title: Treatment with paracetamol, ketorolac or etoricoxib did not hinder alveolar bone healing: a histometric study in rats.
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.
  
  
  OBJECTIVE
  The 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.
  
  
  METHODS
  The 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.
  
  
  CONCLUSIONS
  Histometric results confirmed that none of the tested drugs had a detrimental effect in the volume fraction of bone trabeculae formed inside the alveolar socket.
authors.affiliation: Ribeirão Preto Dental School, University of São Paulo, Ribeirão Preto, SP, Brazil.
authors.forename: Ricardo Nogueira
authors.initials: RN
authors.lastname: Fracon
authors.forename: Juliana Mazzonetto
authors.initials: JM
authors.lastname: Teófilo
authors.forename: Izabela Cristina
authors.initials: IC
authors.lastname: Moris
authors.forename: Teresa
authors.initials: T
authors.lastname: Lamano
mesh_terms: D000082:Acetaminophen / Q000009:adverse effects* / Q000494:pharmacology; D018712:Analgesics, Non-Narcotic / Q000009:adverse effects* / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000494:pharmacology; D001861:Bone Regeneration / Q000187:drug effects*; D051545:Cyclooxygenase 1 / Q000009:adverse effects / Q000494:pharmacology; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors / Q000009:adverse effects* / Q000494:pharmacology; D004195:Disease Models, Animal; D000077613:Etoricoxib; D017102:Fracture Healing / Q000187:drug effects; D020910:Ketorolac / Q000009:adverse effects* / Q000494:pharmacology; D008297:Male; D011725:Pyridines / Q000009:adverse effects* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013450:Sulfones / Q000009:adverse effects* / Q000494:pharmacology; D013997:Time Factors
chemical_list: D018712:Analgesics, Non-Narcotic; D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D011725:Pyridines; D013450:Sulfones; D000082:Acetaminophen; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D000077613:Etoricoxib; D020910:Ketorolac