Background: This study aimed to determine the contribution of cystathionine gamma lyase (CSE) to physiological and orthodontic root resorption in mice.Methods: Mice genetically deficient in the CSE (CSE -/-), the dominant hydrogen sulfide (H 2 S)-generating enzyme in osteoclast were used in this study. Physiological and orthodontic root resorption was assessed with micro computed tomography (micro-CT) and scanning electron microscopy (SEM) in the mice at the age of 8-, 26-, and 52-week and in 8-week old mice following 1-, 2-, and 3-week orthodontic treatment, respectively. Hematoxylin and eosin (HE) and tartrate-resistant acid phosphatase (TRAP) staining were used for further determination of root resorption and the number of osteoclasts. The receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG) level in surrounding alveolar bone of the maxillary first molar after 2-week orthodontic treatment was measured by reverse transcription polymerase chain reaction (RT-PCR).Results: Root resorption lacunae (RRL) gradually and significantly increased with age in wild type (WT) and CSE -/mice. The CSE -/showed less RRL compared with the WT group. At each time point of orthodontic treatment, the CSE -/group had less RRL and osteoclasts than the WT group. The orthodontically induced RANKL/OPG mRNA expression in the periodontal tissue in the CSE -/group was lower than that in the WT group.Conclusions: CSE contributes significantly to physiological and orthodontic root resorption.

Background and objective Though impacts of traumatic occlusion (TO) on periodontal tissues and roles of cystathionine γ‐lyase (Cth) gene in the regulation of bone homeostasis have been studied by many, no consensus has been reached so far on whether TO deteriorates the periodontium and precise roles of Cth in occlusal trauma. Therefore, this study aims to investigate the impacts of TO on periodontal tissues and the involvement of Cth gene. Methods Eighty C57BL/6 wild‐type (WT) mice and Cth knockout (Cth−/−) mice, 8 weeks old, were used in this study. The TO model was established using composite resin bonding on the left maxillary molar for one, two, and three weeks, respectively. Morphological and histological changes in the periodontium were assessed by micro‐computed tomography (micro‐CT), hematoxylin and eosin (H&E) staining, and tartrate‐resistant acid phosphatase (TRAP) staining. Osteoclast‐related genes were analyzed by real‐time polymerase chain reaction (qPCR). Results It was found that decreased alveolar bone height, expanded bone resorption area, and increased width of periodontal ligament (PDL) occurred in TO models, accompanied by an increased number of osteoclasts in a time‐dependent manner by micro‐CT and histological staining. Osteoclast‐related genes including Ctsk, Mmp9, Rank, Trap, and Rankl/Opg were also up‐regulated after one week of modeling. The up‐regulated expressions of Cth gene and its protein CTH were observed in TO mouse models. After 1, 2, or 3 weeks of modeling, WT mice showed more severe alveolar bone resorption, wider PDL, higher osteoclast count, and higher levels of osteoclast‐related genes Ctsk, Rank, and Rankl/Opg than Cth−/− mice. Conclusion TO causes a reduction in alveolar bone height and PDL morphological disorder with their severity increases in a time‐dependent manner. Cth aggravates periodontal damage caused by TO.