•OSTEOARTHRITIS

ARTHRITI •GOUTY ARTHRITIS

DES •RHEUMATOID ARTHRITIS
•SEPTIC ARTHRITIS
OSTEOARTHRITIS
OSTEOARTHRITIS (OA)

 Progressive non inflammatory

joint failure disease in which all
structures of the joint have
undergone pathologic change.
 Joint injury in the setting of a
failure of protective mechanisms.
Types of OA

•Primary OA
• joint de novo
• old age, mainly in weight bearing joints
• more common

•Secondary OA
• underlying primary disease of the joint which leads to degeneration of the joint
• any age after adolescence, mainly in hip
• Predisposing factors:
• congenital maldevelopment of a joint
• irregularity of the joint surfaces from previous trauma
• previous disease producing a damaged articular surface
• malalignment
• obesity
Epidemiology and Risk factors

• most common type of arthritis

• prevalence correlates with age ;
uncommon in <40 and highly
prevalent in >60
• F>M
• joint susceptibility and joint
loading
• influenced by
• Systemic factors
• Local factors
• Loading factors
 Genetic anomalies in
Single large traumatic
cartilage production and
event, repeated Obesity
inborn errors of cartilage
microtrauma
metabolism

Damage to normal
articular cartilage Failure of abnormal Failure of normal cartilage
under normal cartilage under normal joint under abnormal loading
loading loading

Destruction of articular cartilage

Osteoarthritis (weight bearing joints,

PIP, DIP CMC joints in the hand)
•Events following hyaline articular
cartilage loss
• increasing thickness and sclerosis
of the subchondral bone plate
• outgrowth of osteophytes at the
joint margin
• stretching of the articular capsule
• weakness of the muscles bridging
the joint
Clinical Symptoms
manifestations • Use-related pain affecting one or a few joints
(rest and nocturnal pain less common)
• weight-bearing and frequently • Stiffness after rest or in morning may occur
used joints but is usually brief (<30 min)
• hand joints: DIP, PIP, first • Loss of joint movement or functional
carpometacarpal limitation
• Wrist, elbow, ankle – not • Joint instability
affected
• Joint crepitation (“crackling”)
Physical examination

• Chronic monarthritis or asymmetric oligo/polyarthritis

• Firm or “bony” swellings of the joint margins
Heberden’s nodes or Bouchard’s nodes
• Deformity
medial, lateral, or patellofemoral compartments → varus or
valgus deformities
• Objective neurologic abnormalities may be seen with spine
involvement

Varus - stress is placed across the medial compartment of

the knee joint
Valgus - which places excess stress across the lateral
compartment of the knee
Diagnostics
• Diagnosis is usually established on basis of pattern of joint
involvement.
• Plain radiography
-diagnosis of osteoarthritis is mainly radiological AP and Lateral views, showing osteoarthritis of the knee

-may be normal at first but as disease progresses may

show joint space narrowing, subchondral bone
sclerosis, subchondral cysts, and osteophytes.
-Erosions occur subchondrally along the central portion
of the joint surface.

X-ray of knee with medial osteoarthritis.

• Laboratory investigations:
-Routine lab work usually normal.
-ESR usually normal, may be elevated in patients who have synovitis
-Rheumatoid factor, ANA studies negative.
-Joint fluid is straw-colored with good viscosity; fluid WBCs <1000/μL; of value in ruling out
crystal-induced arthritis, inflammatory arthritis, or infection.
Management

Goal: alleviate pain and minimize loss of physical function

• Non pharmacotherapy:
-aimed at altering loading across the painful joint and improving the function of joint protectors
 include patient education
 weight reduction
 appropriate use of cane and other supports
 isometric exercises to strengthen muscles around affected joints
 bracing/orthotics to correct malalignment
• Pharmacotherapy:
-oral, topical, intraarticular

 Acetaminophen – initial analgesic of choice, caution regarding hepatic toxicity

 Oral NSAIDs, COX-2 inhibitors - GI, renal, cardiovascular toxicity, must weigh individual risks and benefits.

