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Pain - Basic Science
Implications for Analgesia & Analgesics
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Definition of pain
www.iasp.org/terms
“Pain is an unpleasant sensory and
emotional experience associated with
actual or potential tissue damage”
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Is there a basis for the separation of pain?
A- Chronicity
B- intensity
C- Mechanism of action
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A- Chronicity
Acute
Sudden onset
Self-limiting
Generally respondsto drug treatment ormanagement of theunderlying cause
Chronic
Onset not well
defined Persistent or
recurring
Triggered by injuryor disease butpersists even withtreatment
Acute at top of
chronic
(Flare up) Sudden onset
Self-limiting
Generally responds
to drug treatment ormanagement of theunderlying cause
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B- Pain Intensity
Mild
Sever
Moderate
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Assessing the efficacy of analgesics
Outcome measures used in clinical studies
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Assessment of pain in clinical studies
Due to its subjective nature, the assessment of pain in clinical studies ischallenging.
There are several standardized pain assessment instruments:
Pain intensity – Visual Analogue Scale (VAS)
Pain intensity – categorical scale
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Pain intensity – Visual Analogue Scale (VAS)
Continuous numerical self-rating pain scale
Patients mark along the line to represent pain intensity
Worst painExperienced
No pain
0 10
VAS score
Joyce C, et al . 1975
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Pain intensity – categorical scale
0 = None
1 = Mild
2 = Moderate
3 = Severe
Pain categorized by number or descriptor
Patients select category to represent pain intensity
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Feminine pain
Physiological
Psychological
Perception
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The Complexity of Feminine Pain …
• Researches over the past twenty years have found significantdifferences between men & women regarding the following aspects
- Physiological response to pain 1
- Psychological perception of pain 2
1.Zubieta et al. 2002; Gear et al. 19962.Campbell, Clauw, & Keefe, 20033.Pain." The Merck Manual of Diagnosis and Therapy,
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Why Females are more sensitive?
Nerve receptorsWomen have averaged double the number of nerve receptors
compared with men.
Hormones
Variations in women's Estrogen levels like those that occurthroughout the monthly menstrual cycle, or duringpregnancy regulate the brain's natural ability to suppressbrain. Endorphins ,Enkphalins ).
Testosterone, appears to raise the pain threshold
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Incidence of acute pain in the US
CDC. 2004
Migraine/severe
headache
0
5
15
35
30
Neck pain Pain in faceor jaw
Lower backpain
10
20
25
US adults (%)
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Prevalence and economic impactof chronic (persistent) pain
Worldwide, 22% of primary care patients suffer from persistent painevery year
75 million US adults experience chronic pain
12.7% of the US work force lose productive time over a 2-weekperiod due to common pain conditions (arthritis, back pain, headacheand other musculoskeletal conditions)
Common pain conditions cost US employers an estimated $61.2billion in lost production time each year
Gureje O, et al . 1998; Schnitzer T. 1998; Stewart W, et al . 2003
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Worldwide impact of chronic pain
Gujere O, et al . 1998
Depression Poor health Workimpaired
Activitylimited
Chronic pain
No pain
0
20
30
50
10
Primary care attendees (%)
40
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Goals of pain management
• Pain control
• Alter disease course (may not be possible)
• Restore function to affected areas (e.g. joints)• Address psychological factors such as stress and
depression
• Maximize quality of life (QoL)
Adapted from Ashburn MA. 1999
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The World Health Organisation (WHO)analgesic ladder
3
2
Simple analgesicse.g. paracetamol , NSAIDs
Weak opiatese.g. codeine or dihydrocodeine +simple analgesics
Strong opiatese.g. morphine or diamorphine+ simple analgesics
I n c r e a s i n g
p a i n
1
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Types of analgesics
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Types of analgesics
• Simple analgesics (paracetamol)
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Weak opiates
• Strong opiates
• Corticosteroids
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History of NSAID to the 21st Century
History: •In 1829, salicin was isolated in a pure form from thewillow bark (spiraer).
•In 1899, introduced into medicine under the name ofaspirin.
•Towards the end of the Nineteenth Century, otherNSAID were discovered.
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PG’s pathway
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PG has a big role to amplification of inflammation -pain - fever .
1. Anti-inflammatory effects
2. Analgesic effects NSAIDs
supp ress synthes is and
release of PGs by
inhib i t ing Cox enzymes
wh ich in turn block the
sensit izat ion o f pain
receptors.
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Biology & Regulation of COX-1& COXII
COX 1 COX 2Constitutive under normal conditions Inducible, COX-2 is typically undetectable
in most tissues under basal conditions, butits expression in many cell types, includingmacrophages, fibroblasts, markedlydepends on stimulation with inflammatorycytokines
COX-1 is expressed in virtually alltissues, most notably:
Platelets ,Endothelial cells ,GIT ,kidney
COX-2 is expressed in a variety tissues in
basal conditions such as:Kidney ,Brain
,Bone &Cartilage
COX-2 is rapidly induced and participatesin pathological and inflammatory tissue
processes.
