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Aging and disease    2020, Vol. 11 Issue (5) : 1317-1328     DOI: 10.14336/AD.2019.1116
Review Article |
Infrapatellar Fat Pad and Knee Osteoarthritis
Ni Zeng1,2, Zhi-Peng Yan2, Xin-Yuan Chen2, Guo-Xin Ni1,*
1School of Sport Medicine and Rehabilitation, Beijing Sport University, Beijing, China
2Department of Rehabilitation Medicine, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China
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Abstract  

Osteoarthritis is the most prevalent arthritis typically characterized by degradation of cartilage. However, its pathogenesis is not fully understood. Currently, osteoarthritis is best considered a disease of the whole “joint organ”. Infrapatellar fat pad (IFP), an adipose tissue near synovium, is now attaching importance to researchers for its inflammatory phenotype. In this narrative review, a large body of evidence has been gathered for the involvement of IFP in the development of knee osteoarthritis. Additionally, the underlying mechanisms of how IFP can be involved in this process have been proposed. However, further investigations are needed to better understand its precise role in this process and its underlying mechanism, and beyond that, to develop new strategies to slow down the degenerative process and explore an effective and timely diagnosis of the disease.

Keywords infrapatellar fat pad      knee osteoarthritis      local inflammation      crosstalk     
Corresponding Authors: Ni Guo-Xin   
About author:

These authors contributed equally to this work.

Just Accepted Date: 06 December 2019   Issue Date: 21 September 2020
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Zeng Ni
Yan Zhi-Peng
Chen Xin-Yuan
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Cite this article:   
Zeng Ni,Yan Zhi-Peng,Chen Xin-Yuan, et al. Infrapatellar Fat Pad and Knee Osteoarthritis[J]. Aging and disease, 2020, 11(5): 1317-1328.
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http://www.aginganddisease.org/EN/10.14336/AD.2019.1116     OR
Ref. (year)SubjectsFindings
33 (2018)KOA patientsIncreased signal intensity in the IFP was associated with knee structural abnormalities in tibiofemoral compartment.
34 (2018)KOA patientsIFP signal intensity is associated with the occurrence of knee replacement.
28 (2017)KOA patients1.The increase in 3D MRI heterogeneity was greater in progressor and OA knees than non-progressor knees and healthy knees, respectively. 2. Increase in 3D IFP MRI signal and signal heterogeneity may be associated with radiographic/symptomatic progression of OA, when compared to non-progressive OA or healthy knees
35 (2016)Older adultsThe IFP signal abnormalities has a potentially important role in OA progression.
81 (2015)Adults without KOA1.IFP at baseline was associated with reduced knee pain at follow-up and lateral tibial cartilage volume loss; 2. IFP size is not simply a marker of systemic obesity.
82 (2015)PFJ OA patients1. IFP volume was greater in the PFJ OA group than controls and it was directly related to PFJ OA pain; 2. Larger IFP was associated with worse pain.
2 (2015)Older adults1.IFP maximal area in women was significantly associated with changes in knee pain and reduced loss of medial and lateral tibial cartilage volume; 2. IFP plays a protective role in joint degeneration in the elderly.
36 (2014)Older adults1.IFP maximum area was significantly associated with joint space narrowing and medial osteophytes, knee tibial and patellar cartilage volume, tibial cartilage defects, any BMLs, and knee pain on a flat surface; 2.IFP maximum area is beneficially associated with radiographic OA, MRI structural pathology and knee pain on a flat surface suggesting a protective role for IFP possibly through shock absorption.
15 (2014)KOA patients1.The severity of inflammation in the IFP were associated with the severity of pain in KOA; 2.DCE-MRI is a promising method to study the impact of inflammation in KOA
30 (2010)KOA patientsSubjects who are prone to growth or enlargement of the IFP may also be more prone to symptomatic OA.
Table 1  The relationship between MRI features of IFP and knee characteristics.
Figure 1.  A mechanistic model depicting how IFP is involved in OA pathogenesis. It is supposed that the IFP may be involved in the local inflammation state and/or that it might interact with other periarticular tissues, thus contributing to the development of KOA. (A). IFP may interact with cartilage, synovial membrane and subchondral bone. IFP may interact with the synovial tissue through affecting the inflammatory response and promoting the fibrosis of the synovial cells. In parallel, IFP plays either a deleterious or a protective role on cartilage by altering the expression of IL-6 or leptin or MMPs. While the influence of IFP on subchondral bone has not yet been investigated clear, IFP may interact with subchondral bone through Wnt signaling pathway. Reciprocally, these joint tissues could also modulate the IFP. (B). Many factors such as obesity, bone fracture, and aging are related to abnormal loading or abnormal cartilage, and eventually lead to cartilage injury. Then, the immune response of IFP may be activated by the cartilage specific autoantigens. The immunophenotype of immune cells of IFP is related to inflammatory phenotype of IFP, which is the potential mechanisms of the involvement of IFP in the development of OA. Macrophages consist of is type M1 and M2 macrophage. PPARγ-regulated genes are upregulated in M2 macrophage. Macrophages can interact with T cells and adipocytes to participate in local inflammation state. First, CD4 ?T cell also called Th cells, it contains two subtypes named Th1 and Th2. The balance between type Th1 and Th2 type signals may affect the recruitment and activation of macrophages in the adipose tissue, resulting in pathogenic and inflammatory conditions or non-inflammatory and protective environments. Then, adipocytes secrete fatty acids and fatty acid derivatives which are highly immune-regulated, to modulate the phenotype of macrophages and CD4+T cells. Moreover, CD8+ T present a higher level of activation in the IFP, and the activated CD8+ T cells in IFP may recruited into the tissues by preactivated circulating peripheral blood. In addition, CD8+T cells may modulate matrix turnover, and thus contribute to the development of OA by up-regulating TIMP-1. These activated immune cells and adipocytes alter the inflammatory phenotype of IFP, participate in the local inflammation of the whole joint, and ultimately lead to KOA. Short title of the first figure. The figure caption should begin with a title (an overall descriptive statement of the figure) followed by additional text. The legends should be placed immediately after each figure.
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