Sirtuin 3 deficiency exacerbates age‐related periodontal disease
Bibliographic record
Abstract
Abstract Background Sirtuin 3 (SIRT3), a mitochondrial NAD+‐dependent deacetylase, has received much attention for its effect on metabolism and aging. However, the role of SIRT3 in periodontal disease remains unknown. Objective This study aimed to investigate the functional role of SIRT3 in age‐related periodontal disease and underlying mechanisms. Methods Sixteen mice were randomly assigned into four groups: the young wild type (WT), the aged WT, the young SIRT3‐knockout (KO), and the aged SIRT3‐KO. SIRT3 and cyclophilin D (CypD) expression and protein lysine acetylation levels in alveolar bones were detected by western blot. The bone architecture and the distance of CEJ‐ABC were assessed using micro‐CT and HE staining. The osteoclast number was observed through tartrate‐resistant acid phosphatase (TRAP) staining. Mitochondrial morphology in SIRT3 knockdown MC3T3‐E1 osteoblastic cells was analyzed by Immunofluorescence staining. In gingival tissues, the NAD+/NADH ratio was measured, and oxidative stress was detected by MitoSOX staining, HO‐1 staining, and MnSOD expression. Mitochondrial biogenesis was measured by PGC‐1α expression and oxygen consumption rate (OCR). Results In parallel with the imbalanced NAD+/NADH ratio, the SIRT3 expression was significantly decreased in the alveolar bones of the aged mice, accompanied by a global elevation of protein acetylation levels. The aged SIRT3‐KO group showed the highest rate of bone resorption and the largest number of TRAP‐positive osteoclasts among the four groups. Moreover, the reactive oxygen species level was up‐regulated in the young and the aged SIRT3‐KO groups. SIRT3 deficiency promoted mitochondrial fission and increased the CypD expression. Furthermore, the lack of SIRT3 reduced the PGC‐1α expression in gingival tissues and exhibited a significant reduction in maximal OCR. Conclusion Reduced SIRT3 abundance contributes to aged‐related periodontal disease via the exacerbation of oxidative stress and mitochondrial dysfunction.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.001 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.004 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".