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 Table of Contents  
Year : 2012  |  Volume : 4  |  Issue : 6  |  Page : 304-306  

NSAIDs in orthodontic tooth movement

Department of Orthodontics, KSR Institute of Dental Science and Research, Tiruchengode, Tamil Nadu, India

Date of Submission01-Dec-2011
Date of Decision02-Jan-2012
Date of Acceptance26-Jan-2012
Date of Web Publication28-Aug-2012

Correspondence Address:
Muthukumar Karthi
Department of Orthodontics, KSR Institute of Dental Science and Research, Tiruchengode, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-7406.100280

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Orthodontic tooth movement is basically a biological response toward a mechanical force. The movement is induced by prolonged application of controlled mechanical forces, which create pressure and tension zones in the periodontal ligament and alveolar bone, causing remodeling of tooth sockets. Orthodontists often prescribe drugs to manage pain from force application to biologic tissues. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the drugs usually prescribed. NSAIDs block prostaglandin synthesis and result in slower tooth movement. Prostaglandins have been found to play a direct role in bone resorption. Aspirin, acetaminophen, ibuprofen, diclofenac, vadecoxib, and celecoxib are the commonly prescribed drugs. Acetaminophen is the drug of choice for orthodontic pain without affecting orthodontic tooth movement.

Keywords: Acetaminophen, NSAIDs, prostaglandins

How to cite this article:
Karthi M, Anbuslevan GJ, Senthilkumar KP, Tamizharsi S, Raja S, Prabhakar K. NSAIDs in orthodontic tooth movement. J Pharm Bioall Sci 2012;4, Suppl S2:304-6

How to cite this URL:
Karthi M, Anbuslevan GJ, Senthilkumar KP, Tamizharsi S, Raja S, Prabhakar K. NSAIDs in orthodontic tooth movement. J Pharm Bioall Sci [serial online] 2012 [cited 2022 Aug 14];4, Suppl S2:304-6. Available from:

Orthodontic tooth movement is based on the biologic principle that prolonged pressure on the teeth results in remodeling of periodontal structures including the alveolar bone and periodontal ligament. The early phase of orthodontic tooth movement involves acute inflammatory response characterized by periodontal vasodilatation. There is inflammatory response surrounding the tissues where osteoblastic and osteoclastic activities are carried out. [1],[2] Depending on the alterations in the periodontium, pain and discomfort are the common experiences among orthodontic patients. Reported pain and discomfort is generally the highest during the first 24 h after the application of an orthodontic force. The periodicity of these complaints peaks at 24 h, but decreases to baseline levels by 7 days. [3]

The most common group of medications used in orthodontics for pain relief consists of nonsteroidal anti-inflammatory drugs (NSAIDs). [4],[5] These drugs function by inhibition of enzyme cyclooxygenase (COX), which modulates the transformation of prostaglandins (PGs) from arachidonic acid in the cellular plasma membrane. PGs such as PGE1 and PGE2 are important mediators of bone resorption. [6]

Several authors have published on the effects of systemic or local application of medicaments and the intake of dietary supplements, such as vitamins and minerals, during orthodontic tooth movement. [4] Most reviews did not report the effect of medications or supplements on the rate of orthodontic tooth movement. The medications can affect the rate of orthodontic tooth movement. [7] We performed a systematic literature review on the effects of NSAIDs in particular on orthodontic tooth movement.

Research in molecular biology on orthodontic tooth movement has identified the main mediators involved in the complex process of extravasation, inflammatory cell chemotaxis, and the recruitment of osteoclast and osteoblast progenitors. [8]

NSAIDs have been classified as analgesic and anti-inflammatory, and analgesic but poorly anti-inflammatory [Table 1]. [9]
Table 1: Classification of NSAIDs

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Though NSAIDs are chemically disparate, they produce their therapeutic effects by the common ability to inhibit the activity of the COX enzymes. [10]

Two isoforms of mammalian COX have been described: the constitutive COX1 and the inducible COX2. COX1 is considered important in tissue homeostasis. COX2 is transcriptionally induced by cytokines and is important in the development of inflammation. [11],[12],[13],[14] NSAIDs have been developed to target these cyclooxygenases, including acetylsalicylate (aspirin), ibuprofen, etc. [15]

Non-selective COX inhibition includes agents such as aspirin, acetaminophen, indomethacin, and naproxen, which provide effective pain relief for inflammatory conditions. All NSAIDs have more or less similar effects and mechanism of action. They suppress the production of prostanoids (thromboxanes, prostacyclines, and PGs) because of their inhibition of COX1 and COX2, which are essential in the synthetic pathways of prostanoids. COX1 is a constitutive form, whereas COX2 is inducible. Acetylsalicylic acid inhibits both types of COX in a non-competitive and irreversible way. [16] Thus, it effectively inhibits PG synthesis.

