Arthritis and Joint Anatomy

ARTHRITIS
MOHD NUR HAZIQ BIN NOOR HAMIZAM SHAH

Arthritis
is a disorder of the joint characterized by pain, swelling
and limitation of movement.
Arthralgia
is pain of a joint, without any associated signs of
inflammation.
Essential Orthopaedics 4th edition

ANATOMY OF A
SYNOVIAL JOINT
ARTICULARCARTILAGE:
-‐ Covered by Hyaline
cartilage.
-‐ Covers weight-‐bearing
surfaces of bones.
-‐ Transmits load
uniformly to bone.
-‐ Decreasesfriction
https://www.orthobullets.com/basic-science/9017/articular-cartilage?expandLeftMenu=true

• ARTICULAR CARTILAGE:
composedof -‐
1. Extracellular matrix
2. Cells
Extracellularmatrix
- matrix of proteogylcans, collagen &
glycoproteins
- makes up the dry weight
- mainly type II collagen & proteoglycan
- provides compressive and tensile strength
- atracts and retains water incartilage
Water
- about 65‐80%of the cartilage mass
- Distribute nutrients to chondrocytes
-providing lubrication
Condrocytes
• produce collagen, proteoglycans and
enzyme
• derive from chondroblasts that are
trapped in lacunae and become
chondrocytes.
Sophia Fox, A. J., Bedi, A., & Rodeo, S. A. (2009). The basic science of articular
cartilage: structure, composition, and function. Sports health, 1(6), 461-468.

ARTICULAR CARTILAGE:nutrition-‐
-‐ Articular cartilage is avascular and
aneural tissue.
-‐ Nourished by diffusion from
synovial fluid at surface
-‐ Nourished by subchrondal bone at
the base
SYNOVIUM:
-‐ Lining the cavity of the joint
-‐ Highly vascularized structure
-‐ Produces synovial fluid responsible
for nutrition and lubrication
-‐ Synovial fluid rich in hyaluronin
and lubricin
CAPSULE &LIGAMENTS:
-‐ The tough fibrous material that covers the entire joint
-‐ Stabilizers of joints
-‐Prevent excessive movement in a joint
-‐Have mechanoreceptors and free nerve endings that help with joint proprioception
https://www.orthobullets.com/basic-science/9016/ligaments?expandLeftMenu=true

OSTEOARTHRTIS
• A chronic jointdisorder in which there is
progressive softening and disintegration of
articular cartilage accompanied by new growth
of cartilage and bone at the joint margins and
capsular fibrosis.
Apley's System of Orthopaedics. and Fractures, Ninth Edition

• Cardinal features are:
1. Progressive loss of articular cartilage thickness
2. Subarticular cyst formation and sclerosis
3. Remodelling of the bone ends and osteophytes formation
4. Synovial irritation
5. Capsular fibrosis
OA is a dynamic phenomenon, which involves both destruction and
repair
PATHOPHYSIOLOGY

Softening of the articular cartilage (normally smooth and glistening surface
become frayed and fibrillated)
Articular cartilage worn away and expose the underlying bone
Subarticular bone changes (attempts to remodel)
High stress area – cyst appear and surrounding trabecular thickened or sclerotic,
vascular congestion and increased intraosseous pressure rise
Low stress area – cartilage proliferate and ossifies producing bony outgrowth
(osteophytes)
Shedding of the fibrilated articular cartilage as well as release of enzyme from
damaged cells lead to synovitis
Later stage, capsular fibrosis lead to joint stiffness

PREVALENCE & RISK FACTORS
• Patients usually present after middle
age, though cartilage changes start
10 - 20 years before.
• Most affectedjoints:
– Knee
– Hip
– Hand
– Spine

RISK FACTORS
• Non-modifiable
• • Advancing age
• • Female
• • Genetic influence on hand and knee OA in women
• Heberden’s nodes in hand
• Modifiable
• Previous knee injury/articular trauma
• Occupation, repetitive knee bending
• Muscle weakness
• BMI >25kg/m2
CPG Management of Osteoarthritis ( Second Edition) 2013

CLASSIFICATION
PRIMARY
No identifiable cause.
A diagnosis by exclusion.
SECONDARY
Has an identifiable cause.
-‐Dysplastic joint.
-‐Trauma/ Infection/
Inflammatory arthritis.
MONO/PAUCI-‐ARTICULAR-‐
Involves only1-‐2joints.
-‐Large weight-‐bearingjoints. (hip,
knees)
-‐Has an underlying bone
dysplasia.
POLYARTICULAR-‐Multiplesmall
jointsinvolved.
eg: hands, MTP, knees, lumbar
facet

