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.