoarthritis although associated with
aging is often unknown since not everybody who ages
will have osteoarthritis or they will have osteoarthritis in
different degrees of severity. Since the cause is unknown,
a definite cure is also unknown but what we know is
that early diagnosis and treatment can help minimize
symptoms and help patients maintain active life. Recent
findings, however, suggest that there may be ways to
slow the progression of osteoarthritis.
To fully understand and recognize osteoarthritis and
thus adequately manage this condition, we need to
understand the relevant structure and functioning of the
synovial joint, the derangement that lead to the symptoms, and current and potential future treatments.
Anatomy and Physiology of Synovial Joints
All synovial joints have the same basic structure of articulating surfaces covered with cartilage and supported
by subchondral and metaphyseal bone and the inner
surfaces of the joint is lined with synovial membranes.
A joint capsule with ligaments that link the bones then
covers the whole structure. In some joints, a dense
fibrous tissue called menisci lie in-between the cartilage
surfaces and attached to the joint capsule. The synovial
176
joints may be simple or complex joints depending on the
number of articulating surfaces that are involved in the
particular joint motion. They can also be a hinge type or
the ball and socket types.
Joint Stability. The joint biomechanics include stability
during motion, lubrication that allows low-friction gliding
of cartilage surfaces and load distri­bution across the joint.
Efficient, controlled movement requires dynamic joint
stability made possible by the muscles acting across the
joint. It is important at this point to stress that anything
that changes this smooth and stable joint motion will lead
to early joint degene­ration. Joint stability are maintained
all throughout, that is alignment and contact of articular
surfaces at rest or during motion are made possible by the
cong­ruence of the joint itself and the restraint afforded by
the muscles and ligaments as it acts across the joint. Any
laxities therefore in the joint capsule, ligaments and/or
muscles are enough to cause joint instability lead­ing to
early degenerative conditions.
Joint Lubrication. As true in the saying that nothing
beats a well-oiled machine the joint in itself is a welllubricated motion and loading machine and much more
complicated in a sense. Lubrication decreases friction and
wear in the articular cartilage, thus, ensuring a smooth
gliding motion of the joint surfaces. Nutrition of the articular cartilage is brought about by the diffusion of the
synovial fluid. Again, any condition that will interfere in
this mechanism will result to a less efficient joint. The very
complex nature of the joint not only involves lubrication
but load distribution as well since the joint is not like the
common ball-bearing wherein load distribution is equally
distributed. The ligaments and muscles participate much
in this sense such that they contract at one end or relaxes
at the other end or vice-versa to help the joint absorb and
distribute the impact or loading. For, example, if one does
a skip and jump the stresses generated across the knee
joint may not be the same all the time since the way you
land on the surface varies. Thus, failure of joint muscular
mechanisms of load distribution can increase stresses
on cartilage and subchondral and metaphyseal bone,
thereby contributing to joint degeneration.
Articular Cartilage. Articular cartilage contains only one
cell type, the chondrocyte. It is believed that they are
avascular and has no nerve cell. They are made up of
spheroid and ellipsoid cells scattered throughout a highly
organized matrix no more than a few millimeters thick.
These thin layers have almost excellent low friction gliding
properties and ability to distribute loads, thus, minimizing
stresses on the subchondral bone. The chondrocytes
depend on diffusion of nutrients and meta­bolites through
the matrix. The matrix consists of a framework of macromolecules filled with water and the macromolecules are
collagens, proteoglycans and noncollagenous proteins.
The collagens form a fibrillar meshwork that gives the
cartilage its tensile strength and form. The proteoglycans
on the other hand consist of protein core filament and
one or more glycosami­no­glycan chains.
Osteoarthritis
Etiology and Pathophysiology
Degenerative joint diseases may be classified into primary or idiopathic and secondary osteoarthritis. Although
mentioned earlier that the condition is age related and
or due to normal “wear and tear”, it remains a fact that
not all joints will end up osteoarthritic or have varying
degrees of osteoarthritis. Degenerative joint disease
with no clear-cut cause is called primary or idiopathic.
Secondary osteoarthritis, on the other hand, are those
with associated known cause and they develop earlier
in life than the age-related joint disease.
The development of primary joint disease as stated
is strongly associated with age. Despite this association, however, the relationship between aging and joint
degeneration remains unclear and normal joint use has
not been shown to cause degeneration. Regular and
moderate or even strenuous activity does not appear to
accelerate degenerative joint disease in normal joints,
meaning those with normal articular surfaces, alignment,
static and dynamic stability, innervation and muscle
control. Any loss of the above will not render the joint
normal. However, we know that any excesses are also
bad because intense repetitive loading will also cause
joint degeneration. Cyclic loading on the joint stimulates
cartilage matrix synthesis, whereas, prolonged static
loading or the absence of it as in pro­longed joint immobilization causes degradation of the matrix and eventually
joint degeneration.
