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Osteoarthritis
Clinical Approach
LEARNING OBJECTIVES
Understand the natural history of osteoarthritis
Learn about the pathophysiological process of
osteoarthritis
Recognize the signs and symptoms of osteoarthritis and
the typical joints involved
Learn about the work up and diagnosis of osteoarthritis
Understand the treatment of osteoarthritis
BACKGROUND
• Osteoarthritis was formerly considered to be a
degenerative process resulting from “wear and tear”.
• Disease process is more complex with multiple factors
contributing to the disease process.

Obesity
Genetic
Gender
Factors

Risk of
Joint
Age Developing injury/
OA
Trauma
BACKGROUND
• 27 million Americans suffer from osteoarthritis
• Most common joint disorder in the US
• OA affects 10% of 40 year-olds and 50% of 60 year-olds.
• Estimated costs due to hospital expenditures of total
knee replacements $28.5 billion (2009)
PATHOGENESIS
PATHOGENESIS
• Osteoarthritis is primarily a disease of the articular
cartilage
• However, it also affects surrounding structures of the
joint (i.e. ligament thickening, subchondral bone
sclerosis, synovial membrane inflammation)
• Therefore, OA is considered a disease of the joint as an
organ.
ARTICULAR CARTILAGE
• Bones at a joint are lined by hyaline cartilage.
• Cartilage functions to improve lubrication and fluidity
at joints.
PHYSIOLOGY REVIEW:
ARTICULAR CARTILAGE
• Cartilage tissue:
• Cellular (chondrocytes): 1-2%
• Extracellular Matrix
• Liquid phase (water): 75%
• Solid phase: 25%
• Collagen: Type II
• Proteoglycans

 Collagen provides tensile strength


 Proteoglycans retain water
PATHOGENESIS
• Normal conditions
• Matrix undergoes dynamic remodeling process
• Synthesizing and degradative factors are in balance

Matrix Matrix
Formation Destruction

Protease
Proteases
Inhibitors
Protease inhibitors:
 MMP inhibitor
 TIMP-1, TIMP-2 Proteases:
 Alpha-2-macroglobulin  Matrix Metalloproteases
PATHOGENESIS
• Osteoarthritic condition
• Imbalance between matrix synthesizing and matrix
degrative factors

Matrix Matrix
Formation Destruction

Protease
?
Inhibitors
Proteases
PATHOGENESIS
What causes this imbalance?
 Proinflammatory factors (i.e. IL-1, TNF-β) stimulate the
production of proteolytic enzymes responsible for the
degradation of the extracellular matrix  leading to joint
tissue destruction.

What causes upregulation of proinflammatory factors?