In the early 1990s, it became apparent that COX1 mediates the synthesis of PGs responsible for the protection of stomach lining, whereas COX2 is induced during inflammatory reaction, thereby mediating the synthesis of PGs responsible for pain. Acetylsalicylic acid and flurbiprofen, [17] indomethacin, [18] and ibuprofen [19] have shown reduction in the rate of orthodontic tooth movement. [20]

Acetaminophen is an NSAID belonging to the family of paraminophenols, which by not inhibiting PGs or by inhibiting them slightly, does not have an effect on orthodontic tooth movement. Its antipyretic and analgesic activities are the same as aspirin. However, its mechanism of action has not been determined, and it is supposed that its analgesic effect is produced at the central nervous system level and does not act over cell membranes, as those described previously do. [19]

Acetaminophen is considered to be a very weak PG inhibitor and possesses no significant anti-inflammatory effects. It has no effect on the rate of tooth movement in rabbits undergoing orthodontic tooth movement. Acetaminophen, a proven analgesic that lacks the anti-inflammatory properties of NSAIDs, appears to be the drug of choice to relieve orthodontic pain. [21],[22],[23],[24],[25] Ibuprofen showed reduced rate of orthodontic tooth movement. [22]

Carlos et al. in their study of orthodontic tooth movement after inhibition of COX2 found that both diclofenac and reofecoxib inhibited tooth movement. [23] Coxibs possess minimal NSAID typical toxicity with full anti-inflammatory efficacy and have been used for orthodontic treatment of pain. [18] Rofecoxib completely inhibited orthodontic tooth movement in rats, whereas celecoxib and parecoxib did not. [23] Long-term effect of celecoxib has shown to reduce the rate of orthodontic tooth movement. [26] Acetaminophen is still the drug of choice for treating the discomfort of tooth movement because no advantages are derived from the use of new COX2 inhibiting drugs. [27]

Recently, rofecoxib and valdecoxib were withdrawn from US and European markets by their manufacturer because of reports of increased cardiovascular events and skin rashes, respectively. Another COX2 inhibitor, celecoxib, is currently FDA approved for treatment of pain syndromes. [28] Celecoxib and parecoxib are better than rofecoxib in orthodontic tooth movement. [23]

The various NSAIDs and their effects on bone metabolism and orthodontic tooth movement are given in [Table 2] and [Table 3], respectively.
Table 2: Groups and subgroups of NSAIDs, and some well-known brand names

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Table 3: Effects of NSAIDs on orthodontic tooth movement

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   Conclusion Top

Acetaminophen [21],[22],[23],[24],[25] and celecoxib [23],[26] are the NSAIDs of choice for relief of orthodontic pain without affecting the rate of orthodontic tooth movement. [29],[30],[31],[32],[33]

