Following corticotomy surgery, patients experience moderate to severe post-operative pain that necessitates prescriptions of analgesics. The prostaglandin inhibitory effect of ibuprofen influences the mobility of teeth during orthodontic treatment. This study aimed to determine how ibuprofen affects histological reactions and dental root resorption during orthodontic tooth movement aided by corticotomy. Forty-two male Wistar rats were divided into three groups by random selection: (1) control group, (2) corticotomy group (CO), and (3) corticotomy with 0.6 mL of 15 mg/kg ibuprofen group (CI). On each buccal and palatal alveolar bone, two decortication points were made. Orthodontic tooth movement was induced on the maxillary first molar for 21 days utilizing a NiTi-closed coil spring with 10 g of force. Hematoxylin and eosin were used to prepare and stain the histological sections. The numbers of osteoclasts on days 0, 7, 14, and 21 were determined, and the root resorption area on days 0 and 21 was measured. Compared to the control group, the osteoclast counts in the CO and CI groups were considerably greater (p < 0.002). No significant differences were observed between the CO and CI groups in the numbers of osteoclasts or the percentages of root resorption (p > 0.05). The amounts of osteoclast activity and root resorption were unaffected by the administration of ibuprofen in corticotomy-facilitated tooth movement.

Asthma is a chronic, heterogeneous respiratory pathology characterized by reversible airway inflammation. Therapeutics focus on symptom reduction and control, aimed at preserving normal pulmonary function and inducing bronchodilatation. The objective of this review is to describe the adverse effects produced by anti-asthmatic drugs on dental health, according to the reported scientific evidence. A bibliographic review was carried out on databases, such as Web of science, Scopus, and ScienceDirect. Most anti-asthmatic medications are administered using inhalers or nebulizers, making it impossible to avoid contact of the drug with hard dental tissues and oral mucosa, and thus promoting a greater risk of oral alterations, mainly due to decreases in the salivary flow and pH. Such changes can cause diseases, such as dental caries, dental erosion, tooth loss, periodontal disease, bone resorption, as well as fungal infections, such as oral candidiasis.

During orthodontic tooth movement (OTM), areas of compressive and tensile forces are generated in the periodontal ligament (PdL), a mechanoreactive connective tissue between the teeth and alveolar bone. Mechanically stimulated PdL fibroblasts (PdLFs), the main cell type of PdL, express significantly increased levels of growth differentiation factor 15 (GDF15). In compressed PdL areas, GDF15 plays a fundamental role in modulating relevant OTM processes, including inflammation and osteoclast activation. However, the specific function of this factor in tensile areas has not yet been investigated. Thus, the aim of this study was to investigate the role of GDF15 in the mechanoresponse of human PdLFs (hPdLFs) that were exposed to biaxial tensile forces in vitro. Using siRNA-mediated knockdown experiments, we demonstrated that GDF15 had no impact on the anti-inflammatory force response of elongated hPdLFs. Although the anti-inflammatory markers IL1RN and IL10, as well as the activation of immune cells remained unaffected, we demonstrated an inhibitory role of GDF15 for the IL-37 expression. By analyzing osteogenic markers, including ALPL and RUNX2, along with an assessment of alkaline phosphatase activation, we further showed that the regulation of IL-37 by GDF15 modulates the osteogenic differentiation potential of hPdLFs. Despite bone resorption in tensile areas being rather limited, GDF15 was also found to positively modulate osteoclast activation in those areas, potentially by adjusting the IL-37 levels. In light of our new findings, we hypothesize that GDF15 modulates force-induced processes in tissue and bone remodeling through its various intra- and extracellular signaling pathways as well as interaction partners. Potentially acting as a master regulator, the modulation of GDF15 levels may hold relevance for clinical implications.