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with additional gratitude  to our scientific partners  AOSSM, FNIH, NIAMS  and  OARSI and to  Gordon & Carole Segal
OPENING SESSION <ul><li>OSTEOARTHRITIS: </li></ul><ul><li>CLASSIFICATION, RISK FACTORS, THERAPEUTIC & CLINICAL TRIAL IMPLI...
JOHN A. HARDIN, MD
A Cause for Urgency -  The personal impact - <ul><li>50 million Americans have arthritis. </li></ul><ul><li>9.5 million Am...
A Cause for Urgency -  The Cost - <ul><li>Arthritis accounts for almost 10% of our nations total health care costs. </li><...
CLINICAL SUBSETS OF OA/UNIQUE  PATHWAYS TO JOINT FAILURE <ul><li>JOEL BLOCK, MD </li></ul><ul><li>CHAIR </li></ul>
<ul><li>DAVID T. FELSON, MD, MPH </li></ul>
An Overview of the Epidemiology of Osteoarthritis  David T. Felson MD MPH Boston University School of Medicine
Definition of Osteoarthritis <ul><li>A painful disorder in which local areas in a joint are damaged </li></ul><ul><li>All ...
 
Outline of Talk <ul><li>The prevalence and impact of OA now  and in the future </li></ul><ul><li>What are the risk factors...
The Prevalence of Osteoarthritis (OA) <ul><li>The most common type of arthritis.  </li></ul><ul><ul><li>Of those  >  65 ye...
Prevalence of Knee Pain and Osteoarthritis in Persons Age 55 and Over  Population of adults aged 55+ years 160 1250 2500 1...
Is Symptomatic OA Much More Common than We Estimated?* *From Cibere et al, AC+R,2010
Impact of Osteoarthritis <ul><li>Cuts 1.9 years on average from the remaining number of healthy years.  (Losina et al, 201...
Painful Osteoarthritis: Future Shock in U.S. <ul><li>27 million currently affected </li></ul>40 million affected in 2020 A...
Systemic  Factors Affecting Joint Vulnerability Older Age Female Gender Caucasian Race (hip) Genetic Susceptibility Intrin...
OBESITY AND KNEE OSTEOARTHRITIS IN CAUCASIAN FEMALES* Percent with Radiographic Knee Osteoarthritis ( >  Grade 2) *from An...
Is Osteoarthritis More than One Disease? (does it consist of >1 phenotype?)
Phenotype <ul><li>Wikipedia: A  phenotype  is an  observable characteristic  or trait of an organism such as its morpholog...
Could Phenotype be Relevant in OA? <ul><li>OA: final common pathway of joint destruction for multiple etiologies (trauma, ...
What Factors Define Phenotypes? <ul><ul><li>Genetics (e.g. BRCA; EGFR Mutation)  </li></ul></ul><ul><ul><li>Risk/Etiologic...
Are Phenotypes Likely to be Important in OA? <ul><ul><li>If treatment only works in phenotype, we will miss effect in all ...
Percent of Knee OA Due to  Hypothesized Causes of Knee OA
Questions Addressed  <ul><li>1  Based on  evidence, what are the likely subtypes of OA? </li></ul><ul><li>2. How will we d...
Which Phenotypes are supported by Evidence in OA? <ul><li>Generalized vs. Joint Specific (Hand/Knee/Hip) OA  </li></ul><ul...
GDF-5 snp  and Hip OA: Meta-analysis   Evangelou et al, 2009
GDF-5 snp  and Knee OA: Meta-analysis
GDF-5 snp  and Hand OA: Meta-analysis
Grade 1 From Rheumatol 2009
Secondary vs. Primary OA   Example: Meniscal Tear and Knee OA
Percentage of Knees with Degenerative Changes after Meniscal Removal  Compared to Opposite (Unoperated) Knee Years of Foll...
Which Phenotypes are supported by Evidence in OA <ul><li>Generalized vs. Joint Specific (Hand/Knee/Hip) OA  </li></ul><ul>...
Evidence of Inadequate Diffuse Noxious Inhibitory Control in Hip OA (generalized pain) Kosek and Ordeberg, OA&Cartilage, 2...
One Probable OA subtype: Malaligned Joints <ul><li>Malaligned vs. nonmalaligned: potent effect on progression </li></ul><u...
BMI and Its Effect on Incident vs. Progressive OA  From  Niu et al, 2008
Which Phenotypes of OA exist based on Current Evidence?  <ul><li>Generalized vs. Localized OA </li></ul><ul><li>Secondary ...
Methods for Finding Distinct OA Phenotypes <ul><ul><li>Factor or Cluster analysis: statistical approach  </li></ul></ul><u...
How to Identify or Confirm Phenotypes? <ul><li>Large studies best for identifying subtypes even initially </li></ul><ul><l...
Conclusions <ul><li>OA is a remarkably common, painful and disabling disorder </li></ul><ul><li>It will become more common...
Conclusions about Phenotypes in OA <ul><li>In OA identifying different phenotypes may be critical to  treatment/prevention...
Appreciations <ul><li>Funding: NIAMS, NIA and the Arthritis Foundation </li></ul><ul><li>Specific thanks for help in think...
 
