In the skeleton, prostaglandins, mainly PGE 2 produced by osteoblasts under COX-2 stimulation, play either a stimulatory or an inhibitory role in bone metabolism, depending on the physiological or pathological conditions. The anabolic effect occurs largely in response to mechanical forces and in bone fracture healing, whereas PGE 2 -mediated resorption contributes significantly to bone loss in inflammatory diseases and in response to prolonged immobilization.

Large bone defects, congenital or caused by diseases, trauma or surgery, do not heal spontaneously and are usually a clinical challenge in the orthopedic and dental practices. A critical review concerning strategies to substitute lost bone or stimulate osteogenesis was undertaken. Pivotal concepts ranging from traditional bone grafting and use of biomaterials to local application of growth factors and gene therapy were addressed, including critical comments on the efficacy and safety, difficulties, advantages and disadvantages of each method. The most predictable results are still obtained with autogenous bone graft, despite the inconveniences of morbidity and limited availability of graft material. Satisfactory results have been reported for recombinant bone morphogenetic proteins (rhBMPs)-2 and -7, which distinguish for their osteoinductive property, the difficulty being the need for a degradable carrier that allows its continuous release in a rate compatible to that of new bone formation. Other bone growth factors are currently under evaluation in preclinical models of bone defects; however their efficacy is also dependent on the competence of a delivery strategy and on an appropriate delineation of "which one", "which dose" and "when". Parameters of efficiency and safety for gene therapy are still being established. In conclusion, given the variety of growth factors involved in the complex cascade of bone repair and the biological interactions between them, it remains a challenge to accomplish the ideal strategy to stimulate reparational bone formation in specific conditions of the medical as in the dental practices.

In conclusion, the study indicates that rhBMP-2 can enhance the bone formation at acute DO, which may potentially reduce the treatment period and complications related to the distraction procedure.

Prostaglandins control osteoblastic and osteoclastic function under physiological or pathological conditions and are important modulators of the bone healing process. The non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX) activity and consequently prostaglandins synthesis. Experimental and clinical evidence has indicated a risk for reparative bone formation related to the use of non-selective (COX-1 and COX-2) and COX-2 selective NSAIDs. Ketorolac is a non-selective NSAID which, at low doses, has a preferential COX-1 inhibitory effect and etoricoxib is a new selective COX-2 inhibitor. Although literature data have suggested that ketorolac can interfere negatively with long bone fracture healing, there seems to be no study associating etoricoxib with reparative bone formation. Paracetamol/acetaminophen, one of the first choices for pain control in clinical dentistry, has been considered a weak anti-inflammatory drug, although supposedly capable of inhibiting COX-2 activity in inflammatory sites.ObjectiveThe purpose of the present study was to investigate whether paracetamol, ketorolac and etoricoxib can hinder alveolar bone formation, taking the filling of rat extraction socket with newly formed bone as experimental model. Material and methodsThe degree of new bone formation inside the alveolar socket was estimated two weeks after tooth extraction by a differential point-counting method, using an optical microscopy with a digital camera for image capture and histometry software. Differences between groups were analyzed by ANOVA after confirming a normal distribution of sample data. Results and conclusionsHistometric results confirmed that none of the tested drugs had a detrimental effect in the volume fraction of bone trabeculae formed inside the alveolar socket.