 Intraarticular injections:
 Glucocorticoids - may provide symptomatic relief but typically short-lived.
 hyaluronans – can be given for symptomatic knee and hip OA, but it is controversial whether it has efficacy
beyond placebo

 Topical:
 capsaicin cream
 NSAIDs - fewer GI and systemic side effects; can cause skin irritation

 Opioid analgesics - considered in selected patients whose symptoms are inadequately controlled with other
measures and who cannot undergo surgery
• Surgery – if the OA fails to respond to a medical management plan
 Osteotomy
-for active patients <60 y/o who has knee OA isolated to medial compartment
-high tibial osteotomy : tibia is broken just below the tibial plateau to shift the weight to healthy
lateral aspect of the knee

 Arthroplasty
-surgical removal of joint surface and insertion of a metal and plastic prosthesis
high tibial osteotomy
GOUTY ARTHRITIS
GOUT

• Monosodium urate  acute arthritis

• middle-aged to elderly men; postmenopausal women
• Filipinos (1.6% prevalence)
• adult men (4:1)
• Females: less dramatic; secondary
PATHOPHYSIOLOGY
CLINICAL FEATURES

• Classical features an acute attack fo

gout:

• Pain that suddenly appears in 12-24

hours

• overnight (metabolic changes)

• Skin over affected joint is red-

purplish, tight and shiny

• Recurrent attacks in single episode

• fever, chills, malaise, tachycardia

• One to two joints

• Podagra or pain in the first MTP

joint (the classic presentation)
 CLINICAL FEATURES
FOUR STAGES
• Asymptomatic hyperuricemia
• Acute gouty arthritis (the gout flare)
• Intercritical (or interval) gout
• Chronic tophaceous gout
FACTORS THAT OFTEN TRIGGER AN ACUTE
ATTACK:
• Injury
• Surgery
• Withdrawal of steroids
• Vascular disturbance
• Consumption of large quantities of alcohol
• Disturbed electrolyte imbalance
• Decreased urinary 17-ketosteroid
• Consumption of large quantities of purine rich foods
• Fatigue
• Emotional stress
• Illness
PREDISPOSING FACTORS FOR CHRONIC
TOPHACEOUS GOUT
• Genetic predisposition
• Obesity
• Hypothyroidism
• Cancers and blood disorders
• Alcohol abuse
• Duration of hyperuricemia
• Starvation
• Renal failure
• High intake of purine containing food
• Lead poisoning
• Radiation treatment
• Age
• Pharmacologic agents
DIAGNOSIS
• American College of Rheumatology - 11 criteria
• Presence of six or more of the following:
1. More than one attack of active arthritis
2. Maximum inflammation develops within one day
3. Oligoarthritis attack
4. Redness observed over joint
5. First MTP joint painful or swollen
6. Unilateral first MTP joint attack
7. Unilateral tarsal joint attack
8. Tophus (proven or suspect)
9. Hyperuricemia
10.Asymmetrical swelling within a joint on radiography
11.Complete terminal of an attack
LABORATORY

• Needle aspiration of involved joint or tophaceous deposits

• Synovial fluid leukocyte counts
• Serum uric acid levels
• Serum urate levels
• 24-hr urine collection for uric acid
• Others: urinalysis, serum crea, hemoglobin, WBC count, liver function tests and lipids
RADIOLOGY

• exclude other causes

• cystic changes, well-defined erosions with sclerotic margin, and soft tissue masses
• Ultrasound: double contour sign
• Dual-energy CT
 MANAGEMENT
Phase 1: Asymptomatic Hyperurecemia
• Asymptomatic hyperurecemia should not be routinely treated with allopurinol. Well-
known associated risk factors of hyperuricemia should be addressed.
• Lifestyle changes recommended include the following:

Adherence to animal or vegetable protein diet as well as intake of dairy products is

recommended.

Avoidance of a high meat and seafood diet and alcoholic beverages most especially
beer should be prescribed.

Low impact and aerobic exercise at least 45 mins 4 times a week, intake of at least 8
glasses of water per day, and maintenance of appropriate BMI, are likewise advised.

