Dr.

Henry Pebruanto, SpOT

CURICULUM VITAE

EDUCATION UNDER-POST GRADUATE TRAININGS

 Medical Faculty of Udayana University, Denpasar – Bali; 2005
 Orthopaedic Training (Airlangga Univ., Sby/ Udayana Univ., Dps); Jan 12
 Overseas Observership Programme (Hip and Knee Arthroplasty): Perth – WA; Nov 10
 ASEAN Cadaveric Knee Course: Chiang Mai Univ. – Thailand; Apr 12.
 Australian Educational Program (Knee &Shoulder): Sydney – NSW; Jun 12
 ASEAN Cadaveric Knee Course: Bangkok – Thailand; May 14.
 ASEAN EASE (Express Arthroplasty and Arthroscopy Skills Education) Knee Course : Bangalore –
India; May 15.

COURSES
 Advanced Trauma Life Support (Denpasar – Bali); Jan 06
 Basic Orthopedic Skill Course (Surabaya – East Java); Aug 07
 Basic Surgical Skills Course (Surabaya – East Java); Jan 08
 Ultrasonography for Abdominal and Chest Trauma Course (Jakarta); Apr 08
 Total Nutritional Treatment Course (Tanah Lot – Bali); Dec 08
 Basic AO Trauma Course (Nusa Dua – Bali); May 09
 Bali Hand Course (Denpasar – Bali); Jul 09
 Post Graduate Course : Musculoskeletal Trauma (Jakarta); Nov 09
 8th Annual Meeting of Indonesian Spine Society & 1st International Society for Minimal
Intervention in Spinal Surgery (Denpasar – Bali); Jun 10
COURSES
 Workshop Hemiarthroplasty and Bone Substitute (Malang – East Java); Jun 10
 Ponsetti Course (Denpasar – Bali); Dec 10
 4th Arthroplasty Workshop : Jump Start on Total Knee Replacement (Jakarta); Apr 11
 3rd Arthroplasty Workshop : Jump Start on Total Hip Replacement (Jakarta); Apr 11
 AO Spine Principles Course (Jakarta); Jun 11
 Current Diagnosis and Comprehensive Treatment of Brachial Plexus Injury (Surabaya –
East Java); Oct 11
 3rd Pelvic and Acetabular Course and Workshop (Surabaya – East Java); Oct 11
 Lower Extremity Trauma Course (Denpasar – Bali); Jan 12
 Osteoarthritis (OA) ~ the most common form
of joint disease throughout the world.
 ~ associated with age
 extremely common in older people;
 > 80% of people > 55 yo have OA
 It mainly affects the hips, knees, spine, hands
and feet.
 Hip and knee OA are the most important
 Because of the high prevalence of pain and disability
 Massive healthcare resource ~ in terms of the
provision of joint replacements.
 OA ~ final common pathway of joint failure
 End result of biochemical and mechanical insult
that exceeds the joint’s ability to repair itself.
 Classification and subtyping
 ~ difficult
 primary versus secondary OA
 asymptomatic versus symptomatic OA
 localized versus generalized OA
 hypertrophic versus atrophic OA
 progressive versus inactive OA
 ‘sporadic’ or ‘common-or-garden OA’ – by far the
most frequent type
 Osteoarthritis (OA or joint failure) is
relatively easy to define pathologically, being
distinguished by focal areas of loss of
articular cartilage within a synovial joint,
accompanied by sclerosis of the underlying
bone, and varying degrees of change in other
joint tissues.
 Thepathology of OA is sometimes associated
with the development of joint pain and other
symptoms and signs,
 Central dilemma of OA:
 pathological changes of OA are very common in
older people, but often asymptomatic;
 joint pain is very common in older people, and
sometimes due to OA.
 This means that clinicians need to think carefully
about the cause of joint signs and symptoms in
older people.
 Thejoint sites most commonly involved :
knees, hips, hands, feet and spine.
 OA affects focal areas within joints:
 early ~ only a localized area is affected
 later on ~ spread to affect the whole joint.
 Knee~ anteromedial compartment of the
TFJ, and the lateral facet of the PFJ,
 Hip ~ superolateral aspect
