Relapse after orthodontic tooth movement (OTM) is an undesirable outcome that involves a number of factors. This study investigated the remodelling of the alveolar bone and related periodontal structures during orthodontic relapse in rat molars. The maxillary right first molars of 35 Wistar rats were moved mesially by a fixed orthodontic appliance for 10 days and the contralateral molars served as controls. The appliances were removed and six animals killed. The molars were allowed to relapse, and the remaining animals were sacrificed at 1, 3, 5, 7, 14, and 21 days. The jaws were sectioned and stained with haematoxylin and eosin and tartrate-resistant acid phosphatase (TRAP). One day after appliance removal, the molars relapsed to a mean 62.5 per cent of the achieved OTM and then steadily relapsed to 86.1 per cent at 21 days. The number of osteoclasts situated along the alveolar bone of the first molars was highest at the end of active treatment and significantly decreased during the relapse period. In the OTM group, osteoclasts were most numerous in the pressure side of the periodontal ligament (PDL). As the molars relapsed over time, the osteoclast distribution shifted, and after 7 days of relapse, TRAP-positive cells were registered in previous pressure and tension sides of the first molars. After 21 days, these cells were concentrated in the distal parts of the PDL of all three maxillary right molars. These results indicate that orthodontic relapse in the rat model occurs rapidly and remodelling of the alveolar bone and PDL plays a central role in the relapse processes of both actively moved and adjacent teeth.

Bone tissue reactions on a molecular level are similar during OTM and orthodontic relapse. These findings validate the importance of immediate retention following active OTM.

These results indicate that LLLT may reduce the relapse tendency, possibly due in part to bone formation in previous tension areas, and to redistribution of osteoclasts following removal of orthodontic force. The role of LLLT in the prevention of orthodontic relapse requires further study.

Class III malocclusion of skeletal origin manifests as a result of skeletal imbalances in the sagittal relationship between the maxilla and mandible. These imbalances are either associated with deviations in the size of the jaws or their position. 1 Different components of the craniofacial complex contribute to the development of a skeletal Class III malocclusion, which is mainly characterized by a retrognathic maxilla, prognathic mandible or a combination of both. [2][3][4][5] The aetiology of Class III malocclusion has been attributed to both environmental and genetic

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