INQUIRY Anticoagulants Chewing gum for orthodontic pain Background.—Orthodontic treatment has the side effect of causing pain as the teeth are moved that is sufficient to lead patients to refuse or eventually abandon therapy. Pain is reported by 70% to 95% of the children having orthodontic treatment, with intensity and duration varying from patient to patient, but roughly beginning 2 to 3 hours after appliance fitting and lasting up to 7 days, with the most intense pain over the first 2 days. The pain can affect eating and sleeping. The analgesics ibuprofen and paracetamol are often prescribed for orthodontic pain, either preemptively or when the teeth become painful after an appointment. However, both of these drugs carry adverse side effects. Chewing gum has been proposed as having the ability to provide relief from orthodontic pain or at least reducing the need for analgesics. A trial was conducted to evaluate the effect of using a sugar-free chewing gum to counteract pain after full maxillary and mandibular fixed appliances were fitted. Secondarily, it looked at the effect of the gum on pain on the 3 days after placement and after archwire changes, on the use of ibuprofen for pain relief, and in connection with appliance breakage. Methods.—One thousand patients at nine sites throughout southwest England took part. All were having fixed maxillary and mandibular appliance therapy, were age 11 to 17 years, and were able to use ibuprofen and chewing gum. They were randomly assigned to an experimental group of 499 patients who used gum to relieve pain and a control group of 491 patients who used ibuprofen. All completed questionnaires for analysis. Pain experience was measured using the mean of three recordings on a scale from 1 to 10. Pain experienced in the subsequent 3 days and after the first archwire change was also noted. Patients in the intervention (gum) group were allowed to use ibuprofen if the gum was insufficient to relieve their pain. Patients in the control group could only use ibuprofen. Results.—Mean pain scores on the day of bond-up were 4.31 for the experimental group and 4.17 in the control group. The mean difference was 0.14. Pain scores
were slightly higher for the gum-chewing group on the day of bond-up but lower on the next 3 days. None of the measures reached significance and were likely not clinically relevant. Eighty-two percent of the patients in the chewing gum group and 91% of those in the control group took ibuprofen after bond-up, with the gum group taking it a mean of 2.1 times and the control group a mean of 3.0 times. After archwire changes, 42% of the gum group and 60% of the control group used ibuprofen, with the gum group taking it a mean of 0.8 times and the control group 1.5 times. The difference in the relative use of ibuprofen between groups differed slightly but with no obvious trend across time. Bracket debonding rates did not differ between the two groups either after bond-up or after the first archwire change. In addition, no other adverse events were noted in either group. Discussion.—The reported pain in the two groups did not differ significantly. However, those using chewing gum had slightly more pain on the day of bond-up but slightly less over the next 3 days compared to those in the ibuprofen group. Patients in the chewing gum group reported less use of ibuprofen for pain relief than those in the control group. Appliance breakage did not differ between the two groups.
Clinical Significance.—Sugar-free chewing gum may be useful for patients undergoing orthodontic treatment. It appears to reduce the need for analgesic usage and has no clinically or statistically significant effect on bracket debonding. Chewing gum may offer a way to avoid the adverse effects of taking ibuprofen or other analgesic drugs, or at least may limit their intake and reduce adverse results.
Ireland AJ, Ellis P, Jordan A, et al: Comparative assessment of chewing gum and ibuprofen in the management of orthodontic pain with fixed appliances: A pragmatic multicenter randomized controlled trial. Am J Orthod Dentofacial Orthop 150:220-227, 2016
Reprints available from AJ Ireland, School of Oral and Dental Sciences, Univ of Bristol, Lower Maudlin St, Bristol BS1 2LY, United Kingdom; e-mail: [email protected]
Endodontics Apical periodontitis Background.—Studies find that apical periodontitis is caused by microbial agents from an infected root canal system. Treatments have been developed to counter these agents, but because of the diversity of the endodontic microbiota and the current poor understanding about specific bacterial species, the role of these organisms remains a mystery. A review was undertaken to summarize the state of knowledge about the microorganisms that contribute to apical periodontitis, identify targets for future research, and suggest appropriate treatments. Methods.—The Dentistry and Oral Sciences Source (EBSCO) and Medline electronic databases were searched for English language articles published between 1995 and 2015 dealing with apical periodontitis and its microbiological ties. A hand search of articles was also conducted. The results of the search were divided into etiologic concerns and identification of species, pathogenesis of apical periodontitis, and treatment implications. Etiologic Concerns and Identification of Species.— Various studies in animals have confirmed that the role of microorganisms in the development of apical periodontitis is essential. The pathogenicity of the species involved is enhanced when more than one is present. The specific bacteria dwelling in root canal infections were predominantly anaerobic, with facultative anaerobes found in the more coronal aspect of the system and obligate anaerobes found apically. The survival of these species depends on the availability of nutrients, oxygen level, and pH level. Fermentable carbohydrates sustain the initial population, which are generally facultatively anaerobic bacteria. As the infection extends deeper into the canals, the decreased oxygen levels and diminished availability of fermentable carbohydrates favors the obligate anaerobic bacteria, which live on protein and glycopeptides that become available through the breakdown of pulpal tissues and serum proteins. This deterioration raises the pH of the environment, and late-stage bacteria take over. The various species seem to be interdependent for nutrition, with the metabolic products of one providing nutrition for others.
The species can now be identified through molecular methods rather than just culture-dependent means. The drawback with molecular methods is their high sensitivity, which increases the risk of including contaminants as well as amplifies the presence of non-prevalent species. As a result the role of unimportant species can be overemphasized. A combination of the molecular and culture-based methods has identified 9 phyla, 4 fungal species, and 1 alchael species in primary root canal infections. However, the prevalence of microbial species differs by study method and sample population. Newer species have been found, with primary intra-radicular infection reportedly consisting of 10 to 30 species per canal, with individual variations. Because of the diversity and breadth of these findings, the exact pathogenic role of each individual species remains undetermined. Microorganisms in the root canal system tend to congregate in biofilms. These allow the creation of niches fostering the survival of the various species, enhance metabolic efficiency, protect the bacteria from host defenses and antimicrobial agents, facilitate cellular communication (specifically, quorum sensing and exchange of genetic materials), and help to retain water to hydrate the microbial cells. Pathogenesis of Apical Periodontitis.—Complex interactions between the microbial factors and host defenses responding to the bacterial invasion produce apical periodontitis. The specific pathogenicity of the invading species is modified by bacterial interactions, host evasive actions, the release of lipopolysaccharides (LPS), and the production of proteolytic enzymes. Microbes grow and avoid detection until the community is large enough to cause host destruction by interfering with host defenses. Porphyromonas gingivalis appears able to avoid triggering a host response because its LPS does not induce chemotaxis. Gram-negative organisms can secrete antigens for antibodies to react against that leave the organism intact. LPS on Gram-negative cell walls