Effect of Obesity on Progression by Limb Alignment Status Felson et al, 2004
Prevalence of Knee Pain and Osteoarthritis in Persons Age 55 and Over  Population of adults aged 55+ years 160* 1250 2500 ...
OA vs. no OA: How big a difference on x-ray? (K/L 2 vs. 1) K/L Grade 1 K/L Grade  2
New Onset vs. Progressive OA <ul><li>To distinguish new onset (de novo; incident) vs. progressive (OA existing at start), ...
Other Possible Phenotypes in OA <ul><li>Within Joint Genetic Phenotypes </li></ul><ul><li>Painful vs. nonpainful (50% of p...
Percent of Progressive Knee OA Among Knee OA cases
<ul><li>Meniscus and OA:  </li></ul><ul><ul><li>Up to 40% of persons age 50/60/older have meniscal tears </li></ul></ul><u...
 
Malalignment & OA Progression  <ul><li>240 subjects with knee OA followed 18 months </li></ul><ul><li>Varus  (bowlegged)  ...
<ul><li>STEFAN LOHMANDER, MD, PhD </li></ul>
<ul><li>NIZAR MAHOMED, MD </li></ul>
<ul><li>RICHARD F. LOESER, JR., MD </li></ul>
<ul><li>JOHN LOUGHLIN, PhD </li></ul>
THE JOINT AS AN ORGAN: Identifying Targets for Intervention <ul><li>MARY GOLDRING, PhD, </li></ul><ul><li>CHAIR </li></ul>
<ul><li>ROBIN A. POOLE, PhD, DSc </li></ul>
<ul><li>STEVEN R. GOLDRING, MD </li></ul>
<ul><li>CARLA R. SCANZELLO, MD, PhD </li></ul>
<ul><li>LAWRENCE BONASSAR, PhD </li></ul>
<ul><li>VANIA APKARIAN, PhD </li></ul>
OA RISK FACTORS: Can They Be Addressed Therapeutically? <ul><li>JOHN SANDY, PhD </li></ul><ul><li>CHAIR </li></ul>
<ul><li>THOMAS ANDRIACCHI, PhD </li></ul>
<ul><li>JOSEPH BUCKWALTER, MD </li></ul>
<ul><li>RICHARD F. LOESER, JR., MD </li></ul>
<ul><li>MARTIN K. LOTZ, MD </li></ul>
EVALUATION OF OA DIAGNOSIS AND PROGRESSION <ul><li>MARC HOCHBERG, MD, MPH </li></ul><ul><li>CHAIR </li></ul>
<ul><li>VIRGINIA KRAUS, MD, PhD </li></ul>
<ul><li>HOLLIS POTTER, MD </li></ul>
<ul><li>GARRY GOLD, MD </li></ul>
<ul><li>TOM ANDRIACCHI, PhD </li></ul>
WHAT HAVE WE LEARNED ABOUT OA FROM ANIMAL MODELS? Kenneth D. Brandt, MD University of Kansas Medical Center
Although the most obvious pathologic  changes in an OA joint are usually seen  in the articular   cartilage,  ALL  of the ...
Previous definitions of OA have  been far too   chondrocentric.   The  etiopathogenesis  of OA is very different from the ...
Advanced OA of  the Knee
 
 
 
Osteoarthritis (OA)  is  NOT   a degenerative joint disease (“DJD”).
 