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Sciops-Medical DivisionPlatelet aggregation Cytoprotection Pain and inflammation
Traditional NSAIDsMechanism of action
Thromboxane
synthase
TxA2
AA
Reduction in
platelet aggregation
Reduced
cytoprotection
Reduced
pain and inflammation
Prostaglandin
isomerase
PGI2PGE2
Prostacyclin
synthase
PGH2 PGH2
AA
Prostaglandin
isomerase
Prostacyclin
synthase
Phospholipids
PGH2
Phospholipids Phospholipids
AA
Platelet Inflamed synoviumGI mucosa
COX-2
COX-2
COX-2
COX-1
COX-1
COX-1
COX-1
COX-1
PGI2PGE2
membrane
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Risk factors for GI ulcer complications
Corticosteroiduse
Wolfe M, et al. 1999
Warfarin use Aspirin use
Cardiovasculardisease
Increasingage
Risk of ulcercomplication
Higher dosesMore thanone NSAID
Previousulcer or bleed
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Strategies to prevent NSAID-associated GI adverseevents
• Administration of concomitant gastroprotectants such as PPIs (e.g. omeprazole; Losec®) prostaglandin analogues (misoprostol) are partiallyeffective but add their own potential side effects1
• Administration of NSAIDs with food reduces gastric irritation
• Enteric-coated tablets release drug in the small intestine, thereby preventingdirect damage to the stomach
1
NICE. 2001
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• It has been demonstrated that upper GI ulcers, gross bleeding or
perforation, caused by NSAIDs, appear to occur in approximately 1%
of patients treated for 3-6 months, and in about 2-4% of patients
treated for one year.
FDA
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Musculoskeletal diseases
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Common musculoskeletal diseases
Osteoarthritis A combination of Predisposing factors &jointBiomechanics(degenerative) which triggers Biochemical(Inflammatory ) changes
Rheumatoid arthritis A chronic, progressive, inflammatory disease of the joints
Ankylosing spondylitis An inflammatory disease of the joints of the back bone
Juvenile arthritis A form of arthritis affecting children
Gout A metabolic disease in which uric acid crystals deposit inthe joints
P l d E i b d f
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Prevalence and Economic burden ofmusculoskeletal disease
More than 33 million people in the US (16% of the population) have a form ofarthritis
• 28 million aged 45 years
• prevalence is projected to increase to 18.2%
by 2020 due to aging population
Worldwide it is estimated that 9.6% of men and 18.0%of women aged 60 years have symptomatic OA
1.0 –2.5% of Gross National Product (GNP) is spent
annually on musculoskeletal disorders in the US,Canada, UK, France and Australia
March L, et al. 1997; Woolf A, et al. 2003
Di bilit b d f l k l t l
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Disability burden of musculoskeletaldiseases
Ischaemic heart disease
Cerebrovascular disease
Total musculoskeletal disease
OAHIV/AIDS
Chronic obstructivepulmonary disease
Liver cirrhosis
Asthma
RA
0 2 106 84Disability –adjusted life years (millions)
Reginster J, et al. 2002
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Rheumatic Disorders Classification
Gout
Tendinitis
Tenosynovitis
Sport Injuries &strains
GoutRheumatoid
Arthritis
AnkylosingSpondylitis
Osteoarthritis
Articulus: Latin word means joint
Bursitis
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Normal Joints
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Normal Joint
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The Articular Cartilage (Hyaline cartilage)
• Avascular ,Aneural
Formed of: Water 69%
Collagen 15%
Proteoglycans 15% Chondrocytes 1%
Matrix
Function: Shock absorbent , distribute load applied on joints
Structure of articular cartilage (hyaline cartilage)
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Structure of articular cartilage (hyaline cartilage)
2. Condrocytes :Mature cartilage,cellular manufacturing sites
Fn: Production & MaintenanceOf surrounding matrix
1. Collagen Fibers: sheets of Fibrous proteins ,Fn:provide high tensile strength to theCartilage, resistant to extension
Protect cartilage from swelling pressuregenerated by proteoglycans
3. Proteoglycans: Large ,high molecular weight molecules ,Available in aggregates,Consist of protein core and Carbohydrate Side chain (Chondroitin sulphate and keratin sulphate)
and long central chain of hyaloronic acid, Hygroscopic i.e. attract water to make a hydrated tissuethat resist compression
protein
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Osteoarthritis
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Prevalence
• Leading cause of chronic disability in elderly
• The most common joint disease.
