Objective The etiology of orthodontic‐induced gingival enlargement (OIGE) or orthodontic‐induced gingival overgrowth (OIGO) is multifactorial and is related to issues such as poor oral hygiene and the hormonal changes that are common during puberty. It is known that brackets facilitate the accumulation of dysbiotic microbial biofilm and that mechanical stress on the periodontium is a possible factor in the development of OIGE. Therefore, the objective of this systematic review was to analyze the principal factors involved in the pathogenesis of OIGE. Methods Independent reviewers performed a systematic literature search of several databases, including PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), Scopus, and Web of Science. The eligibility criteria included clinical studies assessing any type of gingival enlargement/gingival overgrowth (GE/GO) in healthy patients of any age undergoing fixed orthodontic treatment. The outcomes assessed included primary factors (mechanical stress, gingival fibrotic reaction, hormonal changes, nickel (Ni)/titanium (Ti) sensitivity, and genetics) and secondary factors (demographic variables, dysbiotic microbial biofilm, orthodontic variables, periodontal parameters, and mouth breathing). The methodological quality and risk of bias of the studies included were analyzed using the Newcastle–Ottawa Scale. Results Titles and abstracts of 670 articles were screened. Fifty‐six articles were selected for full‐text reading. From these, 27 were included and selected for extraction. From the selected studies, 17 assessed primary factors and 12 assessed secondary factors related to GE. The results of the studies indicated that the appearance of OIGE was associated with increases in matrix metalloproteinases (MMPs) MMP‐8, MMP‐9, collagen, Ni accumulation in gingival samples, increases in estradiol and testosterone in adolescents, and genes associated with the regulation of cell proliferation and migration. The rate of OIGE was higher in males (both in children and in adolescents), and it was most frequently located in the anterior buccal regions of both arches. There was a directly proportional relationship with the duration of orthodontic treatment, probing depth (PPD), and bleeding on probing (BOP). Metal brackets, elastomeric ligatures, excess resin, and change in the polymicrobial profile favored OIGE, and thick periodontal phenotype and mouth breathing were predisposing factors for this condition. The risk of bias was “favorable” for 14‐case control, cohort, and cross‐sectional studies; medium for nine articles; and the assessment was “unfavorable” in four. The level of evidence for the studies selected was adequate, with an acceptable degree of recommendation. Conclusion The results summarized in this systematic review suggest that the mechanical stress generated by the presence of orthodontic devices may be the main cause of the development of GE. The risk and prevalence of OIGE are highest in the adolescent population.
Rocha-Eiroa et al. (Thu,) studied this question.