 Hands and feet ~ DIPJ, first MTP and thumb
base.
 Increasing age ~ strong risk factor
 there are differences in prevalence and
distribution in men and women.
 Some racial/ethnic differences exist in the
prevalence and distribution of OA.
 Eg. Superolateral hip OA ~ very common in
Caucasians
 relatively uncommon in people of Chinese origin.
 ~ may be due to subtle differences in skeletal
shape.
 OA has no single cause
 due to a variable combination of several risk
factors
 OA arises as a result of a mixture of both
systemic predisposition and local biomechanical
risk factors, as shown in Figure 5.4, and Box 5.1
shows the major risk factors currently known.
GENETIC PREDISPOSITION
 ~ 40% may be genetic.
 There is no ‘OA gene
 This increased risk relate to genes important
for
 skeletal development
 bone size and shape
AGE
 OA is strongly associated with increasing age.
 cartilage gets thinner
 muscles get weaker
 stability of major joints such as the knee may be
affected in subtle
 Muscleweakness precedes the development
of knee OA.
GENDER
 The reasons ~ not clear.
 Changes related to the female menopause
appear to be particularly important,
 Knee OA prevalence in women rises sharply after
the menopause,
 Inflammatory OA of the hands often starts during
the menopause.
DIET AND OBESITY
 Obesity is a strong risk factor, particularly for
knee OA.
 also a risk factor for hand OA
 Have some systemic influence ~ changes in
obesity-related biochemical factors such as
leptin levels.
 Vitamin deficiencies may be important in the
development of OA
 including vitamins C, D and K.
ABNORMAL JOINT SHAPE AND SIZE
 Joint shape is an important risk factor,
particularly for hip OA.
 Hip dysplasia
 Abnormalities of the size or shape of the head of
the femur or acetabulum (Femoroacetabular
impingement – FAI)
 Thedifferences in shape of hips in Chinese
from that in Caucasians ~ low prevalence of
hip OA in Chinese people.
 Joint size and shape are also important in knee
OA.
PREVIOUS INJURY
 Injuries that affect the shape or stability of a
joint predispose to OA.
 This is most apparent in joints which have a
low prevalence of ‘common-or-garden’ OA
such as the wrist or ankle.
 Meniscal and ligament injuries, particularly
ACL rupture, are important predisposing
factors for OA.
NEUROMUSCULAR PROBLEMS
 Severe neurological problems ~ ‘Charcot’s
joints’.
 Lesser forms of neurological change, including
weak muscles, and loss of proprioception.
 Joint laxity seems to predispose to OA.
 Spasticity results in very tight joints
accompanied by abnormal joint loading leading
to joint damage and secondary osteoarthritis.
 OA of the hip ~ patients with spastic cerebral palsy.
JOINT LOADING, OCCUPATION AND OBESITY
 Repetitive ‘overuse’ of joints
 eg.‘picca-thumpers thumb’ ~ OA at the base of
the thumb
 in people who spent their working days shifting
printing blocks around with their thumbs.
 Obesity ~ important for knee OA
 due to loading factors, as well as any systemic
influence.
BONE MINERAL DENSITY
 High bone mineral density is a risk factor for
OA,
 low bone mineral density is protective.
 The
OA process is mechanically driven but
chemically mediated.
 The key pathological features of OA are shown
in Table 5.1, and their radiographic correlates.
 The cartilage changes include:
 early softening and swelling or articular cartilage,
with an increase in its water content;
 intermediate fragmentation and fissuring of the
cartilage surface;
 late erosion down to the underlying bone (see
Figure 5.5).
 Outerbridgeclassification is most commonly
used by orthopaedic surgeons.
 Described changes to the articular surface
 particularly as arthroscopy