Excessive or Release of Stimulates


abnormal joint Joint tissue
proinflammatory production of
loading destruction
factors proteases
PATHOGENESIS
PROGRESSION OF OA
• Begins with mild fibrillation which progresses.
• Abrasion of cartilage leads to shearing and thinning.
Necrosis of chondrocytes occurs.
• Subchondral sclerosis and osteophytes form.
Interprofessional Education
Team Based Learning
CASE STUDY 1: MRS. OA
• Mrs. OA is a 62yo lady
• Chief complaint: Bilateral knee pain
• HPI:
• She is having trouble getting up and down from sitting, using
stairs, getting in and out of the car, bathing her grandchildren,
and walking for more than 10 minutes at a time.
• Has had knee pain for ~10 years, but no formal diagnosis for
knee pain. She attributes it to “arthritis”.
• Joint pain is worse during the cold seasons/weather, and better
during warm, sunny days. This summer, however, her knee pain
has not improved and has actually worsened in the past 6
months.
• Reports stiffness after prolonged sitting and in the mornings.
• Experiencing numbness and tingling sensation in both legs,
below the knees.
CASE STUDY 1: MRS. OA
Which of the following parts of the history is
suggestive of osteoarthritis? (select all that apply)
CLINICAL
MANIFESTATION
CLINICAL
MANIFESTATION
• Symptoms:
• Joint pain worse with
use or weight bearing
activity
• Stiffness with inactivity
(gelling)
• i.e. prolonged sitting,
after sleeping
• Morning stiffness
(duration <30min)
• Reduced joint
mobility/range
CASE STUDY 1: MRS. OA
• Past Medical hx:
• DMII, HTN, HLD, obesity
• Surgical hx:
• hysterectomy (’88), R hip fx s/p repair (’10)
• Social Hx:
• Originally from Mexico, but has been living with
daughter in Los Angeles for the past 2 years.
Helps with housework during the day and cares
for the grandchildren.
CASE STUDY 1: MRS. OA
Given her history, what are potential risk factors for
developing OA?
RISK FACTORS
• Various risk factors have been linked to the
pathogenesis of OA:
• Older age
• Hx of joint injury/trauma
• Obesity (increased joint load)
• Genetics
• Female gender
• Occupation
CASE STUDY: MRS. OA
• Physical Exam:
• General exam – notable for obesity (5’2”, 180lbs)
• Focused knee exam -
• Mild quadriceps muscle atrophy L > R.
• Mild effusions, cold, erythematous b/l.
• Pain with passive ROM, joint line tenderness left
worse than right.
• Unable to perform valgus/varus d/t pain
• Hip exam:
• R hip limited ROM, mild pain with passive flexion,
+ crepitus. L hip unremarkable.
CASE STUDY: MRS. OA
What findings on physical exam are concerning for
osteoarthritis of the knee? (select all that apply)
CLINICAL
MANIFESTATION
• Symptoms: • Signs:
• Joint pain worse with • Joint instability
use or weight bearing • Bony enlargement
activity • Joint line tenderness
• Stiffness with inactivity (variable)
(gelling)
• Swelling (variable)
• i.e. prolonged sitting,
after sleeping • Crepitus
• Morning stiffness • Restricted movement
(duration <30min) (mechanical or due to
• Reduced joint pain)
mobility/range
SUBSETS OF OA
• Primary OA
• Affects multiple, typical joints in appendicular and axial
skeleton
• Typical weight bearing joints
• Secondary OA
• Can occur at atypical joints
• Prior injury/ trauma to the joint
• Secondary to a related disease (i.e. endocrinopathy,
neuropathic join, hemochromatosis, etc)
JOINT INVOLVEMENT
• Primary OA can involve
following joints:
• Distal interphalangeal
• Carpometacarpal
• Lower cervical and
lumbar facet joints
• Hip, knee
• Metatarsophalangeal
ANATOMY REVIEW
ANATOMY REVIEW
Loss of articular cartilage at DIP
Hand OA Large Osteophytes and ankylosis
ANATOMY REVIEW
Carpometacarpal OA
•‘Square thumb’ appearance
ANATOMY REVIEW
Cervical Facet OA
ANATOMY REVIEW
Metatarsophalangeal
OA
CASE STUDY: MRS. OA
Which of the following OA subsets does Mrs. OA fit?
What information supports your decision?
DIAGNOSIS
CASE STUDY: MRS. OA
• 62 yo F
• Progressive b/l knee pain and stiffness.
• H/o R hip fx s/p surgical repair.
• PEx:
• Obese.
• Mildly limited R hip flexion
• B/l knee effusions, ttp, ?redness, limited ROM.

What additional information do we need to make a


diagnosis of OA?
CASE STUDY: MRS. OA
What next step is needed to make a diagnosis of OA?
DIAGNOSIS
• Osteoarthritis is primarily a clinical diagnosis
• History and physical exam can establish dx
• Hx:
• Joint pain worsened by movement
• Risk factors support diagnosis
• Physical examination:
• Pain with ROM
• Limited ROM
WHEN SHOULD LABS BE
ORDERED?
• Typically, labs are not required to make diagnosis and not
recommended (high false-positives)
• ACR clinical guideline recommends against the routine
ordering of arthritis panels for patients with joint problems. 2

