Evidence mapPaperPMID 42470255Full record

ArticleMediators of inflammation2026

Combination of High-Fat Diet and Chronic Unpredictable Stress Synergistically Induces Osteoarthritis-Like Changes in Temporomandibular Joints in Rats.

Xi Wang, Ting Hao, Ye-Hua Gan

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Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

3 authors.

Xi WangCentral Laboratory, Peking University School and Hospital of Stomatology, Beijing, China, bjmu.edu.cn.ORCID https://orcid.org/0009-0009-2765-4964
Ting HaoCenter of Stomatology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua Medicine, Tsinghua University, Beijing, China, tsinghua.edu.cn.ORCID https://orcid.org/0000-0003-4667-4556
Ye-Hua GanCentral Laboratory, Peking University School and Hospital of Stomatology, Beijing, China, bjmu.edu.cn.ORCID https://orcid.org/0000-0002-7806-8174

Funding

National Natural Science Foundation of China 82170981
6 · The paper itself

Abstract

objectivesHigh-fat diet (HFD) and chronic unpredictable stress (CUS) are potential risk factors for temporomandibular joint osteoarthritis (TMJOA). This study aimed to investigate whether the combination of HFD and CUS synergistically induces pathological changes in the temporomandibular joints (TMJs) and to explore the underlying molecular mechanisms.

methodsMale Sprague-Dawley rats were assigned to four groups as follows normal diet (ND), HFD, ND with CUS (ND/CUS), and HFD with CUS (HFD/CUS), and were treated with HFD, CUS, or both accordingly. TMJs were harvested after 5 or 10 weeks of HFD, CUS, or combined HFD/CUS treatment. An additional group was used to evaluate whether the TLR4 inhibitor TAK242 could attenuate HFD/CUS-induced TMJOA-like changes. Serum proteins or lipids were measured by enzyme-linked immunosorbent assay (ELISA) or biochemical analysis. Pathological changes were evaluated using microcomputed tomography (micro-CT) for subchondral bone morphometry, histology with Mankin scoring for cartilage degradation, and TUNEL assays for chondrocyte apoptosis. The expression levels of TLR4, NF-κB p65, and IL-1β in condylar cartilage were assessed by immunofluorescence.

resultsThe HFD/CUS group showed serum levels of total cholesterol (TC), triglycerides, and oxidized LDL (ox-LDL) comparable to those in the HFD group, and both groups had significantly higher levels than the ND and ND/CUS groups. Simultaneously, the HFD/CUS group also exhibited the earliest and most severe TMJOA-like pathological changes and highest Mankin score, including cartilage degradation, subchondral bone resorption, and increased chondrocyte apoptosis as early as 5 weeks posttreatment. The ND/CUS and HFD groups only showed slight degenerative changes at 5 weeks posttreatment and obvious TMJOA-like changes at 10 weeks posttreatment. The HFD/CUS group also showed a higher number of TLR4-positive cells, NF-κB p65-nuclear-positive cells, and IL-1β-positive cells in the condylar chondrocytes than those in the ND/CUS and HFD groups at 5 weeks posttreatment. TAK242 significantly alleviated the cartilage degradation, subchondral bone destruction, and chondrocyte apoptosis in the HFD/CUS group.

conclusionHFD and CUS could synergistically induce TMJOA-like changes, potentially by activating the TLR4/NF-κB/IL-1β inflammatory signaling pathway. Our findings suggest an important interplay between metabolic and psychological factors in the pathogenesis of TMJOA.

Indexed as

Diet, High-FatOsteoarthritisStress, PsychologicalTemporomandibular JointAnimalsApoptosisChondrocytesEnzyme-Linked Immunosorbent AssayMaleRatsRats, Sprague-DawleyToll-Like Receptor 4X-Ray MicrotomographyToll-Like Receptor 4

Identifiers

PMID42470255
PMCPMC13379892

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