On the other hand, joints with known abnormalities that
interferes with normal joint function as stated earlier are
the secondary type of osteoarthritis. Any disruption in
joint anatomy and function including incongruity of joint
surfaces, dysplasia, mal-alignment, disturbances in joint
enervation and muscle strength and endurance will lead
to earlier than expected osteoarthritis. Subjecting these
joints to normal loads of daily activities places the joint at
risk of developing arthritis. A patient with developmental
hip dysplasia early on in life will most likely develop
secondary osteoarthritis.
Pathophysiology
Despite the term osteoarthritis, “itis” meaning an inflammation, there is hardly an inflammatory component in
these conditions, unlike in rheumatoid arthritis. The
process involves loss of articular cartilage structure accompanied by an attempt of cartilage repair and bone
remodeling which can be seen radiologically as spur or
osteophyte formations. This process progresses slowly
over many years or may stabilize or even improve spontaneously with a decrease in symptoms. The primary
changes occur on the articular cartilage only but the
symptoms may refer to every structure around the joint.
The symptom of pain for instance is not a direct result
of articular cartilage loss but spasm of muscles and
ligaments around the joint. Progressive cartilage loss
may then involve the subchondral bone and ultimately
to subchondral bone collapse leading to joint deform-
ity. These series of events are seen radiologically as
loss of joint height or thinning of the joint space such
that in severe cases it appears as if there is no more
joint and clinically manifests as severe joint limitation
of motion.
Clinical Manifestations
Pain is by far the most common presenting symptoms that
compels the patient to seek consultation. Joint stiffness
particularly in the morning or after prolonged activity is the
second most important symptom. As joint degeneration
progresses, the joint may continually lose motion and
the patient may complain of crepitus or grinding sensations over the joint in motion. In more severe cases, the
joint may lose motion due to onset of contractures or
even soft tissue or bony ankylosis. Joint involvement in
osteoarthritis are not necessarily symmetric and usually
involves mostly weight-bearing joints, except the hands.
Thus, the most commonly involved joints are the knee,
hip, spine and hands.
Loss of joint motion in varying degrees is next common
complaint of patients with osteoarthritis. Active and passive joint motions should be assessed by the clinician.
The limitation of joint motion maybe due to pain, incongruity or actual deformity, ligament and capsular contracture,
muscle spasm or intra-articular conditions as menisci or
loose fragments of cartilage.
Diagnosis
Based on history and physical examination alone much
of this condition can be diagnosed. Plain radiographs
will confirm the condition and will present the varying
degrees of joint involvement. Invariably, the radiological
picture may not correlate with the clinical picture such
that in some cases, a very severe x-ray picture may
have minimal symptoms or vice versa. Other imaging
studies that may help the clinician are bone scans, CTScans, magnetic resonance imaging (MRI), but these
are rarely indicated but will help in some cases wherein
a closer study of the joint is needed as in pre-operative
planning. In some cases, by the time clinical symptoms
and radiographic evidence of degene­rative joint disease
develop, significant dege­neration has already occurred
which are already irre­versible. Early diagnosis and newer
modalities may make it possible to prevent progression
of the disease condition.
Radiography would usually confirm the diagnosis of osteoarthritis and it would usually show narrowed joint space,
increased density of subchondral bone and osteophyte
formations or spurs. In severe long standing cases the
joint will show radiographically in various stages of malalignment, subluxations, or deformities. Some special
radiographic films may further help in the diagnosis or
even planning for management. Stand­ing films of lower
extremity joints or long leg films that will show the true
picture of alignment will be of help in the evaluation of
patients with osteoarthritis.
177
Osteoarthritis
Although plain radiographs may suffice, other imaging
studies may corroborate not only in the diagnosis but also
in total assessment of patients with osteoarthritis. Bone
scintigraphy, CTScanning, and even MRI will pro­vide
excellent visualization not only of the bony structures but
soft tissue structures as well around the joint.
Laboratory tests are used mostly to rule out other conditions rather than confirm the diagnosis of osteoarthritis.
The most helpful among these tests would be synovial
fluid analyses if the presenting symptom includes joint
effusion although joint effusion are quite rare or minimal
in osteoarthritis.
An exercise program or at least physical therapy would
also be needed in patients who eventually need surgery
as a pre-operative preparation.
Pharmacologic Treatment
• Analgesics remain as the treatment for mild osteoarthritis. These are paracetamol, mefenamic acid
and acetylsalicylic acid. The more potent ones are
opiates and antagonists and the newer classification
such as tramadol. These analgesics are sometimes
used in combination with muscle relaxants such as
eperisone hydrochloride, tizanidine and chlorzoxasone. These combination drugs are given to patients
for relief from pain and muscle spasm associated
with osteoarthritis.
