ABSTRACT
OBJECTIVE: The aim of the investigation was to evaluate the maxillary alveolar bone morphology, bone architecture, and bone turnover in relation to the mechanical strain distribution in rats with dental premature contact. MATERIALS AND METHODS: Fifty 2-month-old male Wistar rats were used. The premature contact group (N=40) received a unilateral (right side) resin cementation on the occlusal surface of the upper first molar. The animals were distributed in 4 subgroups according to the periods of euthanasia: 7, 14, 21, and 28 days after cementation (N=10, for each period). For the control group (N=10), the teeth were kept without resin, featuring a normal occlusion. The pieces including the upper first molars, alveolar bone, and periodontal tissue were processed to histological and immunohistochemical evaluation of RANK-L and TRAP protein expression. A three-dimensional bone microarchitecture analysis was performed, where the heads of animals were scanned using microtomography and analyzed using CT-Analyser software (Bruker, Kontich, Belgium). In the computer simulation by finite element analysis, two micro-scaled three-dimensional finite element models of first molar and dentoalveolar tissues were constructed, in representation of control and premature contact groups, using Materialise MIMICS Academic Research v18 (Materialise, Leuven, Belgium). The analysis was set to simulate a maxillary molar biting during the power stroke phase. The total deformation, equivalent strain, and minimum principal strain distribution were calculated. RESULTS: The expression of RANK-L and TRAP presented higher positive ratio in the 7-day period compared to the control group. The three-dimensional morphometry showed decrease of bone volume in the premature contact, with significant values between the control and the 7-day and 14-day groups (P = 0.007). In FEA, the premature contact model presented a uniform compressive strain distribution in the alveolar bone crest compared to a non-uniform compressive strain distribution in the control model. CONCLUSIONS: The results from FEA, 3D bone microarchitecture, and histological and immunohistochemical analyses showed that a model with dental traumatic occlusion resulted in changes of alveolar bone mechanobiology and, consequently, its morphology. CLINICAL RELEVANCE: These results could be applied in dental treatment planning bringing biological and mechanical feedback to provide an effective mechanism to obtain physiological bone loss responses. Furthermore, this association between experimental and computational analyses will be important to figure out the alveolar bone response to mechanical stimulation in different clinical conditions.
Subject(s)
Alveolar Process , Maxilla , Alveolar Process/diagnostic imaging , Animals , Computer Simulation , Finite Element Analysis , Male , Maxilla/diagnostic imaging , Rats , Rats, WistarABSTRACT
PURPOSE: To investigate the effect of experimental traumatic occlusion (ETO) induced by metal crowns on alveolar bone loss. MATERIALS AND METHODS: Metal crowns were custom-made for the lower first molars with occlusal discrepancy of 0.4 and 0.7 mm from the maximum intercuspation. Thirty-six animals were randomly divided into three groups (n = 12 animals per group): 0.4-mm hyperocclusion group, 0.7-mm hyperocclusion group and the sham group (no metal crown). Twenty-eight days after crown cementation, the animals were euthanized and gingival tissue was collected to assess cytokine levels of IL-17, IL-6, and TNF-α using enzyme-linked immunosorbent assay (ELISA). Mandibles were stained with 1% methylene blue and alveolar bone levels were quantified. Western blotting was used to quantify the expression of receptor activator of nuclear factor κ B (RANK), and its ligand (RANKL), secreted osteoclastogenic factor of activated T cells (SOFAT) and TNF-α-converting enzyme (TACE). Also, mandibles were histologically processed and stained with hematoxylin and eosin, from which the presence of osteoclast-like cells, multinucleated cells containing ≥3 nuclei was counted at 100× magnification. The data were analyzed using one-way ANOVA and Tukey tests. RESULTS: Experimental occlusal trauma for 28 consecutive days significantly increased alveolar bone loss and multinucleated cell counts (p < 0.05). RANK, RANKL, SOFAT, TACE, IL-6, and TNF-α were significantly higher in gingival tissues of ETO groups (p < 0.05). IL-17 titers were unchanged among the groups (p > 0.05). CONCLUSION: Experimental traumatic occlusion activates and sustains bone resorption pathways in the periodontium inducing alveolar bone resorption. As the intensity of occlusal trauma increased, alternative osteoclastic pathways were activated, such as TACE and SOFAT.