SYMPTOMS
• JOINT PAIN
– Insidious onset
– intermittent & relapsing
– increased by joint use & impact
– relieved by rest
– night pain in severe OA
• Stiffness
– due to due to capsular fibrosis, muscle spasms
– only last a few minutes; always < 30minutes
– usually occurs after inactivity

• Swelling
– with or without associated warmth & loss of function
– Bony swelling: in hand OA, hypertrophic bone formation in the IP joint may
result in reduced dexterity & difficulty in performing fine movements such
as sewing
– OA of the first CMC joint may result in writing difficulties
• Gait disturbance
– on weight-bearing joints (hip/knee)
– can produce a prominent limp
– impaired function of a weight-bearing joint will cause added stress on the
contralateral weight-bearing joint e.g. a patient with impaired right knee
function & pain will have difficulty with the left hip & vice versa

• Loss of muscle bulk
– inactivity secondary to pain, may lead to significant
weakness & loss of quadriceps muscle bulk
• Limb deformity
– knock knees’ (valgus) or ‘bowing’ (varus)
• Clicking/ grinding sensation
– clicking or grinding sensation with joint motion
resulting in discomfort or pain
• Instability
– instability in the knee or hip may cause the patient to
seek assistance in ambulation e.g. using a cane or
crutch

SIGNS OF OA
– Look
• Alignment,symmetry
• Muscle wasting
• Swelling
• Scar
• Deformities (Heberden’s
nodes, Bouchard’s
nodes, genu varus,genu
valgus)
• Gait
– Feel
• Tenderness
• Warmness
• Jointeﬀusions
• Crepitus
– Move
• Limited joint
movement
• Locking

• SWELLING-
• Fluctuant (effusion)-‐ fluid shift/ patella tap/
fluid thrill.
• Doughy (synovial hypertrophy).
• Hard immobile (osteophytes).
DEFORMITY-‐HAND-‐
Heberden’s nodes/
Bouchard’s nodes.

DIAGNOTIC CRITERIA
• The diagnostic criteria for classification of OA
are based on the American College of
Rheumatology (ACR) criteria

KNEE OA
• can also be diagnosed using evidence based
recommendations by European League
Against Rheumatism (EULAR) 2010

• In the presence of 3/10 at least 1 point from Domain
II along with all entry criteria, the diagnosis of Knee
OA can be established
2016 ACR REVISED CRITERIA FOR EARLY DIAGNOSIS OF KNEE OA
http://aperito.org/uploads/pdf/ADTAOA-3-118.pdf

INVESTIGATIONS
• Diagnosis of OA is mainly clinical
• Blood investigations - ESR/CRP normal
• Synovial fluid analysis - normal & seldom
required except to exclude septic,
inflammatory & crystal arthropathy
• Plain radiography is the investigation of choice
– should be done in weight bearing position

PLAIN RADIOGRAPH
• Classical features of OA
– narrowed joint space
– subchondral bone
sclerosis
– osteophytes
– subchondral cysts

MANAGEMENT
• NON-PHARMACOLOGICAL TREATMENT
– Patient Education
• nature of the disease
• therapeutic options
• importance of patient participation
– Lifestyle Modification
• weight loss programs
• exercise
– Physiotherapy
– Occupational Therapy
– Orthoses

Physiotherapy:
– improve muscle strength, balance, coordination and joint
mobility
TENS: Trancutaneous Electrostimulation
• patients with chronic moderate to severe pain who are not suitable
for total knee arthroplasty. (ACR 2012)
OCT:
– To improve health, prevent disability & help individuals to
achieve their optimum functional level & independence in
performing ADL
– Joint protection exercises, splinting, assistive devices (walking
stick, tap turners)

PHARMACOLOGICAL
• Oral medication
• Simple analgesics – paracetamol (acetaminophen)
• Weak opioid analgesics – tramadol (combined with pcm or nsaids)
• NSAIDs and COX-2 Inhibitors (diclofenac, celecoxib)
• Nutraceutical - glucosamine, chondroitin, diacerein
• Intraarticular injections
• Steroids – for short term pain relief
• Viscosupplementation – to replace hyaluronic acid in joints,
controversial
• Topical cream
• NSAIDS and LMS cream

