Treatment with paracetamol, ketorolac or etoricoxib did not hinder alveolar bone healing: a histometric study in rats

Ricardo Nogueira Fracon,Izabela Cristina Moris,Teresa Lamano,Juliana Mazzonetto Teófilo

doi:10.1590/s1678-77572010000600016

Abstract

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.

Highlights

The cyclooxygenase enzymes COX-1 and COX2 catalyze the conversion of arachidonic acid to prostaglandins, which, in addition to a variety of physiological functions, are involved in several pathological processes
The skeleton is abundantly supplied with prostaglandins, mainly PGE2, which modulate osteoblastic and osteoclastic function under physiological or pathological conditions
The purpose of the present study was to investigate whether paracetamol, ketorolac or etoricoxib may have a detrimental effect on DOYHRODU ERQH IRUPDWLRQ FRQVLGHULQJ WKH ¿OOLQJ RI rat extraction socket with newly formed bone as experimental model

Summary

Introduction

The cyclooxygenase enzymes COX-1 and COX2 catalyze the conversion of arachidonic acid to prostaglandins, which, in addition to a variety of physiological functions, are involved in several pathological processes. The non-steroidal antiLQÀDPPDWRU\ GUXJV 16$,'V LQKLELW &2; DFWLYLW\ and prostaglandin synthesis. A wide array of NSAIDs is currently available, notably the conventional NSAIDs, which inhibit non-selectively both enzymes COX-1 and COX-2, and a new class of selective COX-2 inhibitors. The skeleton is abundantly supplied with prostaglandins, mainly PGE2, which modulate osteoblastic and osteoclastic function under physiological or pathological conditions. The anabolic effect of PGE2 RQ ERQH RFFXUV FKLHÀ\ LQ UHVSRQVH WR mechanical forces and in the healing process. Considerable experimental and clinical evidence has indicated a risk for reparative bone formation related to the use of selective and non-

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Conclusion