 
The  real  problem isn’t OA;  it’s   painful  OA.
 
 
 
 
 
Neurogenic Acceleration of OA
 
 
 
 
 
 
? Post-Rehabilitation Arthritis
 
ADVANCING THE CARE OF PATIENTS WITH OA <ul><li>THE PATIENT PERSPECTIVE </li></ul><ul><li>KENT KWOH, MD </li></ul><ul><li>C...
Robin Katzanek,  PT, MA, PhD <ul><li>Osteoarthritis Advisory Group </li></ul>
Osteoarthritis Advisory Group <ul><li>We represent a community of people who share a personal and common interest in elimi...
Osteoarthritis Advisory Group <ul><li>We voice the needs of the OA community to Arthritis Foundation leadership regarding ...
We put a face on OA as a life-altering disease
One of 27 million with OA <ul><li>Diagnosed at age 30 years </li></ul><ul><li>Years of running and other athletic pursuits...
Physical Therapist <ul><li>42-year-old groundskeeper </li></ul><ul><li>46-year-old mother of three </li></ul><ul><li>53-ye...
Concerns of People with OA <ul><li>Pain </li></ul><ul><li>Medication </li></ul><ul><li>Surgery </li></ul><ul><li>Lifestyle...
What Do We Want? <ul><li>Limit medications & their side effects </li></ul><ul><li>Work </li></ul>
What Do We Want? <ul><li>Disease control </li></ul><ul><li>Enjoy activities </li></ul><ul><li>Live life to its </li></ul><...
<ul><li>MARCY O’KOON </li></ul>
<ul><li>PATIENCE WHITE, MD </li></ul>
<ul><li>GILLIAN HAWKER, MD, MSc </li></ul>
<ul><li>JOANNE JORDAN, MD, MPH </li></ul>
CLINICAL TRIAL DESIGN <ul><li>THOMAS SCHNITZER, MD, PhD </li></ul><ul><li>CHAIR </li></ul>
<ul><li>MARC HOCHBERG, MD, PhD </li></ul>
<ul><li>ELENA LOSINA, PhD </li></ul>
<ul><li>GAYLE LESTER, PhD </li></ul>
<ul><li>LINDA SANDELL, PhD </li></ul>
<ul><li>JEFFREY KRAINES, MD </li></ul><ul><li>MARIE-PIERE HELLIO LE GRAVERAND-GASTINEAU, MD, DSc, PhD </li></ul><ul><li>PE...
A PLAN FOR ACTION NEXT STEPS <ul><li>JOHN ESDAILE </li></ul><ul><li>CHAIR </li></ul>
AF RESOURCES/PRIORITIES <ul><li>JOHN A HARDIN, MD </li></ul>
PUBLIC/PRIVATE PARTNERSHIPS <ul><li>ERIC NELSON </li></ul>
REPORT FROM THE AOSSM <ul><li>CONSTANCE CHU </li></ul>
BREAKOUT SESSIONS: PURPOSE & GOALS <ul><li>ROBIN A. POOLE, PhD, DSc </li></ul>
GROUP DISCUSSION
<ul><li>FUTURE ACTIVITIES FOR ADVANCING THE GOALS TREATMENT OF OA </li></ul>
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Segal North American Osteoarthritis Worshop

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Segal North American Osteoarthritis Worshop