 Grade 1 : Softening and swelling of the cartilage

 Grade 2 : Fragmentation and fissuring of the
cartilage in an area less than ½ inch in diameter
 Grade 3 : Fragmentation and fissuring of the
cartilage in an area more than ½ inch in diameter
 Grade 4 : Exposure of underlying bone.
 The cartilage changes are accompanied by extensive
changes in the tidemark between bone and cartilage,
 vascular invasion and extension of the calcified zone,
 thickening of the subchondral bone.
 At the margins of the joint, periosteal cells
proliferate and change their phenotype to form bone
(osteophytes).
 Synovial inflammation, which may result in
 joint effusions, thickening and fibrosis of the joint
capsule
 In advanced cases
 formation of cysts, and loss of bone volume
 The radiograph
 the only routinely
available tool to detect

 joint space narrowing,

 osteophyte formation &
 subchondral bone
sclerosis

 ~ which are
pathognomonic of OA
 Kellgren
and Lawrence scoring system (X-ray
changes) :

 0 : Normal
 No features of OA
 1 : Doubtful
 Minimal osteophyte, doubtful significance
 2 : Minor
 Definite osteophyte, no loss of joint space
 3 : Moderate
 Some diminution of joint space
 4 : Severe
 Advanced joint space loss and sclerosis of bone
 OA process is initiated by a mixture of
systemic predisposing factors interacting
with local mechanical influences ~ the
changes are chemically mediated.
 The generation of local cytokines and proteolytic
enzymes within the joint, and cell signalling
pathways that link chondrocyte activity to
changes in the subchondral bone, synovium and
capsule
 Earlychanges in cartilage appear to result
from collagenase enzymes disrupting the
integrity of the type II collagen matrix which
encloses the hydrophilic proteoglycans,
leading to swelling and softening;
 subsequently, more proteolysis and damage to
proteoglycans, as well as collagen, results in the
fissuring and loss of volume.
 One of the problems ~ to detect it in its
earliest stages, before the pathology is
severe enough to become apparent on an X-
ray or be clinically relevant.

 It is not a degenerative process

 The term ‘degenerative joint disease’ should be
avoided
 Repair
of the pathological changes is less
common but can occur:
 joint repair in response to major mechanical
treatment interventions, such as osteotomy at
the knee, or mechanical unloading by use of
Ilizarov frames for ankle OA.
 The repaired OA joint is not normal, as the
hyaline articular cartilage is replaced by
fibrocartilage.
 Pain is the main clinical problem.
 there is a poor correlation between the
radiographic evidence of OA in joints
 The most common symptoms and clinical
signs reported by/seen in people with
clinical OA are documented in Box 5.2.
PAIN
 Dull ache after exercise
 Moderate ~ activity-related pain
 Excruciating continuous pain and pain at night.
 Severe pain that wakes the patient ~ debilitating
symptom  leads to sleep deprivation.
PAIN
 We do not know why OA sometimes causes
pain.
 No nocioceptive receptors in the cartilage,
 Nocioceptive pathways do occur in subchondral
bone, in periosteum and in the synovium and
capsule of the joint.
PAIN
 Once pain has become chronic ~
amplification pathways can be activated
locally and at both spinal and cortical levels,
leading to chronic and more widespread
pain, which is difficult to treat, particularly
if accompanied by mood changes.
 Anxiety and depression both affect the
perception of pain and its response to
interventions.
OTHER SYMPTOMS
 Stiffness, or gelling of the joint after
inactivity
 Difficulty getting moving after resting.
 Common in the early morning after first
awakening.
SIGNS
 The joints ~ swollen, wasting and weakness of
surrounding muscles
 As in quadriceps muscle wasting at the knee, or
 the Trendelenburg sign at the hip ~ signifies weakness
of hip abductors
 Joint deformity.
 Palpation ~ bony swelling at the margin of the
joint, signs of mild inflammation
 such as heat over the joint line, and an effusion.
 On movement ~ reduced range, with pain at the
end of the range, and crepitus
 instability may be detected.
 Joint pain may:
 be referred from above (e.g. hip OA causing knee
pain)
 be due to a periarticular problems
 come from the joint itself
 be due to central nervous system pain
sensitization (as in ‘fibromyalgia’)
 result from a complex mixture of the above.
 Routine investigations do not help.
 All blood tests ~ generally normal
 small rise in CRP levels
 ESR or CRP ~ useful in differentiating OA from
inflammatory forms of joint disease.
 Plainradiograph ~ joint changes
 MRI or scintigraphy ~ not routine to detect
pathophysiology.
 Pain, the main symptom of OA