• NSAIDs or the non-steroidal anti-inflammatory
drugs acemetacin, naproxen, ketoprofen, piroxicam, diclofenac, aceclofenac, ibuprofen and indomethacin. These drugs offer analgesic effect and
anti-inflammatory effect as well. The only adverse
effects of NSAIDs are those pertaining to the gastrointestinal tract of which bleeding is foremost.
• COX2-inhibitors: Meloxicam, cele­coxib, rofe­
coxib.
Diagnostic arthroscopy can be done in some cases
for it allows direct visualization or if other intra-articular
conditions are suspected specially in early stages of
the disease.
Treatment
The goals of treatment of osteoarthritis are directed
towards preserving or at least improving whatever joint
condition of a particular patient has at the moment the
condition was diagnosed. Treatment would vary according to the severity and the patients expectations and level
of activity. In these sense, it may involve simple avoidance of activities that may exacerbate the condition such
as impact loading or strengthening the muscles around
the joint to the occasional use of only mild analgesics/
anti-inflammatory drugs (NSAIDs). Others may already
require physical modalities as physical therapy and still
others may already require adaptive aids. In selected
patients with moderate to severe osteoarthritis, surgical
options may already be required to improve function and
quality of life.
Patient education and counseling. Understanding the
condition on the part of the patient will have a lot to do in
the management. Reassuring patients that there is life
after osteoarthritis, that there are simple measures that
can be resorted to such as exercise programs, physical
therapy, weight loss and occasional anti-arthritic medications. Patient education would include advising patients
the appropriate type of activities that they can still do and
activities that are to be avoided. Some patients may need
counseling in order to cope with chronic pain and disability
and to relieve anxiety and/or depression.
Patients with osteoarthritis involving the weight bearing
joints such as the hips, knees and lumbar spines would
benefit from a weight loss program to help decrease
symptoms and progression of the disease. This is attributed to the decrease in stress loading that the joint
is subjected to.
An exercise program would include maintaining and
increasing whatever range of joint motion that remains.
It will also improve muscle strength for increased mobility and function. The exercise program therefore should
include:
178
1) range of motion and stretching,
2) muscle strengthening and
3) aerobic exercise to increase endurance and
reduce fatigue.
Osteoarthritis being an age-old problem has spurred
tremendous research towards other medical treatment.
A new means of treatment are the “nutriceuticals” such
as glucosamine sulfate, chondroitin sulfate and ginger
extracts.
Treatment has also been brought to where the damage is, such as intra-articular injections of steroids for
its anti-inflammatory effects. There is also the visco­
supplementation with hyaluronic acid which is the main
component of synovial fluid that gives it much viscosity.
Physical Modalities. Local application of heat, ultrasound, and hydrotherapy offer temporary relief.
Supportive Aids and Appliances. The use of splints,
braces, canes, walkers, crutches decrease joint loading in an osteoarthritic joint. Shoe modifications aim to
reduce the impact or load on weight bearing joints. Modifications in the workplace and even at home are also
advocated to make the environment arthritic-friendly.
Surgical Treatment. The surgical treatment is meant
to decrease or eliminate pain, improve function and the
quality of life. This procedure includes techniques that
attempt to preserve or restore articular cartilage, realign
joints or replace joints and even fuse joints. Results of this
procedure are good to excellent although it exposes the
Osteoarthritis
patient to the risk attendant to surgery such as infections,
nerve and blood vessel injuries, venous thrombosis and
pulmonary embolism. If no relief is obtained from medical
and physical treatment, a patient with moderate to severe
osteoarthritis will have to consider surgical options. Delaying surgery until after joint contractures, muscle atrophy
and joint instability occur will compromise the results and
increase probability of complications.
•Cartilage restoration. There are surgical procedures to attempt preserve or restore damaged
articular cartilage. Arthroscopic debridement or perforation of subchondral bone to stimulate cartilage
formation and replacement of damaged articular
cartilage with cultured cartilage grafts had evolved
beyond the experimental stage.
•Joint realignment procedures. Osteoarthritic
joints with identified cause such as mal-alignment are good candidates for these procedures
with the end in view of redistributing loads from
severely degenerated joint areas. The results of
these procedures in certain well selected cases
are comparable to joint replacements. More often
than not, these are the procedures recom­mended
for young patients with earlier than normal osteoarthritis.
Joint replacement with prosthetic implants has over
the years evolved successfully to almost include
many joints. Most procedures done are those of
the hip, knees, shoulder, elbow, ankle and small
joints of the fingers. A better implant design and
materials had led to successful joint replacements
over the years. As stated earlier, total joint replacements are not recommended for younger patients
since they have inherent limitations that they do
not substitute for the mechanical properties of a
normal joint. Implant wear limits its life span, and
loosening and implant failure remains a problem.