• 35% of rheumatic consultations
• 30% of women aged between 45-64 years suffer from O.A
• And 70% for patients with age above than 65 years
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A Multifactorial Disease
Adapted from The Lancet, Vol 365, Dieppe PA, Lohmander S. Pathogenesis and management ofpain in osteoarthritis, Pages 965-973, Copyright 2005, with permission from Elsevier
1
2
3
O.A is a Combination of predisposing factors & jointbiomechanics leading to biochemical Changes.
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Pathogenesis of OA ( Predisposing Factors)
Susceptibility to OA may be increased in part by:
• genetic inheritance (a positive family history increases risk),
• age,
• ethnicity,
• diet and
• female gender
Felson DT (2004a) An update on the pathogenesis and epidemiology of osteoarthritis. Radiologic Clin North Am 42, 1 –9.
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Pathogenesis of OA ( Joint Biomechanics)(Mechanical leads to structural changes)
Loading can also be affected by• Obesity & Joint injury (either acutely as in a sporting injury or after
repetitive overuse such as occupational exposure), both of which canincrease the likelihood of development or progression of OA)
Local mechanical factors that facilitate progression
• Malalignment
• Muscle weakness
• Structural integrity (menisical damage of bone marrow lesions)
Felson DT (2004a) An update on the pathogenesis and epidemiology of osteoarthritis. Radiologic Clin North Am 42, 1 –9.
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Pathogenesis of OA (Biochemical Changes)
OA results from an imbalance in catabolic and anabolicprocesses that lead to progressive cartilage damage anddestruction.
Initially anabolic process such as proteoglycan synthesismaintain balance with catabolic processes and damage tocartilage is repaired. However with time and age ,anabolicprocesses decline and progressive damage ensues.
Osteoarthritis and Cartilage (2008) 16, 624e630
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Often the slow but efficient OA process compensates forthe insults, resulting in an anatomically altered butsymptom free functioning joint (compensated OA)
Sometimes because of severe increased insult or poorrepair response, it fails resulting in progressive tissuedamage and presentation of symptoms due to joint failure.
Pathogenesis of OA (biochemical)
Osteoarthritis and Cartilage (2008) 16, 624e630
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1
12
23
3
44
5
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Joint involvement in OA
Solomon L. Clinical features of osteoarthritis. Textbook Rheum 1997;2:1383 –1393.
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Knee Osteoarthritis
In the early stages of the disease, pain is the
main symptom, yet in advanced stages,
cartilage degeneration takes place and the
patient also complains from asound
.
Main symptoms:
Localized knee Pain during movement ‘movement related pain’
Resting stiffness
In severe cases, pain is continuous even during rest.
Mechanical pain might also increase with excessive use of
the joint, and this appears at night. 54
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Knee joint effusion
Deformities
Osteoarthritis and Cartilage (2008) 16, 624e630
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Heberden’s nodes :Hard or bony swellings which can develop in thedistal interphalangeal joints (DIP).
Bouchard's nodes: bony growths in the proximal interphalangeal (PIP) joints
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Special Investigations
• Blood tests: Normal
• Radiological features:
• Cartilage loss• Narrowed joint space
• Subchondral sclerosis
• Cysts
• Osteophytes
R di hi F t f th
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Radiographic Features of theKnee in OA
Joint space narrowing
Marginal osteophytes
Subchondral cysts
Boney sclerosis
Malalignment
Joint spacenarrowing
Osteoarthritis and Cartilage (2008) 16, 624e630
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Goals of The Treatment
Relief pain, swelling and inflammation.
Inhibit joint degeneration.
Improve quality of life.
Osteoarthritis and Cartilage (2008) 16, 624e630
Components of Multimodal Osteoarthritis
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Components of Multimodal OsteoarthritisTreatment
Non-pharmacological TherapyEducation Physical therapy ExerciseOccupational therapy Weight Control Assistivedevices Nutraceuticals
Pharmacological TherapyNSAIDs Topical
DMAs
Intra-articular Injection
Hyaluronic acidsCorticosteroids
Surgery
Osteoarthritis and Cartilage (2008) 16, 624e630
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Rheumatoid arthritis
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What is Rheumatoid Arthritis ( RA )
Systemic multi-organ inflammatory disease Of unknownaetiology.
NORMAL RA
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What is rheumatoid arthritis ?
• It is a systemic multi organ inflammatory disease of unknown etiology.
• Associated with characteristics of joint pathology.