Philippine Clinical Practice Guidelines for the Management of Gout 2008

 MANAGEMENT
Phase 2: Acute Gout
• In the absence of contraindications, the use of colchicine, traditional NSAIDs, or COX-2
inhibitors is recommended for the treatment of acute gouty arthritis.

Colchicine should not exceed 4 tablets in divided doses per day.

Prednisone, initially at 30 mg and rapidly tapered over 6 days, can be given as

alternative if colchicine, traditional NSAIDs or COX-2 inhibitors are contraindicated
or not tolerated by the patient.

Absence of response after a week should prompt reevaluation of the diagnosis and
referral to a rheumatologist.
• Ice compress is recommended in combination with pharmacologic agents for relief of
joint pain and swelling of acute gouty arthritis.

Philippine Clinical Practice Guidelines for the Management of Gout 2008

 MANAGEMENT
Phase 3-4: Intercritical and Chronic Tophaceous Gout
• Serum uric acid (SUA) levels should be reduced to and maintained at
<6 mg/dl (0.36 mmol/L).
• Continuous long-term therapy with allopurinol is advised to achieve a
target serum uric acid level of <6 mg/dl.
• Allopurinol should be started at 100 mg/day 2 weeks after the pain
and swelling of gouty arthritis has subsided. The dose is titrated by
50-100 mg/day every 2-4 weeks to achieve serum uric acid <6 mg/dl.
• Max. dose: 300 mg/day. Refer to Rheumatologist if SUA persistently remains
>6 mg/dl despite max. dose

Philippine Clinical Practice Guidelines for the Management of Gout 2008

 MANAGEMENT
Phase 3-4: Intercritical and Chronic Tophaceous Gout
• Colchicine should be used at 0.5 mg/tab OD-BID to prevent gout
flares when initiating allopurinol. This should be maintained for 3-6
months from the last occurrence of gout flare and after the optima
SUA target is achieved. In the event that adverse events like diarrhea
occur, a lower dose of colchicine should be used. NSAIDs should not
be used for prevention of gout flares.
• Dietary modification and avoidance of alcohol should be prescribed.
• Low impact exercises (walking, biking, swimming, ballroom dancing)
may also be advised.

Philippine Clinical Practice Guidelines for the Management of Gout 2008

RHEUMATOID
ARTHRITIS
RHEUMATOID ARTHRITIS

• Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of unknown etiology

whose hallmark feature is a persistent symmetric polyarthritis (synovitis) that affects the
hands and feet.
• Any joint lined by a synovial membrane may be involved, however, and extra-articular
involvement of organs such as the skin, heart, lungs, and eyes can be significant.
• RA is theorized to develop when a genetically susceptible individual experiences an external
trigger (eg, cigarette smoking, infection, or trauma) that triggers an autoimmune reaction.
EPIDEMIOLOGY, GENETIC, ENVIRONMENTAL
FACTORS
• Female > Male (2-3:1)
• RA increases between 25 and 55 years of age, after which it plateaus until the age of 75 and then
decreases
• 1st degree family history 2-10x affected
• Mostly associated with allelic variation in the HLA-DRB1 gene, which encodes the MHC II β-chain
molecule.
• Genes other than those of the major histocompatibility complex (MHC) are also involved. Results
from sequencing genes of families with RA suggest the presence of several resistance and
susceptibility genes, including PTPN22, PAD14,CTLA4 and STAT4
• Cigarette smoking
• Infectious etiology
Mycoplasma, Epstein-Barr virus, cytomegalovirus, parvovirus and rubella virus have all
been suggested, but mechanism is undefined.
CLINICAL MANIFESTATIONS