•Arthrodesis or fusion of joints in advanced osteo­
arthritis relieves pain and restore stability. However,
this totally eliminates joint motion and thus, transmits joint loading to other adjoining joints, and thus,
might accelerate degeneration of these joints. This
also does not restore the mobility that the patient
may want.
• Joint replacement procedures are done for
severe cases where the articular cartilage is replaced with metal (stainless steel alloy) or plastic
(poly­ethylene). This procedure is done in elderly
patients mainly because in the young the possibility
of revision in the patient is highly possible.
179
Osteoarthritis
Recommended Therapeutics
(Drugs Mentioned in the Treatment Guideline)
The following index lists therapeutic classifications as recommended by the treatment guideline. For the prescriber's
reference, available drugs are listed under each therapeutic class.
Analgesics
Non-Narcotic Analgesics
Coxibs
Etoricoxib
Arcoxia/Arcoxia AC
Celecoxib
Celebrex
Celexib
Flamar
NSAIDS
Aceclofenac
Clanza
Acemetacin
Rantudil
Diclofenac
Abicfen
Cataflam
Cataflam Qs
Denkoran
Difenax
Dolfastad
Doloflam
Drugmaker’s Biotech Diclofenac
Neo-Pyrazon/Neo-Pyrazon SR
Nepenthe
Voltaren
Voltaren Emulgel
Glucosamine sulfate
Viartril-S
Ibuprofen
Advil
Alaxan
Alaxan FR
Anoflam
Dolan FP
Drugmaker’s Biotech
Paracetamol + Ibuprofen
Idyl SR
Laberfen
Medicol
Midol
Muskelax
Nurofen Syrup
Relaxid
Restolax
Restolax Forte
Selxan
Skelan Forte
Indomethacin
Drugmaker’s Biotech Indomethacin
Infree
Ketoprofen
Drugmaker’s Biotech
Ketoprofen
Ketotop
Orudis EC
Orudis IV
Ketorolac
Kortezor
Remopain
Toradol
Mefenamic Acid
Algifort
180
Analcid
Aprostal
Atmose
Calibral
Dli Mefenamic Acid
Dolfenal
Dolmetine
Dolsten
Drugmaker’s Biotech Mefenamic Acid
Eurostan
Gardan
Gisfen
Icelax
Istan
Mecid-A
Medianon
Mefedon
Mefenax
Pacimic
Pharex Mefenamic Acid
Ponstan
Ralgec
Revalan
Ritemed Mefenamic Acid
Selmac
Sigarax
Spegic
Stangesic
Tynostan
Zapan
Meloxicam
Meloflam
Melora
Mobic
Naproxen
Agapro
Alpron
Drugmaker’s Biotech
Naproxen
Flanax/Flanax Forte
Naprosyn Lle/Naprosyn Lle Forte
Piroxicam
Drugmaker’s Biotech
Piroxicam
Feldene/Feldene Flash
Flamastat
Macroxam
Parixam
Pirostad
Proximax
Proglumetacin Afloxan
Tenoxicam
Tilcotil
Para-Aminophenol Derivatives
Paracetamol
Aldep
Alvedon
Baropyrine
Biogesic
Calpol/Calpol Six Plus
Crocin
DLI Paracetamol
Dolexpel
Drugmaker’s Biotech Paracetamol
Geran
Medgenol
Meforagesic
Naprex
Naprinol
Neo-Kiddielets
Opigesic
Pharex Paracetamol
Pynal
Rexidol
Ritemed Paracetamol
Saridon
Temperal
Tempra/Tempra Forte
Tylenol
Ultragesic
Paracetamol/Vitamin B-Complex
Dolo-Neurobion
Paracetamol/Chlorzoxazone
Parafon Forte
Salicylates
Aspirin (Acetylsalicylic acid)
Bayer Aspirin
Cortal
OPIATES & ANTAGONISTS
Butorphanol
Stadol
Fentanyl Durogesic
Sublimaze
Morphine sulfate Hizon Morphine Sulfate
Relimal CR
Nalbuphine Nubain
Tramadol
Dolcet
Dolotral
Milador
Milador Inj
Milador-Retard
Siverol
Tdl
Tramal
Skeletal Muscle Relaxants
Carisoprodol
Lagaflex*
Baclofen
Lioresal
Onelaxant-R
Eperisone HCl
Myonal
Orphenadine
Norgesic/Norgesic Forte*
Tizanidine
Sirdalud
Ternelax
Topical Analgesics
Diclofenac
Voltaren Emulgel