SURGICAL MANAGEMENT
• Considered if symptoms are significant:
– Pain
– Limitation of ADL
– Psychosocial health (psychological well being)
– Economic impact
– Recent deterioration

OPERATIVE
• Arthroscopic surgery
– indicated in patients with OA associated with
mechanical symptoms such as locking, catching or
giving way of the joint caused by presence of loose
bodies or flaps of meniscus or cartilage
• High Tibial Osteotomy
• Total Joint Replacement
• Partial Joint Replacement
• Arthrodesis

- Osteotomised at its upper end and repositioned
- To realign the mechanical axis of the limb away from the diseased area
- Allows the joint to glide freely and distribute weight evenly
In isolated medial compartment knee OA or varus malalingment
• <50 years old
• Good knee ROM (>120⁰)
• Realign to correct mechanical axis
• Load distributed more on normal knee compartment
High Tibial Osteotomy

ARTHROPLASTY
-‐ Replacing the joint with implant
-‐ Results in dramatic reduction of pain and
-‐ Causes significant improvement in ADL
-‐ Active infection is absolute contraindication
INDICATIONS FOR JOINT REPLACEMENT
• Pain
• Severe disability
• Deformity
• Limited function (ADL)
• Fail conservative treatment

ARTHRODESIS
• Surgical fusion of the involvedjoint in optimal
position
• Provides pain relief &stability despite stiff joint
Indications:
• Young active labourer with
unilateral painful OA
• Severe OA with combined
ligamentous injury
• Uncontrolled septic arthritis &
complete joint destruction
• Failed and/or infected
arthroplasty
Advantages:
• Stable pain free knee allowing
long-term ambulation
Disadvantages:
• Stiff joint
• Abnormal gait after surgery
• Late back pain
• Conversion to TKR or THR give
unpredictable result

(a)High Tibial Osteotomy.
(b)Arthroplasty.
(c)Arthrodesis.

RHEUMATOID ARTHRITIS
• Rheumatoid arthritis (RA) is a chronic
inflammatory disease characterized by joint
swelling, joint tenderness, and destruction of
synovial joints, leading to severe disability and
premature mortality
Aletaha, D., Neogi, T., Silman, A. J., Funovits, J., Felson, D. T., Bingham, C. O., ... & Combe, B. (2010). 2010
rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against
Rheumatism collaborative initiative. Arthritis & Rheumatology, 62(9), 2569-2581.

RISK FACTORS
1. Gender
Women are affected 3 times more often than men
2. Genetic factors
Human Leucocyte Antigen (HLA)- DR4 and HLA-DR1
confer susceptibility to RA and are associated with
development of more severe erosive disease
3. Agents such as mycoplasma, clostridium and EB
virus

Exposure of genetically predisposed individual to infectious agent
Formation of immune complexes with IgM antibodies in the serum
Immune complexes deposited in synovial membrane and initiate
chronic granulamatous inflamation
Synovium is edematous and filled with fibrin exudates and cellular
infiltrates
Synovium becomes hypertrophied and has effusion (reversible)
Synovium surrounds articular cartilage to form pannus which cause
reduction in joint space, early cartilage erosions and soft tissue
destruction
(controllable but irreversible)
Pannus ultimately destroys articular cartilage, burrows into the
subchondral bone to erode it (irreversible)
Fibrous ankylosis and joint deformity
Essential Orthopaedics 4th edition

CLINICAL FEATURES
Symptoms
• insidious onset
• morning stiffness >1 hour
• polyarthropathy
• usually affects hands and feet
– (DIP joint of hand is usually
spared)
• may also affect other joints
https://www.orthobullets.com/basic-science/9085/rheumatoid-arthritis

ARTICULAR SIGNS
• Red, warm, tender and swollen small joints of the
hands and feet, excluding DIP, first MTP, and first
CMC joint.
• Symmetrical
• Polyarthritic.
Atlas of rheumatoid arthritis 2015

Rheumatoid nodulesPIP Swelling

Forefoot
-Hyperpronation of
rheumatoid foot
-Metatarsalgia
-Claw toes
-Hallux valgus
Midfoot
-Talonavicular arthritis
-Midfoot hyperpronation
Hindfoot
-Calcaneovalgus