 Forresearch purposes a number of

instruments are available to assess the
severity and impact of OA.
 ‘WOMAC’, Oxford hip, knee and shoulder scores,
Hip Dysfunction and Osteoarthritis Outcome
Score ‘HOOS’ (for hips), Knee Dysfunction and
Osteoarthritis Outcome Score ‘KOOS’ (for knees)
and the Australian–Canadian Hand Osteoarthritis
Index ‘AUSCAN’ (for hands)
 Semi-objective tests of function
 such as walking speed
 MRI ~ to assess the degree of joint damage
 Plain radiographs are so characteristic as to
make other imaging studies unnecessary.
 Four cardinal signs are osteophyte formation, joint
space narrowing, sclerosis of the underlying bone, and
subchondral bone cysts.
 Many different interventions are available
 Divided into symptomatic therapies and
disease-modifying therapies.
 There are no drugs with proven ability to modify
the disease process
 Disease modification can occur in response to
mechanical interventions, such as joint distraction and
osteotomy.
 All other interventions are symptomatic.
 The main symptoms of OA (pain, stiffness, fatigue,
and anxiety/depression) are very susceptible to so-
called ‘placebo’ and ‘nocebo’ effects.
 Placebo is generally thought of as a sham or dummy
intervention, and we know that sham surgery can work
well in OA,
 Symptoms of conditions such as OA are highly responsive
to the whole context in which any therapy is
administered.
 If patients and clinicians feel safe and trusting of each
other, and if the clinician is able to validate the
patient’s experiences (i.e. the patient feels fully
understood), then outcomes will be good, whatever the
intervention. And the opposite is also true.
SYMPTOMATIC THERAPY
 Figure 5.12 illustrates the basic principles of
the symptomatic management of OA.

 UK National Institute for Health and Care

Excellence (NICE) 2014 guideline CG177:
Osteoarthritis: Care and Management, which
recommends that clinicians follow the steps
described below.
SYMPTOMATIC THERAPY
 Step 1 Take a holistic approach and
encourage self-management.
 alterations of diet (particularly to lose weight),
 alteration in activities,
 changing footwear,
 taking a more positive approach to the condition
 exercising more.
SYMPTOMATIC THERAPY
 Step 2 Introduce the ‘core treatments’
appropriate for most people with OA.

 increase their exercise level and to do specific

exercises to strengthen muscles around affected
joints,
 footwear advice,
 weight loss for those who are obese.
SYMPTOMATIC THERAPY
 Step 3 Introduce specific non-surgical interventions.
 pharmacological or non-pharmacological.
 Non-pharmacological interventions of proven value
 physical therapy, the use of aids and devices to reduce
instability, walking aids such as sticks or crutches, some
electrotherapy techniques, such as TENS machines for pain
control
 Pharmacological options
 paracetamol, and topical NSAIDs
 Intra-articular local anaesthetic and corticosteroid injections
 hyaluronan injections
 Glucosamine and chondroitin are not recommended
because of lack of the lack of robust evidence to support
their use.
SYMPTOMATIC THERAPY
 Step 4 Consider surgical options.

 Joint realignment, joint fusion, joint excision and

joint replacement (arthroplasty), which may be total
or partial (such as unicompartmental knee
replacement).
 Joint debridement such as arthroscopic knee
debridement
 ~ usually confined to end-stage disease
 Hip and knee replacements ~ successful treatments
for advanced OA
 often resulting in complete resolution of pain and a
dramatic improvement in function and quality of life.