• Auto antibodies
• Immunologic hyperactivity
• The cause is unknown ,however the following factors contribute to theetiology:
• Heredity
• Infections
• Rheumatic factor : IgM detected in 85% of R.A patients (seropostive),associated with more severe joint disease and subcutaneous nodes
• Over activity of immune system over individual’s own cells
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Risk Factors
• Genetic
• Age ( ↑ with age)
• Sex (> female)
• Obesity
• Joint trauma and injury
• Repetitive occupational joint use
• Physical inactivity
RA - Pathology & Pathogenesis
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RA - Pathology & Pathogenesis
• Active chronic inflammation of the synovial membrane
• Synovial membrane proliferation and out-growth
• Erosion of the articular cartilage and sub-chondral bone
• Formation of the characteristic pannus
• First affects the small joints
• Order of involvement : fingers, toes, hands, knees, elbows,
shoulders and hips.
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Signs and symptoms of R
Signs
Hand joint deformities suchas Boutonnière and Swan
neck & subcutaneousnodules
Synovium hypertrophy
Bone erosion
Rheumatoid factor present in85% of patients
Symptoms
Joint swelling, warmth andtenderness
Pain and stiffness
Weakness, fatigue
Fever
Depression
Hope R, et al . 1998
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RA - Hand Involvement
Subcutaneous NodulesOver Elbow in Rheumatoid Arthritis Severely Affected Hand With
S b t N d l O K kl S N k D f it Of Middl Fi W ti Of
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Subcutaneous Nodules Over Knuckle, Swan – Neck Deformity Of Middle Finger, Wasting Of
Hand, and Ulnar Drift of Fingers
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RA - Laboratory Findings
• The erythrocyte sedimentation rate (ESR) is elevated
in most patients.
• The presence of RF (85%)
• Antinuclear antibodies (30-40%)
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RA – Management Goal
1. Relief of pain
2. Reduction of inflammation
3. Preservation of muscle strength and joint function
4. Return as rapidly as possible to a normal lifestyle
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Management
• Pain relief with NSAIDs
• Adequate rest
• Weight reduction
• Immunosuppressive
• Local corticosteroid injections
• Long term corticosteroids (should be preserved for pts with aggressive joint
reaction whose ability to function is threatened)
• Prolonged home exercise program
ff f O f
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Differential diagnosis of OA from RA
OA RA
More common inhip and knee
More common inwrist, elbow and shoulder
Joint tenderness Joint warmth and redness
Patient typically >45 yearsat onset
Usually symmetrical joint involvement
Patient typically 25 –55years at onset
Asymmetrical joints
Joint space narrowing
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Ankylosing Spondyltis
Classic areas of inflammation in ankylosing
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y gspondylitis
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Ankylosing Spondylitis
Ankylosing spondylitis (AS) is a chronic inflammatory disease of the axialskeleton manifested by back pain and progressive stiffness of the spine.
AS is one of the spondyloarthropathies which show inflammation around theenthesis (the site of ligament insertion into bone) and an association with thehuman leukocyte antigen HLA-B27.
It characteristically affects young adults with a peak age of onset between 20and 40 years. Although classically thought of as a spinal disease, transientacute arthritis of peripheral joints (hips, shoulders, knees) occurs in up to 50 percent of patients
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Ankylosing spondylitis
There are three clinical criteria:
• Low back pain
• Morning stiffness of greater than threemonths duration, improving with exercisebut not relieved by rest
• Limitation of motion of the lumbar spine
It can result in the following
• Fused vertebrae
• Rigid spine, and• Flattening of the lower back.
• The joints and ligament becomeinflamed.
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Ankylosing Spondylitis {AS}
Investigations:
X-ray findings (bilateral sacrolitis; bamboo spine..)
ESR
HLA-B27
(95% of cases) (human leukocytic antigen) not all
RF -ve
Treatment:
Active mobilisation and spine exercises are very important.
NSAIDs
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Non Articular RheumatismSoft Tissue Rheumatism
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Non Articular Rheumatic disorders
• Most common Rheumatic disorders where joints aren’taffected .
• Referred to muscular , adipose tissue , tendons , jointcapsules and bursa.
• Both inflammatory & Degenerative processes play role.
• Most prominent symptoms are pain and tenderness.
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Non Articular Rheumatic disorders
Disorder Pathology
Bursitis Pleural of bursa is synovial sacs that lies betweentendons ,bones and muscles or tendons and skin
Function is to minimize friction
Inflammation of bursa is associated with swelling ,redness of skin and limitation of movement of nearby joints
Tendonitis /Tenosynovitis
Changes affecting tendons and their sheath due to microtrauma or occupational origin
Synovitis Inflammation in synovial membrane
Periarthritis Inflammation in the tissues surrounding the joints , thebursae is often involved
Myositis Pain , tenderness , due to acute or chronic inflammation
of muscles
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Sciops-Medical Division
Management of Non Articular Rheumatic disorders
Rest
NSAIDS
Local steroids
Physiotherapy
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Thank you