Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway
Periodontitis, a common dental illness, causes periodontal tissue inflammation and irreversible bone loss, inevitably resulting in tooth loss. Hyperhomocysteinaemia (HHcy), defined as blood total homocysteine (Hcy) levels greater than 15 µmol/L, is linked to increased cardiovascular disease risk. Mo...
Saved in:
| Main Authors: | , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2025-12-01
|
| Series: | Redox Report |
| Subjects: | |
| Online Access: | https://www.tandfonline.com/doi/10.1080/13510002.2025.2475691 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850139637242134528 |
|---|---|
| author | Kaiqiang Yang Yuting Yang Ting Long Xiaoxue Wang Yeke Chen Chenjiang He Li Li Xinbo Yang Meixiu Jiang Yichen Hu Fang Dai Li Song |
| author_facet | Kaiqiang Yang Yuting Yang Ting Long Xiaoxue Wang Yeke Chen Chenjiang He Li Li Xinbo Yang Meixiu Jiang Yichen Hu Fang Dai Li Song |
| author_sort | Kaiqiang Yang |
| collection | DOAJ |
| description | Periodontitis, a common dental illness, causes periodontal tissue inflammation and irreversible bone loss, inevitably resulting in tooth loss. Hyperhomocysteinaemia (HHcy), defined as blood total homocysteine (Hcy) levels greater than 15 µmol/L, is linked to increased cardiovascular disease risk. Mounting evidence indicates a connection between HHcy and periodontitis; however, the underlying processes remain unknown. Herein, we explored the mechanisms by which HHcy exacerbates periodontal tissue inflammation and osteoclast formation. In an animal model of periodontitis treated with HHcy, periodontal attachment loss was aggravated, and both systemic and gingival tissue inflammation levels tended to increase; additionally, antioxidant-related proteins were suppressed and expressed at low levels, whereas oxidative damage-related protein expression increased. In RAW264.7 cells treated with LPS or LPS + Hcy, the LPS + Hcy group presented increased reactive oxygen species (ROS) fluorescence intensity, and Nrf2/HO-1 signalling pathway suppression was associated with inflammatory cytokine (TNF-α) expression. In monocyte osteoclasts treated with Rankl or Rankl + Hcy, the Rankl + Hcy group presented Nrf2/HO-1 signalling pathway suppression, an increase in osteoclast-related proteins (NFATc-1 and CTSK), and a more pronounced osteoclastic phenotype. Therefore, HHcy may exacerbate inflammation severity and osteoclast generation in periodontitis by promoting ROS production and inhibiting the Nrf2/HO-1 signalling pathway. |
| format | Article |
| id | doaj-art-a55b7b6cf4854af8bb702e3870bd41f9 |
| institution | OA Journals |
| issn | 1351-0002 1743-2928 |
| language | English |
| publishDate | 2025-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Redox Report |
| spelling | doaj-art-a55b7b6cf4854af8bb702e3870bd41f92025-08-20T02:30:12ZengTaylor & Francis GroupRedox Report1351-00021743-29282025-12-0130110.1080/13510002.2025.2475691Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathwayKaiqiang Yang0Yuting Yang1Ting Long2Xiaoxue Wang3Yeke Chen4Chenjiang He5Li Li6Xinbo Yang7Meixiu Jiang8Yichen Hu9Fang Dai10Li Song11Center of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaInstitute of Translational Medicine, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaCenter of Stomatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of ChinaPeriodontitis, a common dental illness, causes periodontal tissue inflammation and irreversible bone loss, inevitably resulting in tooth loss. Hyperhomocysteinaemia (HHcy), defined as blood total homocysteine (Hcy) levels greater than 15 µmol/L, is linked to increased cardiovascular disease risk. Mounting evidence indicates a connection between HHcy and periodontitis; however, the underlying processes remain unknown. Herein, we explored the mechanisms by which HHcy exacerbates periodontal tissue inflammation and osteoclast formation. In an animal model of periodontitis treated with HHcy, periodontal attachment loss was aggravated, and both systemic and gingival tissue inflammation levels tended to increase; additionally, antioxidant-related proteins were suppressed and expressed at low levels, whereas oxidative damage-related protein expression increased. In RAW264.7 cells treated with LPS or LPS + Hcy, the LPS + Hcy group presented increased reactive oxygen species (ROS) fluorescence intensity, and Nrf2/HO-1 signalling pathway suppression was associated with inflammatory cytokine (TNF-α) expression. In monocyte osteoclasts treated with Rankl or Rankl + Hcy, the Rankl + Hcy group presented Nrf2/HO-1 signalling pathway suppression, an increase in osteoclast-related proteins (NFATc-1 and CTSK), and a more pronounced osteoclastic phenotype. Therefore, HHcy may exacerbate inflammation severity and osteoclast generation in periodontitis by promoting ROS production and inhibiting the Nrf2/HO-1 signalling pathway.https://www.tandfonline.com/doi/10.1080/13510002.2025.2475691Periodontitisoxidative stressROSNrf2bone lossinflammation |
| spellingShingle | Kaiqiang Yang Yuting Yang Ting Long Xiaoxue Wang Yeke Chen Chenjiang He Li Li Xinbo Yang Meixiu Jiang Yichen Hu Fang Dai Li Song Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway Redox Report Periodontitis oxidative stress ROS Nrf2 bone loss inflammation |
| title | Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway |
| title_full | Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway |
| title_fullStr | Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway |
| title_full_unstemmed | Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway |
| title_short | Hyperhomocysteinaemia aggravates periodontitis by suppressing the Nrf2/HO-1 signalling pathway |
| title_sort | hyperhomocysteinaemia aggravates periodontitis by suppressing the nrf2 ho 1 signalling pathway |
| topic | Periodontitis oxidative stress ROS Nrf2 bone loss inflammation |
| url | https://www.tandfonline.com/doi/10.1080/13510002.2025.2475691 |
| work_keys_str_mv | AT kaiqiangyang hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT yutingyang hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT tinglong hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT xiaoxuewang hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT yekechen hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT chenjianghe hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT lili hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT xinboyang hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT meixiujiang hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT yichenhu hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT fangdai hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway AT lisong hyperhomocysteinaemiaaggravatesperiodontitisbysuppressingthenrf2ho1signallingpathway |