Obesity and OsteoarthritisMore than just wear and tear

Jonathan T. Bravman, MDCU Sports MedicineDivision of Sports Medicine and Shoulder SurgeryUniversity of Colorado Department of Orthopedics Denver, Colorado

Basis of the talk

Journal of the American Academy of Orthopaedic Surgery, March 2013

Purpose

Present data available in 2013 regarding: The effect of obesity on osteoarthritis The effect of weight loss and exercise for

treatment of osteoarthritis in obese patients

The traditional orthopaedic approach to obesity

Obesity and Osteoarthritis

OA

Biomechanical

Theories

Systemic Theories

Osteoarthritis is strongly correlated with high BMI

The Biomechanical Theories

The intuitive theoriesMost studies involve the kneeSurprising lack of data to support

them (presented evidence here is weak)

#1 Increased load and wear theory

Increased load = increased wear = increased pain

Load exerted on knee: 3x body weight with walking

5x body weight with stairs

200 lb 1000 lb (1/2 ton)

=

Increased load and wear

Obesity increases subchondral bone density and stiffness

Load is redistributed on cartilage causing increased wear

#2 Muscular deconditioning theory

Obese are generally deconditioned Relative quadriceps weakness, muscle

imbalance, and impaired control have been observed in adults with OA vs. none

Decreased muscle mass is associated with increased knee cartilage (Arthritis Rheum. 2005 Feb;52(2):461-7)

Reduced muscle strength relative to body weight causes early quadriceps fatigue in the obese: Reduced shock attenuation Increased loading Increased WEAR Increased variability in loading

BMI is associated with severity of joint space narrowing of the knee in varus malalignment (but not valgus)

Increased adduction moment increases medial compartment wear

Adduction moment increases with age in the obese but not in normal-weight individuals

#3 Malalignment causes increased wear theory

Malalignment smaller role than originally thought mediates other risk factors such as

obesity “The clinician should focus on what is

definitively modifiable…obesity, in particular”

Systemic Effects of Obesity Less intuitive, newer, possibly more important Adipose tissue is not just an energy depot White adipose tissue = immunologically active

organ Cytokines: small cell-signaling peptides Adipokines: pro-inflammatory cytokines

derived primarily from adipose tissue

The Adipokine Family

Important members: Leptin Resistin Adiponectin Visfatin

Active in cartilage regulationExact role of each is unclear but

many studies are currently underway

Leptin Present in synovial fluid of joints with OA levels in both synovial fluid and plasma

correlate closely with BMI Marked expression in OA cartilage and

osteophytes compared to minimal in normal cartilage

First to suggest that leptin plays an important role in pathophysiology of OA

Leptin paved the way for adipokines

Acts on hypothalamus to decrease food intake and increase energy expenditure

Closely linked to the immune systemSynovial fluid levels strongly linked

to radiographic severity of OA!!

Cartilage taken from TKA proceduresLeptin upregulated multiple MMPs in

cartilageLeptin levels correlate with multiple

MMPs in synovial fluid from OA pts

Conclusion: Leptin has a catabolic effect in OA joints

Adiponectin

Adipocyte-derived hormone with known anti-diabetic and anti-atherogenic properties

Found in OA synovial fluid and chondrocytes

Upregulates TIMP-2 and downregulates MMP-13

Researchers feel it is critically involved in pathogenesis of OA

Hand xrays compared at baseline and 6 years

Serum adipokines measured at baseline

Obesity causes a low-grade inflammatory state

Increased levels of adipokines Elevated inflammatory markers in obese:

CRP, ESR, IL-6, and TNF Inflammation plays a role in OA,

cardiovascular disease, DM, dyslipidemia, respiratory disorders, autoimmune disorders, and cancer

Development of OA is both mechanical and metabolic

Mechanoreceptors on chondrocyte surfaces may detect obesity load and trigger intracellular signaling cascades

Adiposity is highly metabolic and inflammatory

Development of OA appears strongly correlated with disordered glucose and lipid metabolism

Adipokines may cause direct cartilage degredation

Is OA an inflammatory arthropathy?

Leptin and adiponectin are key mediators in inducing cartilage breakdown

Work with MMPs, nitric oxide, and interleukins

Therapeutic targets for OA treatment??

The Metabolic Syndrome

“a cluster of conditions…that occur together increasing your risk of heart disease, stroke, and diabetes”1. excess body fat around the waist2. increased blood pressure3. elevated insulin levels4. abnormal cholesterol levels

Being overweight and inactive are “major contributors”

Treatment: exercise, weight loss, eat healthy, and stop smoking

Combing Biomechanical and Systemic TheoriesPredominant theory behind OA now

is that it occurs from local mechanical factors acting in the context of systemic susceptibility

Black box

MSK pain in the obese patient Obesity and overweight are associated

with increased musculoskeletal pain The impact of pain on functional status

and health-related quality of life is greater in the the obese

The metabolic syndrome is associated with chronic pain

Central obesity is the metabolic syndrome component most directly associated with pain (beyond OA or neuropathy)

There is a strong relationship:

obesity depression

55%

58%

The question:

Is the patient’s knee pain caused by obesity or osteoarthritis or both?

How do we figure this out? 1. Weight loss trial2. Surgical trial (knee scope vs. TKA)

Is the risk of surgery justifiable to answer this?

Weight Loss as a Treatment for Joint Pain

Weight loss is difficult for physician and patient

Unfortunately, few studies have looked at MSK outcomes after weight loss: Wt loss reduces risk of symptomatic OA Bariatric surgery: decreases overall joint

pain

48 morbidly obese subjects → bariatric surg

Lost avg 90 lbs

MSK pain complaints:

100% preop 23% postop

Few new risk factors for OA have been identified in the past few years

The only 2 modifiable risk factors with sufficient evidence to support intervention for preventing OA: Weight loss Avoiding traumatic injury

Myokines: the anti-inflammatory effect of exercise

Exercise increases production of myokines from muscles → induces lypolysis + inhibits TNF + decreases insulin resistance

Summary

• Obesity is an epidemic in the US• Osteoarthritis is not just “wear and tear” and

adipose tissue is not just an energy storage organ• The medical risk:benefit ratio for weight loss in

obese patients approaches ZERO• Orthopaedic surgery is not a cure for obesity, but

weight loss has potential to cure orthopaedic conditions

Thank You References available:

ryanckoonce@gmail.com

Talk to him…please

Jonathan T. Bravman, MD

Jonathan.Bravman@UCDenver.edu