  1. 3. with additional gratitude to our scientific partners AOSSM, FNIH, NIAMS and OARSI and to Gordon & Carole Segal
  2. 4. OPENING SESSION <ul><li>OSTEOARTHRITIS: </li></ul><ul><li>CLASSIFICATION, RISK FACTORS, THERAPEUTIC & CLINICAL TRIAL IMPLICATIONS </li></ul>
  3. 5. JOHN A. HARDIN, MD
  4. 6. A Cause for Urgency - The personal impact - <ul><li>50 million Americans have arthritis. </li></ul><ul><li>9.5 million Americans are disabled by arthritis. </li></ul><ul><li>8 million Americans are disabled by </li></ul><ul><ul><li>back pain. </li></ul></ul><ul><li>In contrast, 3 million Americans are </li></ul><ul><ul><li>disabled by heart disease. </li></ul></ul>
  5. 7. A Cause for Urgency - The Cost - <ul><li>Arthritis accounts for almost 10% of our nations total health care costs. </li></ul><ul><li>Back pain is a leading cause of lost productivity in the workplace. </li></ul>
  6. 8. CLINICAL SUBSETS OF OA/UNIQUE PATHWAYS TO JOINT FAILURE <ul><li>JOEL BLOCK, MD </li></ul><ul><li>CHAIR </li></ul>
  7. 9. <ul><li>DAVID T. FELSON, MD, MPH </li></ul>
  8. 10. An Overview of the Epidemiology of Osteoarthritis David T. Felson MD MPH Boston University School of Medicine
  9. 11. Definition of Osteoarthritis <ul><li>A painful disorder in which local areas in a joint are damaged </li></ul><ul><li>All structures within the joint can be affected: </li></ul><ul><ul><li>Hyaline Cartilage loss (the defining feature) and fibrocartilage degeneration/loss </li></ul></ul><ul><ul><li>Bone remodelling and sclerosis </li></ul></ul><ul><ul><li>Chondro-osteophytes </li></ul></ul><ul><ul><li>Capsular thickening and distension </li></ul></ul><ul><ul><li>Synovial inflammation </li></ul></ul><ul><ul><li>Muscle atrophy and weakness </li></ul></ul>
  10. 13. Outline of Talk <ul><li>The prevalence and impact of OA now and in the future </li></ul><ul><li>What are the risk factors for OA? </li></ul><ul><li>Could OA be several different diseases and which ones? </li></ul>
  11. 14. The Prevalence of Osteoarthritis (OA) <ul><li>The most common type of arthritis. </li></ul><ul><ul><li>Of those > 65 years, </li></ul></ul><ul><ul><ul><li>11% have painful knee OA </li></ul></ul></ul><ul><ul><ul><li>5 % have painful hip OA </li></ul></ul></ul><ul><ul><li>Of those age 30 and over, 6% have knee OA; </li></ul></ul><ul><ul><ul><li>2% have hip OA ; </li></ul></ul></ul><ul><ul><li>Risk rises with age: by age 85, 45% of persons will get painful knee OA (higher if obese) </li></ul></ul>
  12. 15. Prevalence of Knee Pain and Osteoarthritis in Persons Age 55 and Over Population of adults aged 55+ years 160 1250 2500 10000 Shading represents the proportion in each category with radiographic evidence of knee osteoarthritis .
  13. 16. Is Symptomatic OA Much More Common than We Estimated?* *From Cibere et al, AC+R,2010
  14. 17. Impact of Osteoarthritis <ul><li>Cuts 1.9 years on average from the remaining number of healthy years. (Losina et al, 2011) </li></ul><ul><li>In the elderly, accounts for more lower extremity disability than any other disease (Guccione et al, 1994) </li></ul><ul><li>Accounts for most total knee and hip replacements </li></ul><ul><li>Shortens life (Nuesch et al, 2011) </li></ul>
  15. 18. Painful Osteoarthritis: Future Shock in U.S. <ul><li>27 million currently affected </li></ul>40 million affected in 2020 Aging of the population Increasing obesity Increased sports related injuries