   References Top

1.Proffit W. Contemporary orthodontics. 3 rd ed. St Louis: Mosby; 2000. p. 302-5.  Back to cited text no. 1
2.Graber, Vanasdrall, Vig. Orthodontics current principles and techniques 2009.  Back to cited text no. 2
3.Grieve WG, Johnson GK, Moore RN, Reinhardt RA, DuBois LM. Prostaglandin E and IL-1β levels in gingival crevicular fluid during human orthodontic tooth movement. Am J Orthod Dentofacial Orthop 1994;105:369-74.  Back to cited text no. 3
4.Gameiro GH, Pereira-Neto JS, Magnani MB, Nouer DF. The influence of drugs and systemic factors on orthodontic tooth movement. J Clin Orthod 2007;41:73-8.  Back to cited text no. 4
5.Krishnan V. Orthodontic pain: From causes to management- a review. Eur J Orthod 2007;29:170-9.  Back to cited text no. 5
6.De Carlos F, Cobo J, Diaz-Esnal B, Arguelles J, Vijande M, Costales M. Orthodontic tooth movement after inhibition of cyclooxygenase-2. Am J Orthod Dentofacial Orthop 2006;129:402-6.  Back to cited text no. 6
7.Krishnan V, Davidovitch Z. The effect of drugs on orthodontic tooth movement. Orthod Craniofac Res 2006;9:163-71.  Back to cited text no. 7
8.Krishnan V, Davidovitch Z. Cellular, molecular and tissue level reaction to orthodontic forces. Am J Orthod Dentofacial Orthop 2006;129:469-72.  Back to cited text no. 8
9.Tripathi KD. Essentials of Medical Pharmacology 3 rd edition:166.  Back to cited text no. 9
10.Vane JR. Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nat New Biol 1971;231:232-5.  Back to cited text no. 10
11.O'Banion MK, Winn VD, Young DA. cDNA cloning and functional activity of a glucocorticoid-regulated inflammatory cyclooxygenase. Proc Nat Acad Sci U S A 1992;89:4888-92.  Back to cited text no. 11
12.Winn VD, O'Banion MK, Young DA. Anti-inflammatory glucocorticoid action: Inhibition of griPGHS, a new cyclooxygenase. J Lipid Mediat 1993;6:101-11.  Back to cited text no. 12
13.Smith WL, Garavito RM, De Witt DL. Prostaglandin endoperoxide H synthases (cyclooxygenases)-1 and -2. J Biol Chem 1996;271:33157-60.  Back to cited text no. 13
14.Smith WL, Dewitt DL. Prostaglandin endoperoxide H synthases- 1 and -2. Adv Immunol 1996;62:167-215.  Back to cited text no. 14
15.Smith WL, Meade EA, Dewitt DL. Interaction of PGH synthase isozymes-1 and -2 with nonsteroidal anti-inflammatory drugs. Adv Exp Med Biol 1997;400A:189-96.  Back to cited text no. 15
16.Wong A, Reynolds EC, West VC. The effect of acetylsalicylic acid on orthodontic tooth movement in the guinea pig. Am J Orthod Dentofacial Orthop 1992;102:360-5.  Back to cited text no. 16
17.Sandy JR, Harris M. Prostaglandins and tooth movement. Eur J Orthod 1984;6:175-82.  Back to cited text no. 17
18.Giunta D, Keller J, Nielsen FF, Melsen B influence of indometacin in bone turnover related to orthodontic tooth movement in miniature pigs. Am J Orthod Dentofacial Orthop 1995;108:361-6.  Back to cited text no. 18
19.Arias OR, Marquez-Orozco MC. Aspirin, acetaminophen, and ibuprofen: Their effects on orthodontic tooth movement. Am J Orthod Dentofacial Orthop 2006;130:364-70.  Back to cited text no. 19
20.Kehoe MJ, Cohen SM, Zarrinnia K, Cowan A. The effect of acetaminophen, ibuprofen, and misoprostol on prostaglandin E2 synthesis and the degree and rate of orthodontic tooth movement. Angle Orthod 1996;66:339-49.  Back to cited text no. 20
21.Roche JJ, Cisneros GJ, Acs G. The effect of acetaminophen on tooth movement in rabbits. Angle Orthod 1997;67:231-6.  Back to cited text no. 21
22.Reza S, Larry JO, W. Craig, Sheldon MN Comparison of the efficacy of ibuprofen and acetaminophen in controlling pain after orthodontic tooth movement. Am J Orthod Dentofacial Orthop 2009;135:516-2.  Back to cited text no. 22
23.Felix de Carlos, Juan Cobo Orthodontic tooth movement after inhibition of cyclooxygenase-2. Am J Orthod Dentofacial Orthop 2006;129:402-6.  Back to cited text no. 23
24.Fidan Alakus S, Elchin Esenlik Pakistan Oral Dent J 2010;30:45-50  Back to cited text no. 24
25.Carmen G, Hitoshi H, Ken M, Tatsunori S, Joseph HY. Effects of Steroidal and Non-steroidal drugs on tooth movement and root resorption in rat molar. Angle Orthod 2009;29:715-25.  Back to cited text no. 25
26.Gustavo HG, Darcy FN, Joao Sarmento PN, Vania CS, Eduardo DA, Pedro DN, et al. Effects of short- and long-term celecoxib on orthodontic tooth movement. Angle orthod 2008;78:860-5.  Back to cited text no. 26 Carlos F, Cobo J, Diaz Esnal B, Arquelles J, Vijiande M, Costales M. Orthodontic tooth movement after inhibition of cyclooxygenase 2. Am J Orthod Dentofacial Orthop 2006;129:402-6.  Back to cited text no. 27
28.Young AN, Taylor RW, Taylor SE, Linnebur SA, Buschang PH. Evaluation of preemptive valdecoxib therapy on initial archwire placement discomfort in adults. Angle Orthod 2006;76:251-9.  Back to cited text no. 28
29.Katzung BG ed. Basic clinical pharmacology. 5 th ed. Appleton and Lange; 1992; p. 180.  Back to cited text no. 29
30.Sari E, Olmez H, Gurton AU. Comparison of some effects of acetylsalicylic acid and rofecoxib during orthodontic tooth movement. Am J Orthod Dentofacial Orthop 2004;125:310-5.  Back to cited text no. 30
31.Arias O, Marquez-Orozco MC. Aspirin, acetaminophen, and ibuprofen: Their effects on orthodontic tooth movement. Am J Orthod Dentofacial Orthop 2006;130:364-70.  Back to cited text no. 31
32.Paula A, Giovanni O, Cesar A, Olga V, Alejandro J, Diego T, et al. Pulp-dentine complex changes and root resorption during intrusive orthodontic tooth movement in patients prescribed nabumetone. J Endod 2004;31:61-6.  Back to cited text no. 32
33.Theodosia B, Jens CT, Edith M, Jaap CM. Medication effects on the rate of orthodontic tooth movement: A systematic literature review. Am J Orthod Dentofacial Orthop 2009;135:16-26.  Back to cited text no. 33


  [Table 1], [Table 2], [Table 3]

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