EXTRA-ARTICULAR MANIFESTATION
• Systemic symptoms
• fever
• fatigue
• malaise
• weight loss
• Musculoskeletal
• osteoporotic #
• tenosynovitis and
bursitis
• rupture of tendons &
ligaments
Face and neck
-Mouth dryness
-Atlanto axial
subluxation
Eyes
-Conjuctival pallor
-Schirmer’s filter paper
test
-Episcleritis
-Scleritis
-Cataracts
-Keratoconjuctivitis
sicca
Chest
-Pericardial rub +-
effusion
-Myocarditis
-Pleural rub +-
effusion
-Fine crepitus
-Vasculitis
Abdomen
-Splenomegaly
Legs
-Mononeuritis
multiplex

DIAGNOSTIC
CRITERIA
JOINT DISTRIBUTION (0-5)
1 large joint 0
2-10 large joints 1
1-3 small joints (large joints not counted) 2
4-10 small joints (large joints not counted) 3
>10 joints (at least one small joint) 5
SEROLOGY (0-3)
Negative RF AND negative ACPA 0
Low positive RF OR low positive ACPA 2
High positive RF OR high positive ACPA 3
SYMPTOM DURATION (0-1)
<6 weeks 0
≥6 weeks 1
ACUTE PHASE REACTANTS (0-1)
Normal CRP AND normal ESR 0
Abnormal CRP OR abnormal ESR 1
2010 ACR/ EULAR
CLASSIFICATION CRITERIA
≥6 = Definite RA
Aletaha, D., Neogi, T., Silman, A. J.,
Funovits, J., Felson, D. T., Bingham, C. O.,
... & Combe, B. (2010). 2010 rheumatoid
arthritis classification criteria: an
American College of
Rheumatology/European League Against
Rheumatism collaborative
initiative. Arthritis &
Rheumatology, 62(9), 2569-2581.

Definition of “JOINT INVOLVEMENT”
- Any swollen or tender joint (excluding DIP
of hand and feet, 1st MTP, 1st CMC)
- Additional evidence from MRI / US may be
used for confirmation of the clinical findings
Definition of “SMALL JOINT”
MCP, PIP, MTP 2-5, thumb IP, wrist
NOT: DIP, 1st CMC, 1st MTP
Definition of “LARGE JOINT”
Shoulder, elbow, hip, knee, ankles
Definition of “>10 JOINTS”
- At least one small joint
- Additional joints include:
temporomandibular, sternoclavicular,
acromioclavicular, and
others (reasonably expected in RA)
Definition of “SEROLOGY”
Negative: ≤ULN (for the respective lab)
Low positive: >ULN but ≤3xULN
High positive: >3xULN
Definition of “SYMPTOM DURATION”
Refers to the patient’s self-report on the
maximum duration of signs and
symptoms of any joint that is clinically
involved at the time of assessment.

Subchondral
erosion
Periarticular
osteopenia
Reduced
joint space

Useful for diagnosis
• normochromic normocytic
anaemia
• elevated ESR
• elevated CRP
• anti-CCP (most sensitive &
specific)
• positive RF titer
• elevated in 75-80% of
patients with RA
• joint fluid testing
• decreased complement
• may have elevated RF levels
Useful for differential diagnosis
• serum uric acid
• antinuclear antibodies
Useful to detect complications
• chest xray
Investigations for follow up and
treatment
• ESR
• FBC
• RP
• LFT
• Chest xray

Categories of Synovial Fluid Based upon Clinical and Laboratory Findings
There is no single diagostic test for RA. Investigationsare used largely to support clinical
diagnosis and negative results does not exclude the diagnosis of RA.

MANAGEMENT
• Principle of treatment
• Induction of remission and it’s maintenance: disease
activity is brought under control by drugs
• Preservation of joint functions and prevention of
deformities during the activity of the disease and
thereafter, by physiotherapy and splinting
• Repair of joint damage which already exists, if it will
relieve pain or facilitate functions

TREATMENT MODALITIES FOR RA
• NSAIDS
• Steroids
• DMARDs
• Biological therapies
• Surgery
• Physiotherapy
• Occupational therapy
• Rehabilitation

• Treatment with DMARD should be initiated as soon as a
diagnosis of RA is made, with the aim of reaching a target
of remission or low disease activity
• EULAR recommends rheumatologists administer
methotrexate (MTX) or combination therapy of MTX with
other conventional synthetic DMARDs.
• Low-dose glucocorticoids should also be considered in
combination with DMARDs for up to six months, but should
be tapered as soon as clinically feasible
EULAR 2013 Rheumatoid Arthritis Management Recommendations, EULAR Data on File, 2013.