  16. 19. Systemic Factors Affecting Joint Vulnerability Older Age Female Gender Caucasian Race (hip) Genetic Susceptibility Intrinsic Joint Vulnerabilities (Local Environment): Previous Damage (e.g. torn meniscus; ACL) Bridging Muscle Weakness Cartilage unable to repair Periph. Nervous System impairment Malalignment across joint Misshapen Joint (hips) Joint Susceptible to O.A. Loading Factors Acting on Joints : Obesity Injurious Physical Activities Osteoarthritis or Its Progression
  17. 20. OBESITY AND KNEE OSTEOARTHRITIS IN CAUCASIAN FEMALES* Percent with Radiographic Knee Osteoarthritis ( > Grade 2) *from Anderson and National Center for Health Statistics
  18. 21. Is Osteoarthritis More than One Disease? (does it consist of >1 phenotype?)
  19. 22. Phenotype <ul><li>Wikipedia: A phenotype is an observable characteristic or trait of an organism such as its morphology, development, biochemical or physiological properties, or behavior. </li></ul><ul><ul><ul><li>Observable characteristic: observable by naked eye/images/blood tests </li></ul></ul></ul><ul><ul><ul><li>Genotype expression can create phenotype variation </li></ul></ul></ul><ul><li>Phenotype = subtype </li></ul><ul><li>We shall define a subtype ONLY when it is important as follows: </li></ul><ul><ul><li>Affects treatment (e.g. estrogen receptor +/- breast cancer) </li></ul></ul><ul><ul><li>Changes prevention approach (e.g. BRCA) </li></ul></ul><ul><ul><li>Alters conceptual approach/biology of disease (e.g. H Pylori) </li></ul></ul>
  20. 23. Could Phenotype be Relevant in OA? <ul><li>OA: final common pathway of joint destruction for multiple etiologies (trauma, developmental, primary cartilage disorder, crystal) </li></ul><ul><li>OA: collection of different disorders producing common phenotype </li></ul><ul><li> IDENTIFYING PHENOTYPES (SUBTYPES) MAY BE CRITICAL TO DEVELOPMENT OF EFFECTIVE TREATMENT/PREVENTION </li></ul>
  21. 24. What Factors Define Phenotypes? <ul><ul><li>Genetics (e.g. BRCA; EGFR Mutation) </li></ul></ul><ul><ul><li>Risk/Etiologic Factors: (e.g. developmental abnormalities in hip OA  early surgery) </li></ul></ul><ul><ul><li>Severity (e.g. TNM classification for a variety of cancers) </li></ul></ul>
  22. 25. Are Phenotypes Likely to be Important in OA? <ul><ul><li>If treatment only works in phenotype, we will miss effect in all disease patients (e.g. treatment targeted to bone marrow lesions) </li></ul></ul><ul><ul><li>If treatment does not work in subtype and subtype is common, may miss effect of treatment on disease (e.g. malalignment of knee creates too much stress for chondroprotective agent to work. </li></ul></ul>
  23. 26. Percent of Knee OA Due to Hypothesized Causes of Knee OA
  24. 27. Questions Addressed <ul><li>1 Based on evidence, what are the likely subtypes of OA? </li></ul><ul><li>2. How will we determine/confirm subtypes? </li></ul>
  25. 28. Which Phenotypes are supported by Evidence in OA? <ul><li>Generalized vs. Joint Specific (Hand/Knee/Hip) OA </li></ul><ul><li>Secondary (Cause identified; acts alone) vs. Primary OA (idiopathic; network of risk factors) </li></ul><ul><li>Painful vs. nonpainful joints (50% of persons with X-ray OA have little, if any, pain in affected joint) </li></ul><ul><li>-Dysfunctional vs. functional pain </li></ul><ul><li>Malaligned vs. nonmalaligned joints </li></ul>
  26. 29. GDF-5 snp and Hip OA: Meta-analysis Evangelou et al, 2009
  27. 30. GDF-5 snp and Knee OA: Meta-analysis
  28. 31. GDF-5 snp and Hand OA: Meta-analysis
  29. 32. Grade 1 From Rheumatol 2009
  30. 33. Secondary vs. Primary OA Example: Meniscal Tear and Knee OA
  31. 34. Percentage of Knees with Degenerative Changes after Meniscal Removal Compared to Opposite (Unoperated) Knee Years of Follow-up <10 10-19 20-29 30-40 Meniscectomy 21% 23% 53% 67% Contralateral Knee 4% 4% 13% 0%