Joint Involvement

• Initially involves small joints of hands and feet

• May be monoarticular, oligoarticular (≤4 joints), or polyarticular (>5 joints)
• Early morning stiffness >1 hour easing with physical activity
• Most frequently involved joints: wrists, MCP, PIP (DIP involvement usually a sign of coexistent OA)
• Swan neck deformity: hyperextension of the PIP with flexion of the DIP joint
• Boutonniere deformity: flexion of the PIP with hyperextension of the DIP joint
• Z-line deformity: subluxation of the first MCP with hyperextension of 1st IP joint
• Flexor tendon tenosynovitis: frequent hallmark of RA. Leads to decreased range of motion,
reduced grip strength, and “trigger” fingers
Flexor tendon tenosynovitis
• Chronic inflammation of the ankle and midtarsal regions comes later and may result to:
 Pes planovalgus - “flat feet”
• Atlantoaxial involvement of the cervical spine
 Cause compressive myelopathy and neurologic dysfunction
 Neurologic manifestations are rare but may evolve over time with progressive
instability of C1 on C2
DIAGNOSIS

The clinical diagnosis of RA is largely based on signs and symptoms of a chronic

inflammatory arthritis, with laboratory and radiographic results providing important
corroborating information.
• The new criteria include as an item a positive test for serum anti-CCP antibodies (also
termed ACPA, anti-citrullinated peptide antibodies), which carries greater specificity for the
diagnosis of RA than a positive test for RF.

• The newer classification criteria also do not take into account whether the patient has
rheumatoid nodules or radiographic joint damage because these findings occur rarely in
early RA.

• The presence of radiographic joint erosions or subcutaneous nodules may inform the
diagnosis in the later stages of the disease.
 DIAGNOSTIC TESTS

Serum Markers

• Patients with systemic inflammatory diseases such as RA will often present with elevated
nonspecific inflammatory markers such as an ESR or CRP
• Detection of serum RF and anti-CCP antibodies is important in differentiating RA from other
polyarticular diseases, although RF lacks diagnostic specificity and may be found in
association with other chronic inflammatory diseases in which arthritis figures in the clinical
manifestations.
• The presence of serum anti-CCP antibodies has about the same sensitivity as serum RF for
the diagnosis of RA. However, its diagnostic specificity approaches 95%, so a positive test
for anti-CCP antibodies in the setting of an early inflammatory arthritis is useful for
distinguishing RA from other forms of arthritis.
Synovial Fluid Analysis

• Synovial fluid white blood cell (WBC) counts can vary widely, but generally range between
5000 and 50,000 WBC/μL with Predominance of neutrophil compared to <2000 WBC/μL for
a noninflammatory condition such as osteoarthritis.

• Clinically, the analysis of synovial fluid is most useful for confirming an inflammatory arthritis
(as opposed to osteoarthritis), while at the same time excluding infection or a crystal-induced
arthritis such as gout or pseudogout.
Joint Imaging
• Joint imaging is a valuable tool not only for diagnosing RA, but also for
tracking progression of any joint damage. Plain x-ray is the most common
imaging modality.
Plain Radiography
• Classically in RA, the initial radiographic finding is periarticular osteopenia.
Practically speaking, however, this finding is difficult to appreciate on plain
films and, in particular, on the newer digitalized x-rays. Other findings on plain
radiographs include soft tissue swelling, symmetric joint space loss, and
subchondral erosions, most frequently in the wrists and hands (MCPs and
PIPs) and the feet (MTPs).
MRI

• MRI offers the greatest sensitivity for detecting synovitis and joint effusions, as well as
early bone and bone marrow changes. These soft tissue abnormalities often occur
before osseous changes are noted on x-ray.

Ultrasound

• Ultrasound, including power color Doppler, has the ability to detect more erosions than
plain radiography, especially in easily accessible joints. It can also reliably detect
synovitis, including increased joint vascularity indicative of inflammation.
CLINICAL COURSE

• Naturally history depends on the following: age of onset, gender, genotype, phenotype and
comorbid conditions
• 10% of patients with inflammatory arthritis will undergo a spontaneous remission within 6
months
• Gradual worsening of disability if with poorly controlled disease activity and disease
progression
• Ischemic heart disease being the most common cause of death followed by infection
• Median life expectancy is shortened by an average of 7 years for men and 3 years for
women
• Low survival rates: systemic extraarticular involvement, low functional capacity, low
socioeconomic status, low education, and chronic prednisone use
MANAGEMENT

