Gingival recession has direct causes and predisposing factors.
Orthodontic treatment is able to prevent recession and even contribute to its treatment, with or without periodontal approach, depending on the type and severity of gingival tissue damage.
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There is no evidence on the fact that orthodontic treatment alone might induce gingival recession, although it might lead the affected teeth (usually mandibular incisors or maxillary canines) to be involved in situations that act as predisposing factors, allowing direct causes to act and, therefore,
trigger recession, especially when the buccal bone plate is very thin or presents with dehiscence.
Several aspects regarding the relationship between orthodontic treatment and gingival recession have been addressed, and so has the importance of the periosteum to the mechanism of gingival recession formation.
Clinical as well as experimental trials on the subject would help to clarify this matter, of which understanding is not very deep in the related literature. Gingival recession is represented by atrophic periodontal changes.
The term "atrophy" makes reference to all processes of cell lesion characterized by a decrease in volume and cell population of a given organ or tissue, resulting from sublethal cell aggression, such as hypoxia, mechanical compression, local reduced vascularization, among others. Sublethal cell aggression is essentially reversible.
Atrophic cells have a decrease in volume, they eat themselves up and cause their structural components as well as their organelles to be digested. Thus, their level of energy consumption is reduced and they are able to survive within a hostile environment.
Once the causal factor is removed, the process ceases and the number and size of cells might be restored to normal levels; however, it all depends on the severity of tissue lesion and the type of tissue involved.
°Dental Press Journal of Orthodontics
°Ana Suzy Jati, Laurindo Zanco Furquim, Alberto Consolaro
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