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ORIGINAL ARTICLE
Year : 2022  |  Volume : 25  |  Issue : 2  |  Page : 57-60

Osteoarthritis of the knee joint in the obese patient: Do metabolic factors play a role?


Department of Orthopaedic Surgery, Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State, Nigeria

Date of Submission07-Jul-2020
Date of Decision10-Dec-2020
Date of Acceptance24-Feb-2021
Date of Web Publication22-Aug-2022

Correspondence Address:
Dr. Obinna Henry Obiegbu
Department of Orthopaedic Surgery, Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/smj.smj_79_20

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  Abstract 


Introduction: Osteoarthritis (OA), a disease process characterized by progressive softening of the articular cartilage, sclerosis of subchondral bone, and cyst formation often affects the knee joint. Although OA has traditionally been interpreted as wear and tear, its etiology is now thought to be multifactorial with both biomechanical and metabolic factors implicated. Of the metabolic factors, leptin a glycosylated peptide hormone produced by the adipocytes has received major attention because of its correlation to body size. The aim of this study was to determine the correlation between the clinical severity of knee OA and serum leptin in obese patients. Materials and Methods: This was a prospective study; recruiting 100 patients (50 obese and nonobese patients) with OA of the knee joint. The severity of knee OA was ascertained using the WOMAC scoring system, and serum leptin of all patients was determined. Results: The age group most commonly affected by knee OA was 51–60 years. The mean serum leptin level in nonobese patients was 4.88 ± 5.08, compared to 20.11 ± 15.04 in obese patients. There was a statistically significant correlation between the severity of knee OA (using WOMAC score) and serum leptin level; P = 0.001. Conclusion: This study shows a statistically significant positive correlation between serum leptin and severity of clinical symptoms in obese patients with knee OA.

Keywords: Leptin, obesity, osteoarthritis, WOMAC score


How to cite this article:
Obiegbu OH. Osteoarthritis of the knee joint in the obese patient: Do metabolic factors play a role?. Sahel Med J 2022;25:57-60

How to cite this URL:
Obiegbu OH. Osteoarthritis of the knee joint in the obese patient: Do metabolic factors play a role?. Sahel Med J [serial online] 2022 [cited 2022 Oct 2];25:57-60. Available from: https://www.smjonline.org/text.asp?2022/25/2/57/354191




  Introduction Top


Osteoarthritis (OA), one of the leading causes of disability, refers to a disease process that is characterized by a progressive softening of the articular cartilage, sclerosis of the subchondral bone, cyst formation, and synovitis that is usually limited to the affected joint.[1] OA of the knee joint (which is the largest of all the synovial joints in the body) tends to affect all three compartments-medial, lateral and patellofemoral, usually culminating in debilitating symptoms, with the interference of activities of daily living.[2]

Although OA has been traditionally interpreted as “wear and tear” of the articular cartilage, the pathophysiology is now thought to be multifactorial. Causative factors that have been implicated include family history, age, obesity, diabetes mellitus, systemic inflammatory mediators, lower limb malalignment (genu valgum and genu varum), joint dysplasia, trauma, and others.[3],[4] The association between obesity and OA is well described;[5] with an associated increase in the incidence of mobility disability in obese patients. Activities such as walking, chair rise, and climbing of stairs are performed at slower speeds and are more challenging for obese patients.[6] Felson et al.[7] reported that obese individuals had 1.5–2 times the risk of developing knee OA than their nonobese counterparts.

The mechanism by which obesity causes OA of the knee joint has been a topic of considerable debate, with studies citing biomechanical and metabolic factors.[8] Biomechanical factors play an important role in the health of most diarthrodial joints including the knee joint. Altered joint loading from obesity has been noted to be a critical risk factor for joint degeneration, whereas weight loss and exercise have been shown to be beneficial to osteoarthritic joints.[9] Of the metabolic factors, adipokines, especially leptin has received major attention because of its correlation to body size. Leptin, a glycosylated peptide hormone mainly produced by adipocytes, may produce pro-inflammatory and catabolic effects on cartilage through the induction of matrix metalloproteinases or through the production of pro-inflammatory cytokines.[10] Leptin is synthesized and secreted by the fat cells and functions as a part of a lipostatic signaling pathway that modulates energy balance by its effects centrally as well as peripherally, with an increased circulation of leptin directly associated with an increase in fat cells.[11]

Some studies have also correlated the severity of knee OA and leptin levels in the synovial fluid. In a study by Ku et al.,[12] a positive correlation was noted between synovial levels of leptin and the severity of knee OA. This has also prompted the identification of both leptin and its receptors in many joint tissues including human chondrocytes, osteophytes, and infrapatellar fat pad.[13] The Western Ontario (WOMAC) score was developed as an OA-specific measure of disability.[14] WOMAC is a self-administered health status questionnaire that accesses joint stiffness, function, and pain in patients with OA of the hip or knee joint.