• ESR/CRP:
• markers of inflammation; typically negative
• Rheumatoid factor:
• only considered if high suspicion for autoimmune
arthritis (i.e. RA)
• Uric acid:
• only if there is suspicion for gout
WHEN SHOULD FILMS BE
ORDERED?
• Not required to make a diagnosis
• But they can help confirm dx and rule out other
conditions
• Benefits:
• Useful for determining severity of hip and knee OA and
planning management.
• Shortcomings:
• Films have poor correlation with symptoms
MANAGEMENT
CASE STUDY: MRS. OA
Mrs. OA is diagnose with OA (primary and secondary to R
hip fracture). She reveals that she’s been taking
ibuprofen with no relief. Is ibuprofen a good medication
for this patient?
MANAGEMENT
•Four categories:
•Nonpharmacologic
•Pharmacologic
•Complementary & alternative
•Surgical
MANAGEMENT
Stepped-approach (based on ACR guidelines) 1, 13

Am Fam Physician. 2012;85(1):49-56.


NONPHARMACOLOGIC
MANAGEMENT
• Exercise
• First line management
• Improves arthritis symptoms 15
• Land-based exercises demonstrate significant improvement
in pain symptoms over water-based exercise (for hip and
knee OA) 4,8
• Weight loss
• Loss of 5% from baseline can significantly reduce disability 6
PHARMACOLOGICAL
MANAGEMENT
• Acetaminophen
• Acetaminophen better than placebo for mild OA and
fewer adverse effects than NSAIDs16
• Max dose 4g/day
• Nonsteroidal Anti-Inflammatory (NSAIDs)
• Superior to acetaminophen for moderate/ severe
symptoms
• Topical preferred over PO due to adverse effects of
NSAIDs (i.e. gastrointestinal bleed, renal injury)
PHARMACOLOGICAL
MANAGEMENT
• Opioids
• Less favorable alternative
• Concerns: constipation, fall risk, potential for abuse
• Considered when acetaminophen and NSAIDs have
failed but patient has not tolerated them
INTRAARTICULAR
INJECTIONS
• Corticosteroid Injections
• Proven efficacy for knee injections 3,15
• Efficacy of shoulder or hand are not supported 1,11
• Perceived benefits last 4-8 weeks
• Administered q3mo
• Hyaluronic Acid Injections
• Treatment effect can last up to 4 months with
improvement in pain and function 5
• Expensive($1300 per injection)
COMPLEMENTARY /
ALTERNATIVE MEDICINE
• Acupuncture
• Chiropractic care
• Supplements
• Glucosamine, Chondroitin
• Glucosamine/Chondroitin Arthritis Intervention Trial (GAIT) in
2006
• 1500 patients, 5 arm study
• Glucosamine + chondroitin effective for moderate to severe
arthritis 7
SURGICAL INTERVENTION
What surgical interventions are available?
 Arthroscopy:
 Debridement, resection, meniscectomy, synovectomy
 Arthroplasty (joint replacement)
 Hip, knee, shoulder 3
ARTHROSCOPY STUDY
• Randomized Controlled Study – NEJM 12
• Method:
• 180 patients enrolled and divided into 3 groups
• Arthroscopic debridement
• Arthroscopic lavage
• Placebo surgery (incisions only)
• Outcomes (pain, functional capacity) assessed over 24
month period
• Conclusion: Arthroscopic interventions were not
superior to placebo procedure.
ARTHROPLASTY
• Total joint replacement for knee, hip, shoulder
• Indications
• Chronic, debilitating pain
• Functional loss
• Failed medical therapy
• Contraindications
• Poor operative candidate (CV disease, DM, smoker)
CASE STUDY: MRS. OA
Which treatment plan would your team recommend to
Mrs. OA?
QUESTIONS?
REFERENCES
1. American Academy of Orthopaedic Surgeons. The treatment of glenohumeral joint osteoarthritis: guide- line and evidence
report. Rosemont, Ill.: American Academy of Orthopaedic Surgeons; 2009. http://
www.aaos.org/research/guidelines/gloguideline.pdf. Accessed August 9, 2011.
2. American College of Rheumatology. Practice guidelines. Recommendations for the medical management of osteoarthritis
of the hip and knee. http://www. rheumatology.org/practice/clinical/guidelines/ oa-mgmt.asp. Accessed August 9, 2011.
3. Arroll B, Goodyear-Smith F. Corticosteroid injections for osteoarthritis of the knee: meta-analysis. BMJ. 2004 Apr
10;328(7444):869. PubMed PMID: 15039276; PubMed Central PMCID: PMC387479.
4. Bartels EM, Juhl CB, Christensen R, Hagen KB, Danneskiold-Samsøe B, et al. Aquatic exercise for the treatment of knee
and hip osteoarthritis. Cochrane Database Syst Rev. 2016 Mar 23;3:CD005523. PubMed PMID: 27007113.
5. Bellamy N, Campbell J, Robinson V, Gee T, Bourne R, et al. Viscosupplementation for the treatment of osteoarthritis of
the knee. Cochrane Database Syst Rev. 2006 Apr 19;(2):CD005321. PubMed PMID: 16625635.
6. Christensen R, Bartels EM, Astrup A, Bliddal H. Effect of weight reduction in obese patients diagnosed with knee
osteoarthritis: a systematic review and meta-analysis. Ann Rheum Dis. 2007 Apr;66(4):433-9. PubMed PMID: 17204567;
PubMed Central PMCID: PMC1856062.
7. Clegg DO, Reda DJ, Harris CL, Klein MA, O'Dell JR, et al. Glucosamine, chondroitin sulfate, and the two in combination
for painful knee osteoarthritis. N Engl J Med. 2006 Feb 23;354(8):795-808. PubMed PMID: 16495392.
8. Fransen M, McConnell S. Exercise for osteoarthritis of the knee. Cochrane Database Syst Rev. 2008 Oct 8;(4):CD004376.
PubMed PMID: 18843657.
9. Fry V, Davis C. Painless nodules in the fingers. Am Fam Physician. 2011 May 15;83(10):1203-5. PubMed PMID:
21568256.
10. Guidelines for the initial evaluation of the adult patient with acute musculoskeletal symptoms American College of
Rheumatology Ad Hoc Committee on Clinical Guidelines. Arthritis Rheum. 1996 Jan;39(1):1-8. PubMed PMID: 8546717.
REFERENCES

