The Evolving Role of Obesity in Knee Osteoarthritis

MaryFran R. Sowers; Carrie A. Karvonen-Gutierrez

Disclosures

Curr Opin Rheumatol. 2010;22(5):533-537. 

In This Article

Abstract and Introduction

Abstract

Purpose of review The frequency of knee osteoarthritis continues to accelerate, likely because of the increasing proliferation of obesity, particularly in men and women 40–60 years of age at the leading edge of the 'baby boom' demographic expansion. The increasing pervasiveness of obesity and the growing appreciation of obesity's accompanying metabolic/inflammatory activities suggest rethinking the knee osteoarthritis paradigm.
Recent findings Whereas once knee osteoarthritis was considered a 'wear-and-tear' condition, it is now recognized that knee osteoarthritis exists in the highly metabolic and inflammatory environments of adiposity. Cytokines associated with adipose tissue, including leptin, adiponectin, and resistin, may influence osteoarthritis though direct joint degradation or control of local inflammatory processes. Further, pound-for-pound, not all obesity is equivalent for the development of knee osteoarthritis; development appears to be strongly related to the co-existence of disordered glucose and lipid metabolism. Additionally, obesity loads may be detected by mechanoreceptors on chondrocyte surfaces triggering intracellular signaling cascades of cytokines, growth factors, and metalloproteinases.
Summary This review summarizes recent literature about obesity, knee osteoarthritis and joint pain. Consideration of adipocytokines, metabolic factors, and mechanical loading-metabolic factor interactions will help to broaden the thinking about targets for both prevention and intervention for knee osteoarthritis.

Introduction

This review will address recent literature about knee osteoarthritis and obesity: two conditions whose prevalence is accelerating worldwide. The review includes the potential association of knee osteoarthritis and selected adipocytokines including leptin, adiponectin, and resistin, the group of cytokines related to fat cells. In addition, the co-occurrence of obesity plus cardiometabolic factors appears to alter risk of knee osteoarthritis as compared with obesity without these cardiometabolic factors. Considering interactions between mechanical loading and these metabolic factors can help broaden approaches to both prevention and intervention for knee osteoarthritis.

Osteoarthritis is a highly prevalent joint disorder estimated to affect more than 37% of adults over the age of 60;[1] it is a leading cause of pain and disability. Osteoarthritis is associated with considerable loss in productivity and healthcare expenditures, accounting for 97% of the total knee replacements and 83% of the total hip replacements in 2004.[2] Using national data, the Healthcare Cost and Utilization Project showed that osteoarthritis accounted for US$ 10.5 billion in hospital charges in 2006, making it a more expensive condition than pneumonia, stroke, or complications from diabetes. Hospital admissions for arthritis more than doubled from 1993 to 2006.[2]

The frequency of knee osteoarthritis continues to accelerate, likely because of the aging of the population and the increasing proliferation of the primary risk factor, obesity. There is an increasingly greater proportion of the total population, both in the United States and worldwide,[3] over age 60, the age range typically associated with having osteoarthritis. Although the prevalence of obesity is rising in this elderly segment of the population, it is the escalating prevalence of obesity in those men and women aged 40–60 years, who are simultaneously at the leading edge of the baby boomer demographic expansion, that are the major contributors to the burgeoning osteoarthritis population.

Obesity has long been recognized as a risk factor for prevalent osteoarthritis, especially knee osteoarthritis[4–9] although the obesity definition based on a BMI more than 30 kg/m2 was not widely adopted until the 1990s.[10] Data from a study of a general British population suggested that women in the highest tertile of BMI had six-fold increased odds of knee osteoarthritis (OAK) and nearly 18 times higher odds of bilateral OAK, compared with women in the lowest tertile of BMI.[11] Similarly, a study of US African-American and Caucasian women identified higher risk of prevalent knee osteoarthritis with higher BMI levels.[12] Longitudinal studies show that increased weight precedes the presentation of OAK; in a longitudinal study of men and women aged 40–64 years, Manninen et al.[8] reported that for every standard deviation increase in BMI (3.8 kg/m2), there was a 40% increased risk [relative risk (RR) = 1.4; 95% confidence interval (CI) 1.2–1.5] for developing OAK.

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