This study was done to determine if there is any correlation between the clinical severity of knee OA and serum leptin levels in obese patients.


  Materials and Methods Top


This was a hospital-based prospective study carried out at the outpatient department of a tertiary hospital. The subjects comprised of new patients attending the orthopedic outpatient department with features of OA of the knee joints. One hundred patients were recruited into this study.

Subject selection

The subject selection was by purposive sampling method. One hundred patients attending the orthopedic outpatient department, diagnosed of OA of the knee joints, and voluntarily gave their consent were recruited into this study.

Fifty of these patients were obese, while the other fifty patients were nonobese on the basis of their body mass index (BMI). BMI is defined as weight in kilograms divided by a square of height in meters (kg/m2). A BMI value of ≥30 was used as an indicator for obesity.

The WOMAC standardized questionnaires were administered to each test subject. A maximum score of 96 and a minimum score of 0 were obtainable. The scores were grouped into three: mild symptoms denoting a score between 0 and 30; moderate symptoms denoting a score between 31 and 60; and severe symptoms denoting a score between 61 and 96.

Diagnostic Automation Leptin Human in vitro ELISA kit was utilized for this study [Figure 2]. No form of inducement, financial, or otherwise was offered to subjects to take part in this study. Ethical approval was gotten from the institution (on December 3, 2019) before the commencement of this study; with protocol number-NAUTH/CS/66/Vol 8/34.
Figure 2: Diagnostic leptin automation kit used in the analysis of serum leptin

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  Results Top


Age distribution of the patients

The age range of patients recruited into this study was between 40 and 76 years. The 40–50 year age group made up 13% of patients, while the 51–60 year age group accounted for 47%; the 61–70 and >70 year age groups accounted for 36% and 4%, respectively.

Sex distribution of the patients

There was a female predominance noted in this study, with females accounting for 71% of subjects and males 29%.

[Table 1] shows that the serum leptin levels were significantly higher in the obese patients.
Table 1: Comparison between serum leptin level and body mass index

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One-way analysis of variance was used to analyze the correlation between serum leptin and the clinical severity of symptoms (using WOMAC scoring system).

The mean leptin level of the patients with WOMAC score between 0 and 30 (mild symptoms) was 5.05 ± 4.7 ng/ml, while the leptin levels in patients with WOMAC score between 31 and 60 (moderate symptoms) and 61–96 (severe symptoms) were 11.48 ± 9.3 ng/ml and 17.87 ± 13.8 ng/ml, respectively. This difference between the groups was found to be statistically significant (P = 0.001) - as shown in [Figure 1].
Figure 1: Comparison between serum leptin level and the severity of clinical symptoms

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  Discussion Top


In this study, a comparison between serum leptin level and severity of clinical symptoms in obese patients with OA of the knee joint was sought. The mean age of patients with OA of the knee joint in this study was 59 ± 7.2, and this agrees with the mean age reported by Akinpelu et al.[15] in their series.

With regard to the BMI, the serum leptin level in nonobese patients in this study was 4.88 ± 5.09 ng/ml, while that in obese patients was 20.11 ± 15.04 ng/ml, and this difference was statistically significant. This agrees with the findings reported by Al Maskari and Alnaqdy[16] where the mean leptin level was 34.78 ± 13.96 ng/ml. A statistically significant difference was also found in this study.[14]

In a study done by Kazmi et al.[17] to determine serum leptin level between obese and nonobese subjects in Rawalpindi, the mean serum leptin level in obese patients was significantly higher than in nonobese patients (P < 0.001). The reason for higher serum leptin levels in obese patients when compared to nonobese patients is not very clear. However, leptin is an adipose tissue-derived hormone, and obese patients typically have an increased adipose tissue volume.

The severity of clinical symptoms in this index study was determined by the WOMAC scoring system. A positive correlation was found between serum leptin and the severity of clinical symptoms of knee OA. Similarly, in a study by Nagla and Giham,[18] the serum leptin levels of the patients with knee OA were compared to their clinical symptoms using the visual assessment score. A statistically significant correlation was found between serum leptin and clinical symptoms of knee OA. Also in the study by Nagla and Giham,[18] tumor necrosis factor-α and interleukin-1 were also found to be significantly higher in patients with more severe clinical symptoms. In another study by Misra et al.,[19] there was also a statistically significant correlation between serum leptin level and symptomatic OA of the knee joint in both men and women. Similarly, this is also in agreement with the findings of Lübbeke et al.,[20] who concluded that high synovial leptin is associated with severe preoperative pain in obese women with hip and knee OA. However, in this study by Lübbeke et al.,[20] synovial leptin was used. The cause of this correlation has not been fully ascertained. However, given that leptin is a pro-inflammatory cytokine, it could contribute to synovial inflammation leading to pain.