11. Meenagh GK, Patton J, Kynes C, Wright GD. A randomised controlled trial of intra-articular corticosteroid
injection of the carpometacarpal joint of the thumb in osteoarthritis. Ann Rheum Dis. 2004 Oct;63(10):1260-3.
PubMed PMID: 15361383; PubMed Central PMCID: PMC1754748.
12. Moseley JB, O'Malley K, Petersen NJ, Menke TJ, Brody BA, et al. A controlled trial of arthroscopic surgery for
osteoarthritis of the knee. N Engl J Med. 2002 Jul 11;347(2):81-8. PubMed PMID: 12110735
13. Scott DL, Shipley M, Dawson A, Edwards S, Symmons DP, Woolf AD. The clinical management of
rheumatoid arthritis and osteoarthritis: strategies for improving clin- ical effectiveness. Br J Rheumatol.
1998;37(5):546-554.
14. Stephens MB, Beutler AI, O'Connor FG. Musculoskeletal injections: a review of the evidence. Am Fam
Physician. 2008 Oct 15;78(8):971-6. PubMed PMID: 18953975.
15. Thomas KS, Muir KR, Doherty M, Jones AC, O'Reilly SC, et al. Home based exercise program for knee pain
and knee osteoarthritis: randomised controlled trial. BMJ. 2002 Oct 5;325(7367):752. PubMed PMID: 12364304;
PubMed Central PMCID: PMC128377.
16. Towheed TE, Maxwell L, Judd MG, Catton M, Hochberg MC, et al. Acetaminophen for osteoarthritis. Cochrane
Database Syst Rev. 2006 Jan 25;(1):CD004257. PubMed PMID: 16437479.

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