  32. 35. Which Phenotypes are supported by Evidence in OA <ul><li>Generalized vs. Joint Specific (Hand/Knee/Hip) OA </li></ul><ul><li>Secondary (Cause identified; acts alone) vs. Primary OA (idiopathic; acts with network of other factors) </li></ul><ul><li>Painful vs. nonpainful joints (50% of persons with X-ray OA have little, if any, pain in affected joint) </li></ul><ul><li>-Dysfunctional vs. functional pain </li></ul><ul><li>Malaligned vs. nonmalaligned joints </li></ul>
  33. 36. Evidence of Inadequate Diffuse Noxious Inhibitory Control in Hip OA (generalized pain) Kosek and Ordeberg, OA&Cartilage, 2000
  34. 37. One Probable OA subtype: Malaligned Joints <ul><li>Malaligned vs. nonmalaligned: potent effect on progression </li></ul><ul><li>-high focal stress with malalignment that may transcend ability of joint cartilage/bone to withstand it. </li></ul><ul><li>-bone marrow lesions, traumatic lesions in bone, associated with malalignment  malalignment damages bone </li></ul><ul><li>In malaligned knees, effects of other risk factor eliminated </li></ul><ul><li>Implications  Treatment targeted to cartilage protection will not work in malaligned knees </li></ul>
  35. 38. BMI and Its Effect on Incident vs. Progressive OA From Niu et al, 2008
  36. 39. Which Phenotypes of OA exist based on Current Evidence? <ul><li>Generalized vs. Localized OA </li></ul><ul><li>Secondary vs. Primary OA? (secondary more common than previously believed) </li></ul><ul><li>Painful vs. Nonpainful OA; subtype with dysfunctional pain </li></ul><ul><li>Malaligned vs. nonmalaligned Joints with OA: response to treatment may differ </li></ul>
  37. 40. Methods for Finding Distinct OA Phenotypes <ul><ul><li>Factor or Cluster analysis: statistical approach </li></ul></ul><ul><ul><li>Genome Wide Association Study (GWAS) : investigate phenotype specific SNP’s (must have good data on phenotypes in the data sets) </li></ul></ul><ul><ul><li>Epidemiologic: test if other major risk factors affect risk the same way in those with and without the phenotype (e.g.malalignment) </li></ul></ul><ul><ul><li>Make guesses based on biology and confirm them in 2 or more studies (e.g. from lung cancer) </li></ul></ul>
  38. 41. How to Identify or Confirm Phenotypes? <ul><li>Large studies best for identifying subtypes even initially </li></ul><ul><li>Subtype must define response to treatment or prevention strategy or must provide evidence that there are important biologic differences among types of disease </li></ul><ul><li>Confirmation in independent studies critical (see work by Ioannidis in GWAS studies) </li></ul>
  39. 42. Conclusions <ul><li>OA is a remarkably common, painful and disabling disorder </li></ul><ul><li>It will become more common </li></ul><ul><li>Risk factors include: aging, obesity, genetics, joint injury and as yet other unknown factors </li></ul>
  40. 43. Conclusions about Phenotypes in OA <ul><li>In OA identifying different phenotypes may be critical to treatment/prevention/disease biology </li></ul><ul><li>Phenotypes of OA include: </li></ul><ul><ul><li>Generalized vs. Joint Specific OA </li></ul></ul><ul><ul><li>Painful vs. Nonpainful (and in those with pain, functional vs. dysfunctional pain likely subtypes) </li></ul></ul><ul><ul><li>Secondary vs. Primary OA (more secondary) </li></ul></ul><ul><ul><li>Malaligned vs. neutrally aligned knee OA (probable) </li></ul></ul><ul><li>Identifying new phenotypes will be challenging and requires multiple replicative studies </li></ul>
  41. 44. Appreciations <ul><li>Funding: NIAMS, NIA and the Arthritis Foundation </li></ul><ul><li>Specific thanks for help in thinking about phenotypes go to: Tuhina Neogi, Yuqing Zhang, Jingbo Niu and the Clin Epi Group at B.U. </li></ul>