SURGERY
Preventive surgery:
– To prevent damage to the joint and nearby tendons by the inflamed,
hypertrophied synovium. It consists of synovectomy of the wrist, knee
and MP joints
Palliative surgery :
– Done in situations where condition of the patient doesn’t permit
corrective surgery, but some relief can be provided by bone block
operations or tendon lengthening
Reconstructive surgery :
– This has revolutionised the rehabilitation of patients with deformed and
painful joints. It includes tendon transfers and total joint replacement.

SEPTIC ARTHRITIS
Septic arthritis refers to infection in a joint; it is
usually caused by bacteria but can be caused by
fungi or mycobacteria.
https://www.uptodate.com/contents/septic-arthritis-in-adults

RISK FACTORS
Adults:
• Age > 80 years
• Medical conditions
• diabetes
• rheumatoid arthritis
• cirrhosis
• HIV
• History of crystal arthropathy
• Endocarditis or recent
bacteremia
• IV drug user
• Recent joint surgery
Neonates:
• Prematurity
• Cesarean section
• Patients treated in the NICU
• Invasive procedures leading to
transient bacteremia
https://www.orthobullets.com/trauma/1058/septic-arthritis--adult?expandLeftMenu=true

PATHOPHYSIOLOGY
Routes of inoculation
Direct inoculation from
trauma or surgery
Hematogenous seeding
(bacteremia)
Extension from adjacent bone
(osteomyelitis)

a) In the early stage, there is an acute synovitis with a purulent joint effusion
b) Soon the articular cartilage is attacked by bacterial and cellular enzyme.
c) If infection is not arrested , the cartilage may be completely destroyed
d) Healing then leads to ankylosis

If left untreated, it will spread to the
underlying bone
and out of joint to form abscess and sinus.
Healing with:
1.Complete resolution
2.Partial loss of articular cartilage and fibrosis of
joint
3.Loss of articular cartilage and bony ankylosis
4.Bony destruction and permanent deformity

PHYSICAL EXAMINATIONS
• i)Temp. and vital signs
• Fever
• ii)Look
• Localized swelling and erythema
• Affected joint lies in a position of
ease
Joint Position of ease
Shoulder Adduction, internal rotation
Elbow Flexion, mid pronation
Wrist Flexion
Hip Flexion, abduction, ext rotation
(FABER)
Knee Flexion
Ankle Plantar-flexion
iii) Feel
Effusion
Warm to touch
Tenderness
iv) Move
Severe pain with passive
motion
Unwillingness to move joint
(pseudoparalysis)

INVESTIGATION
1. WBC raised (>10k with left shift)
2. ESR raised (>30)
• ESR is often elevated but may be normal early in process
• rises within 2 days of infection and can rise 3-5 days after initiation of
appropriate antibiotics, and returns to normal 3-4 weeks
3. CRP raised (>5)
• best way to judge efficacy of treatment, as CRP rises within few hours
of infection, and may normalize within 1 week of treatment
4. Joint aspiration (gold standard)
– should be analyzed for
• cell count with differential
• gram stain
• culture
• glucose level
• crystal analysis

More than 50k is considered diagnostic

5. USG (most reliable)
-widening of space between capsule and bone >2mm
-able to confirm effusion in large joint such as hip
-can be used in guiding aspiration
6. X-ray (AP & lateral of the joint, or frog leg lateral pelvic
xray in paeds)
-normal in early stages
-widening of radiographic joint space or effusion
-subluxation or dislocation
-bone lesions (assc. osteomyelitis)
7. MRI
-detects effusion and also adjacent bone
involvement
-helpful in determining operative treatment

MANAGEMENT
1. URGENT surgical I&D
2. IV Antibiotics
• Initiate empiric therapy prior to C&S based on age and risk
factors
• Transition to organism specific antibiotics after cultures obtained
• Monitor efficacy of treatment using WBC, ESR and CRP
• Paeds: Penicillinase-resistant penicillins+ 3rd generation
cephalopsporins
• Adults: Cloxacillin, or Flucloxacillin and Furisidic acid
3. Analgesia
4. Splintage: joint rested

Arthritis and Joint Anatomy

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