NSAIDS
• Formerly viewed as the core of all other RA therapy
• Now viewed as adjunctive agents for management of symptoms uncontrolled by other measures.
• Chronic use should be minimized
• side effects, including gastritis and peptic ulcer disease as well as impairment of renal function

Glucocorticoids
• Low-moderate doses for rapid disease control before the onset of fully effective DMARD therapy
1- to 2-week burst of glucocorticoids for acute disease flares
• Long-term complication of chronic prednisone use = osteoporosis
Disease-Modifying Anti-
Rheumatic Agents (DMARDS)
• Slow or prevent structural
progression of RA
• Cornerstone of therapy
• They exhibit a delayed onset of
action of approximately 6-12
weeks
Biologics
Protein therapeutics designed mostly to target cytokines and cell-surface
molecules. Share the common adverse effect of a potentially increased
risk for infection
SMALL-MOLECULE INHIBITORS

• Tofacitinib is a small-molecule inhibitor that primarily inhibits JAK1 and JAK3, which mediate signaling
of the receptors for the common γ-chain-related cytokines IL-2, 4, 7, 9, 15, and 21 as well as IFN-γ
and IL-6.
• These cytokines all play roles in promoting T and B cell activation as well as inflammation.
TREATMENT OF EXTRAARTICULAR
MANIFESTATIONS
• In general, treatment of the underlying RA favorably modifies extraarticular manifestations, and it
appears that aggressive management of early disease can potentially prevent their occurrence in the
first place.
• RA-ILD, however, can be particularly challenging to treat because some of the DMARDs used for the
treatment of RA are associated with pulmonary toxicity, such as methotrexate and leflunomide. High
doses of corticosteroids and adjunctive immunosuppressive agents, such as azathioprine,
mycophenolate mofetil, and rituximab have been used for treatment of RA-ILD.
SEPTIC ARTHRITIS
SEPTIC/INFECTIOUS ARTHRITIS
• Refers to an inflammation of a joint caused by various
microorganisms (ie. bacteria, virus, fungi and spirochetes)
• Most common cause: bacteria (ie. Staphylococcus aureus,
Neisseria gonorrhoeae)
Overview
Types
Acute bacterial infection
Subacute or chronic monarthritis
or oligoarthritis
Episodic inflammation
Acute polyarticular inflammation
*Rheumatoid arthritis
Involvement/ Etiology
Single joint or a few joints
involvement
Mycobacterial or fungal infection
Syphilis, Lyme disease, and the
reactive arthritis that follows
enteric infections and chlamydial
urethritis
Endocarditis, rheumatic fever,
disseminated neisserial infection,
and acute hepatitis B
Bacteria
Hematogenous route of infection – most common route in all age groups
Route Pathogens
Surgical procedures or penetrating MC: S. Aureus
injuries
Occasionally :
other gram-positive bacteria
or gram-negative bacilli
Implantation of prosthetic joints or Infections with coagulase-negative
arthroscopy staphylococci
Human bites MC: Anaerobic organisms,
Decubitus ulcers often in association with aerobic
Intraabdominal abscesses or facultative bacteria
Bites and scratches from cats and other Pasteurella multocida
animals Bartonella henselae
Human bites Eikenella corrodens or other
components of the oral flora
Penetration of Pseudomonas aeruginosa
a sharp object through a shoe
Non-gonococcal Bacterial Arthritis
EPIDEMIOLOGY
High Risk Individuals Pathogen
Patients with rheumatoid arthritis S. aureus

- With Diabetes mellitus S. aureus and gram-negative

- In Glucocorticoid therapy bacilli
- In Hemodialysis
- Has Malignancy
-Alcoholics Pneumococcal
- Deficient of humoral immunity infections
-- With hemoglobinopathies

Persons infected with HIV Pneumococci

Salmonella species
H. Influenzae
Non-gonococcal Bacterial Arthritis
EPIDEMIOLOGY
High Risk Individuals Pathogen
Persons Mycoplasma
with primary
immunoglobulin deficiency
IV drug users Staphylococci
Streptococci

