Effects of testosterone and high-dose anabolic steroids on orthodontic-induced bone remodeling and root resorption: An animal study.

BACKGROUND

This study investigates the impact of disruptions in testosterone levels on bone remodeling, root resorption, and periodontal ligament (PDL) during orthodontic tooth movement (OTM) in a pubertal male rat model.

METHODS

Testosterone deficiency was induced through orchiectomy, and the anabolic-androgenic steroid (AAS, testosterone undecanoate) was administered in both replacement and high doses. OTM was simulated using a closed-coil spring on the maxillary right first molar. The surrounding tissues-alveolar bone and periodontal ligament-of both the moved tooth and the contralateral (control) tooth were analyzed 5 and 10 days post-OTM using micro-CT, reverse-transcription quantitative polymerase chain reaction (RT-qPCR), and immunohistochemistry. Root resorption, testosterone, and adrenocorticotropic hormone plasmatic levels were also evaluated.

RESULTS

Both testosterone deficiency and high-dose AAS lead to significant changes in bone microarchitecture, resulting in reduced trabecular thickness, decreased bone connectivity, and bone lacunae. Testosterone dysfunction was associated with greater rotation and intrusion of the moved tooth. High-dose AAS intensified the inflammatory infiltrate and root resorption. Moreover, testosterone dysfunction altered the expression of key genes involved in bone metabolism, including Runx2, Bmp2, Spp1, and Bglap. The Rank/Rankl/Opg pathway was also deregulated due to testosterone disturbances. AAS at replacement doses did not normalize the inflammatory infiltrate, OTM, and the expression of the studied genes to control levels.

CONCLUSIONS

Testosterone dysfunction whether from deficiency or high-dose AAS exposure negatively impacts OTM, increasing bone resorption and promoting inflammation, potentially leading to long-term consequences for bone health and periodontal support. AAS at replacement doses may also impact PDL and bone during OTM.