  Conclusion Top


Although this study has clearly shown a positive correlation between serum leptin and severity of clinical symptoms in obese patients with knee OA, further works need to be conducted to determine if a reduction in serum leptin levels in obese patients leads to a reduction in clinical symptoms.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ishiguro N, Kojima T, Poole AR. Mechanism of cartilage destruction in osteoarthritis. Nagoya J Med Sci 2002;65:73-84.  Back to cited text no. 1
    
2.
Roos EM, Arden NK. Strategies for the prevention of knee osteoarthritis. Nat Rev Rheumatol 2016;12:92-101.  Back to cited text no. 2
    
3.
Varady NH, Grodzinsky AJ. Osteoarthritis year in review 2015: Mechanics. Osteoarthritis Cartilage 2016;24:27-35.  Back to cited text no. 3
    
4.
Orlowsky EW, Kraus VB. The role of innate immunity in osteoarthritis: When our first line of defense goes on the offensive. J Rheumatol 2015;42:363-71.  Back to cited text no. 4
    
5.
Felson DT, Lawrence RC, Dieppe PA, Hirsch R, Helmick CG, Jordan JM, et al. Osteoarthritis: New insights. Part 1: The disease and its risk factors. Ann Intern Med 2000;133:635-46.  Back to cited text no. 5
    
6.
Buchanan W, Kean F. Osteoarthritis: Epidemiological risk factors and historical considerations. Inflammopharmacology 2002;10:5-21  Back to cited text no. 6
    
7.
Felson DT, Anderson JJ, Naimark A, Walker AM, Meenan RF. Obesity and knee osteoarthritis. The Framingham Study. Ann Intern Med 1988;109:18-24.  Back to cited text no. 7
    
8.
Mundermann A, Dyrby CO. secondary gait changes in patients with compartment knee OA. Increased load at the ankle, knee and hip joints during walking. Arthritis Rheum 2002;52:2835-7.  Back to cited text no. 8
    
9.
Farshid G. Biomechanical factors in osteoarthritis. Best Pract Res Clin Rheumatol 2011;25:815-23.  Back to cited text no. 9
    
10.
Tilg H, Moschen AR. Adipokines; mediators linking adipose tissue, inflammation and immunity. Nat Rev Immunol 2006;13:772-83.  Back to cited text no. 10
    
11.
Lönnqvist F, Nordfors L, Schalling M. Leptin and its potential role in human obesity. J Intern Med 1999;245:643-52.  Back to cited text no. 11
    
12.
Ku JH, Lee CK, Joo BS, An BM, Choi SH, Wang TH, et al. Correlation of synovial fluid leptin concentration with the severity of osteoarthritis. Clin Rheumatol 2009;28:1431-5.  Back to cited text no. 12
    
13.
Presle N, Pottie P, Dumond H, Guillaume C, Lapicque F, Pallu S, et al. Differential distribution of adipokines between serum and synovial fluid in patients with osteoarthritis. Contribution of joint tissues to their articular production. Osteoarthritis Cartilage 2006;14:690-5.  Back to cited text no. 13
    
14.
Bellamy N, Buchanan WW, Goldsmith CH, Campbell J, Stitt LW. Validation study of WOMAC: A health status instrument for measuring clinically important patient relevant outcomes to antirheumatic drug therapy in patients with osteoarthritis of the hip or knee. J Rheumatol 1988;15:1833-40.  Back to cited text no. 14
    
15.
Akinpelu AO, Alonge OO, Babatunde A, Odole A. Pattern of osteoarthritis seen in physiotherapy facilities in Ibadan and Lagos, Nigeria. Afr J Biomed Res 2007:111-5.  Back to cited text no. 15
    
16.
Al Maskari MY, Alnaqdy AA. Correlation between Serum Leptin Levels, Body Mass Index and Obesity in Omanis. Sultan Qaboos Univ Med J 2006;6:27-31.  Back to cited text no. 16
    
17.
Kazmi A, Sattar A, Hashim R, Khan SP, Younus M, Khan FA. Serum leptin values in the healthy obese and non-obese subjects of Rawalpindi. J Pak Med Assoc 2013;63:245-8.  Back to cited text no. 17
    
18.
Nagla A, Giham S. Correlation between serum leptin, cytokines, cartilage degradation and functional impact in obese knee osteoarthritis patients. Egypt Rheumatol 2016;38:117-22.  Back to cited text no. 18
    
19.
Misra D, Niu J, Felson D, Lewis C, Jinno S. Serum leptin and risk of knee pain and osteoarthritis: Multicentre osteoarthritis study. Arthritis Rheum 2015;67:189-91.  Back to cited text no. 19
    
20.
Lübbeke A, Finckh A, Puskas GJ, Suva D, Lädermann A, Bas S, et al. Do synovial leptin levels correlate with pain in end stage arthritis? Int Orthop 2013;37:2071-9.  Back to cited text no. 20
    


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