Pseudomonas
Other gram-negative
infections
ACUTE BACTERIAL ARTHRITIS
PATHOPHYSIOLOGY
Entry of Bacteria
Bone or soft tissue Bloodstream Direct inoculation

Hematogenous Spread
Synovial capillaries

Neutrophilic Infiltration (synovium)

Neutrophils and bacteria enter the joint space
ACUTE BACTERIAL ARTHRITIS
PATHOPHYSIOLOGY
Bacteria adhere to articular cartilage

Degradation of cartilage

Increased intraarticular pressure

ACUTE BACTERIAL ARTHRITIS
PATHOPHYSIOLOGY
Synovial Proliferation
Release of proteases and cytokines from Bacteria and inflammatory cells invades
chondrocytes and synovial macrophages cartilage

Formation of a pannus over the cartilage

Thrombosis of inflamed synovial vessels

Clinical finding/ manifestation
IN CHILDREN
• Irritable
• Refuse to feed
• Fever
• Joints are warm, tenderness,
resistance to movement
• Rapid pulse
 IN ADULT
• Often in the superficial joint (knee, wrist or ankle)
• Joint painful, swollen & inflamed
• Warmth and marked local tenderness
• Movement restricted
• Look for gonococcal infection or drug abuse.
• Patient with rheumatoid arthritis and especially those on
corticosteroid may develop “silent” joint infection
DIAGNOSIS
• DIFFERENTIAL DIAGNOSIS
• Acute osteomyelitis
• Trauma
• Hemophilic bleed
• Rheumatic fever
• Juvenile rheumatoid arthritis
• Sickle-cell disease
• Gaucher’s disease
• Gout and pseudo-gout
INVESTIGATION
SEPTIC ARTHRITIS SUSPECTED

BLOOD AND SYNOVIAL FLUID SAMPLE

EMPIRIC PARENTERAL ANTIBIOTICS BASED ON GRAM STAIN

JOINT DRAINAGE

ADJUST ANTIBIOTIC BASED ON CULTURE AND SESNSITIVITY RESULT

LABORATORY FINDING
• 1. BLOOD INVESTIGATIONS
• Raised WBC
• Raised ESR and CRP
• Blood culture (positive)
2. IMAGING
• X-ray
o Early stage: May look normal except widening of joint space,
ultrasound helpful
o Late stage: Narrowing and irregularity of joint space;

• MRI and radionuclide imaging are helpful in diagnosing arthritis in

obscure sites such as the sacroiliac and sterno-clavicular joint.
FINDINGS
 WIDENED JOINT
SPACE
LATER STAGE
• 3. SYNOVIAL FLUID ANALYSIS
MANAGEMENT
• 1st priority - aspirate the joint and examine the fluid.
• General supportive care - analgesics and IV fluid
• Splintage
• Antibiotics
a) Neonates and infants up to 6 months - penicillin (flucloxacillin) + 3rd
gencephalosporin
b) Children from 6 months to puberty – similar to above.
c) Older teenager and adults - flucloxacillin and fusidic acid and
3rdgeneration cephalosporin

Antibiotics given IV for 4-7 days, then orally for 3 weeks.

COMPLICATION
1. Bone destruction and dislocation of the joint (especially hip)
2. Cartilage destruction
3. May lead to either fibrosis or bony ankylosis
4. In adult partial destruction of the joint will result in secondary
osteoarthritis
5. Growth disturbance
6. Presenting as either localized deformity or shortening of the
bone
Thank you
References:
Osteoarthritis
Harrison’s Principles of Internal Medicine 20th ed
Essential Orthopedics 5th ed by J. Maheshwari
Gouty Arthritis
Harrison's Principle of Internal medicine 20th ed
Essential ORTHOPEDICS (Principles and Practice) by Manish Kumar Varshney
Rheumatoid Arthritis: Common Questions About Diagnosis and Management - American Family Physician (aafp.
org)
Rheumatoid arthritis (RA): Pathogenesis and Joint diseases features | Calgary Guide (ucalgary.ca)
Rheumatoid Arthritis
Septic Arthritis
Harrison’s Principles of Internal Medicine 20th ed