  42. 46. Effect of Obesity on Progression by Limb Alignment Status Felson et al, 2004
  43. 47. Prevalence of Knee Pain and Osteoarthritis in Persons Age 55 and Over Population of adults aged 55+ years 160* 1250 2500 10000 * The proportion with radiographic evidence in this category is not known, though seems likely to be high. Dark shading represents the proportion in each category with radiographic evidence of knee osteoarthritis . Persons with X-ray OA
  44. 48. OA vs. no OA: How big a difference on x-ray? (K/L 2 vs. 1) K/L Grade 1 K/L Grade 2
  45. 49. New Onset vs. Progressive OA <ul><li>To distinguish new onset (de novo; incident) vs. progressive (OA existing at start), must be able to distinguish OA vs. nonOA. </li></ul><ul><li>Vs. OA as continuum of severity </li></ul><ul><li>Evidence: </li></ul><ul><li>->90% of Framingham Study Community Knee MRI’s show osteophytes (?OA) </li></ul><ul><li>-Reader disagreement maximal for Kellgren/Lawrence grade 1 (nonOA) vs. mild OA (K/L grade 2) </li></ul>
  46. 50. Other Possible Phenotypes in OA <ul><li>Within Joint Genetic Phenotypes </li></ul><ul><li>Painful vs. nonpainful (50% of persons with X-ray OA have little, if any, pain in affected joint) </li></ul><ul><li>-Generalized pain vs. functional pain </li></ul><ul><li>Malaligned vs. nonmalaligned (is this real or a function of difficulties studying progression) </li></ul>
  47. 51. Percent of Progressive Knee OA Among Knee OA cases
  48. 52. <ul><li>Meniscus and OA: </li></ul><ul><ul><li>Up to 40% of persons age 50/60/older have meniscal tears </li></ul></ul><ul><ul><li>Those with tears have marked increased risk of OA (Englund, A+R, 2009) </li></ul></ul><ul><ul><li>Up to half of knee OA may be due, in part, to tears </li></ul></ul><ul><ul><li>Could other more subtle injuries account for the rest? </li></ul></ul>Englund et al, NEJM, 2008
  49. 54. Malalignment & OA Progression <ul><li>240 subjects with knee OA followed 18 months </li></ul><ul><li>Varus (bowlegged) 3.5 fold increased risk (p<.001) for medial progression </li></ul><ul><li>Valgus (knockneed) 3.8 fold increased risk (p<.001) for lateral progression </li></ul><ul><li>Severe varus or valgus knees with worsening pain and disability </li></ul>Sharma, L et al ,, JAMA, 2001 .
  50. 55. <ul><li>STEFAN LOHMANDER, MD, PhD </li></ul>
  51. 56. <ul><li>NIZAR MAHOMED, MD </li></ul>
  52. 57. <ul><li>RICHARD F. LOESER, JR., MD </li></ul>
  53. 58. <ul><li>JOHN LOUGHLIN, PhD </li></ul>
  54. 59. THE JOINT AS AN ORGAN: Identifying Targets for Intervention <ul><li>MARY GOLDRING, PhD, </li></ul><ul><li>CHAIR </li></ul>
  55. 60. <ul><li>ROBIN A. POOLE, PhD, DSc </li></ul>
  56. 61. <ul><li>STEVEN R. GOLDRING, MD </li></ul>
  57. 62. <ul><li>CARLA R. SCANZELLO, MD, PhD </li></ul>
  58. 63. <ul><li>LAWRENCE BONASSAR, PhD </li></ul>
  59. 64. <ul><li>VANIA APKARIAN, PhD </li></ul>
  60. 65. OA RISK FACTORS: Can They Be Addressed Therapeutically? <ul><li>JOHN SANDY, PhD </li></ul><ul><li>CHAIR </li></ul>
  61. 66. <ul><li>THOMAS ANDRIACCHI, PhD </li></ul>
  62. 67. <ul><li>JOSEPH BUCKWALTER, MD </li></ul>
  63. 68. <ul><li>RICHARD F. LOESER, JR., MD </li></ul>
  64. 69. <ul><li>MARTIN K. LOTZ, MD </li></ul>
  65. 70. EVALUATION OF OA DIAGNOSIS AND PROGRESSION <ul><li>MARC HOCHBERG, MD, MPH </li></ul><ul><li>CHAIR </li></ul>
  66. 71. <ul><li>VIRGINIA KRAUS, MD, PhD </li></ul>
  67. 72. <ul><li>HOLLIS POTTER, MD </li></ul>
  68. 73. <ul><li>GARRY GOLD, MD </li></ul>
  69. 74. <ul><li>TOM ANDRIACCHI, PhD </li></ul>
  70. 75. WHAT HAVE WE LEARNED ABOUT OA FROM ANIMAL MODELS? Kenneth D. Brandt, MD University of Kansas Medical Center
  71. 76. Although the most obvious pathologic changes in an OA joint are usually seen in the articular cartilage, ALL of the tissues of the joint are involved, including the subchondral bone, synovium, muscles, nerves and ligaments.
  72. 77. Previous definitions of OA have been far too chondrocentric. The etiopathogenesis of OA is very different from the pathogenesis of articular cartilage breakdown in OA. ETIOPATHOGENESIS OF OA
  73. 78. Advanced OA of the Knee
  74. 82. Osteoarthritis (OA) is NOT a degenerative joint disease (“DJD”).
  75. 85. The real problem isn’t OA; it’s painful OA.
  76. 91. Neurogenic Acceleration of OA
  77. 98. ? Post-Rehabilitation Arthritis
  78. 100. ADVANCING THE CARE OF PATIENTS WITH OA <ul><li>THE PATIENT PERSPECTIVE </li></ul><ul><li>KENT KWOH, MD </li></ul><ul><li>CHAIR </li></ul>
  79. 101. Robin Katzanek, PT, MA, PhD <ul><li>Osteoarthritis Advisory Group </li></ul>
  80. 102. Osteoarthritis Advisory Group <ul><li>We represent a community of people who share a personal and common interest in eliminating arthritis as the leading source of disability in this country </li></ul>
  81. 103. Osteoarthritis Advisory Group <ul><li>We voice the needs of the OA community to Arthritis Foundation leadership regarding the prevention, control and cure of osteoarthritis </li></ul>
  82. 104. We put a face on OA as a life-altering disease
  83. 105. One of 27 million with OA <ul><li>Diagnosed at age 30 years </li></ul><ul><li>Years of running and other athletic pursuits </li></ul><ul><li>Multiple meniscectomies </li></ul>
  84. 106. Physical Therapist <ul><li>42-year-old groundskeeper </li></ul><ul><li>46-year-old mother of three </li></ul><ul><li>53-year-old laborer </li></ul>
  85. 107. Concerns of People with OA <ul><li>Pain </li></ul><ul><li>Medication </li></ul><ul><li>Surgery </li></ul><ul><li>Lifestyle </li></ul><ul><li>Disease Progression </li></ul>
  86. 108. What Do We Want? <ul><li>Limit medications & their side effects </li></ul><ul><li>Work </li></ul>
  87. 109. What Do We Want? <ul><li>Disease control </li></ul><ul><li>Enjoy activities </li></ul><ul><li>Live life to its </li></ul><ul><li>fullest </li></ul>
  88. 110. <ul><li>MARCY O’KOON </li></ul>
  89. 111. <ul><li>PATIENCE WHITE, MD </li></ul>
  90. 112. <ul><li>GILLIAN HAWKER, MD, MSc </li></ul>
  91. 113. <ul><li>JOANNE JORDAN, MD, MPH </li></ul>
  92. 114. CLINICAL TRIAL DESIGN <ul><li>THOMAS SCHNITZER, MD, PhD </li></ul><ul><li>CHAIR </li></ul>
  93. 115. <ul><li>MARC HOCHBERG, MD, PhD </li></ul>
  94. 116. <ul><li>ELENA LOSINA, PhD </li></ul>
  95. 117. <ul><li>GAYLE LESTER, PhD </li></ul>
  96. 118. <ul><li>LINDA SANDELL, PhD </li></ul>
  97. 119. <ul><li>JEFFREY KRAINES, MD </li></ul><ul><li>MARIE-PIERE HELLIO LE GRAVERAND-GASTINEAU, MD, DSc, PhD </li></ul><ul><li>PETER MITCHELL, PhD </li></ul><ul><li>GLORIA MATTHEWS, DVM </li></ul><ul><li>ROY BLACK, PhD </li></ul><ul><li>BROOKS STORY </li></ul>
  98. 120. A PLAN FOR ACTION NEXT STEPS <ul><li>JOHN ESDAILE </li></ul><ul><li>CHAIR </li></ul>
  99. 121. AF RESOURCES/PRIORITIES <ul><li>JOHN A HARDIN, MD </li></ul>
  100. 122. PUBLIC/PRIVATE PARTNERSHIPS <ul><li>ERIC NELSON </li></ul>
  101. 123. REPORT FROM THE AOSSM <ul><li>CONSTANCE CHU </li></ul>
  102. 124. BREAKOUT SESSIONS: PURPOSE & GOALS <ul><li>ROBIN A. POOLE, PhD, DSc </li></ul>
  103. 125. GROUP DISCUSSION
  104. 126. <ul><li>FUTURE ACTIVITIES FOR ADVANCING THE GOALS TREATMENT OF OA </li></ul>

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