Vol. 119 No.

3 March 2015

Clinical implications of prescribing nonsteroidal

anti-inflammatory drugs in oral health careda review
Ravleen Nagi, BDS, MDS,a B.K. Yashoda Devi, BDS, MDS,b N. Rakesh, BDS, MDS, PhD,c
Sujatha S. Reddy, BDS, MDS, PhD,d and Deepa Jatti Patil, BDS, MDSe

Nonsteroidal anti-inflammatory drugs (NSAIDs), including both the traditional nonselective NSAIDs and the
selective cyclooxygenase (COX)-2 inhibitors, are widely used for their anti-inflammatory and analgesic effects. They are
routinely prescribed in dental practice for the management of pain and swelling. Their use in treating acute dental pain and
chronic orofacial pain, as adjuncts to the treatment of periodontal disease, and to minimize edema following surgical
procedures is well documented. However, long-term utilization of nonselective NSAIDs could increase the risk of
gastrointestinal symptoms, ranging from mild (e.g., dyspepsia, nausea, or vomiting) to serious gastric problems (e.g., gastric
bleeding or perforation). Therefore, selective COX-2 inhibitors have been developed with fewer GI side effects but the recently
identified cardiovascular adverse reactions limit their routine use in dental practice. Another major concern for oral physicians
is NSAID-induced mucosal lesions and prolongation of bleeding time during invasive dental procedures. This article reviews
therapeutic and analgesic uses of NSAIDs in dentistry. The various issues surrounding NSAID-induced adverse reactions and
their implications in dentistry are also discussed. (Oral Surg Oral Med Oral Pathol Oral Radiol 2015;119:264-271)

The primary goal of oral health care providers is to (CV) safety is a major concern and has resulted in
relieve dental pain for the optimal well-being of pa- NSAID withdrawal in many patients. Therefore, den-
tients. Nonsteroidal anti-inflammatory drugs (NSAIDs) tists should assess the risk and benefits of each medi-
provide important analgesic and anti-inflammatory cation, taking into account the medical history and
benefits to millions of patients. They are widely used analgesic requirement of each individual. These drugs
therapeutic agents for the treatment of a wide spectrum should be prescribed in appropriate doses and durations
of pathophysiologic conditions. Due to their effective- to reduce or avoid NSAID-associated complications.4
ness in reducing mild to moderate pain, they are This review discusses the mechanisms of action,
commonly prescribed in dental practice.1 therapeutic uses, and potential side effects associated
Vane discovered that aspirin and related drugs act by with the use of NSAIDs in dental practice.
inhibiting prostaglandin (PG) biosynthesis.2 The
principal pharmacologic effects of NSAIDs are MECHANISM OF ACTION
attributed to their ability to inhibit PG activity by NSAIDs act as nonselective inhibitors of the tissue
blocking the activity of both cyclooxygenase 1 (COX- COX, which exists in two well-known subtypes: COX-
1) and COX-2.2,3 Although NSAIDs relieve symp- 1 and COX-2. COX catalyzes the formation of PGs and
toms, they are not without potentially significant thromboxanes (TXA2) from arachidonic acid. COX-1 is
adverse effects. The most noteworthy adverse effect is constitutively expressed in various tissues, whereas
upper gastrointestinal (GI) toxicity. Cardiovascular COX-2 is a largely inducible form found predominantly
in the kidneys and the central nervous system.COX-1
a
Senior Lecturer, Department of Oral Medicine and Radiology, D.J. generates PGs for the body’s housekeeping functions,
College of Dental Sciences & Research, Modinagar, Ghaziabad, Uttar such as gastric mucosal integrity, platelet homeostasis,
Pradesh, India. and regulation of renal blood flow. TXA2 generated
b
Senior Professor, Department of Oral Medicine and Radiology, initiates platelet aggregation. COX-2 synthesizes
Faculty of Dental Sciences, MS Ramaiah University of Applied
“proinflammatory PGs” that mediate pain and inflam-
Sciences, MSRIT Post, Mathikere, Bangalore, Karnataka, India.
c
Associate Professor, Department of Oral Medicine and Radiology, mation at the site of tissue damage, such as in pulpitis,
Faculty of Dental Sciences, MS Ramaiah University of Applied
Sciences, MSRIT Post, Mathikere, Bangalore, Karnataka, India.
d
Professor and Head, Department of Oral Medicine and Radiology, Statement of Clinical Relevance
Faculty of Dental Sciences, MS Ramaiah University of Applied
Sciences, MSRIT Post, Mathikere, Bangalore, Karnataka, India. Acute pain is the most common complaint that
e
Senior Lecturer, Department of Oral Medicine and Radiology, causes patients to seek help from oral health care
Swami Devi Dyal Dental College and Hospital, Panchkula, Haryana,
professionals. Nonsteroidal anti-inflammatory drugs
India.
Received for publication May 4, 2014; returned for revision Oct 28, are routinely prescribed but have been associated
2014; accepted for publication Dec 2, 2014. with adverse reactions. Therefore, consideration of
Ó 2015 Elsevier Inc. All rights reserved. the medical history and the analgesic requirement of
2212-4403/$ - see front matter patients are essential.
http://dx.doi.org/10.1016/j.oooo.2014.12.002

264
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Volume 119, Number 3 Nagi et al. 265

Fig. 1. Mechanism of action of nonsteroidal anti-inflammatory drugs (NSAIDs).

periodontitis, or pain from surgery. Thus, the thera- chronic orofacial pain; as an adjunct in the treatment of
peutic anti-inflammatory effects of NSAIDs are pri- periodontal disease; and to minimize postoperative
marily due to COX-2 inhibition, whereas undesirable edema, endodontic pain, and bone pain from oral can-
side effects are due to COX-1 inhibtion.5 cer.9 Ibuprofen is the prototypical nonselective NSAID
Commonly used nonselective or traditional NSAIDs and represents the gold standard against which new
block both COX-1 and COX-2, but serious GI effects analgesic agents are evaluated. Shorter-acting (4-6
have been reported with their long-term use. This has hours and 6-8 hours) nonselective NSAIDs are more
led to the development of selective COX-2 inhibitors appropriate for treating acute dental pain with fewer GI
(rofecoxib, celecoxib, valdecoxib), also known as the side effects when used on a short-term basis. Recently
“coxibs,” which have an improved gastric safety pro- introduced selective COX-2 inhibitors are being widely
file. In addition, selective inhibitors of COX-2 depress prescribed by health care professionals to manage
prostacyclin (PGI2), an atheroprotective agent, but not chronic pain in certain conditions, such as temporo-
COX-1ederived TXA2, a proaggregatory and vaso- mandibular disorders (TMDs), due to their improved
constrictor mediator, which might predispose patients gastric tolerability in conjunction with the comparable
to heart attack and stroke6 (Figure 1). efficacy of nonselective NSAIDs.10,11 Table I lists the
NSAIDs commonly used in dental practice.
ANALGESIC AND THERAPEUTIC USES OF
NSAIDS IN DENTISTRY Prescribing considerations
The introduction of NSAIDs into clinical practice has NSAIDs have been established as the drugs of first choice
dramatically improved pain management in dentistry.7 for the management of mild-to-moderate dental and
Drugs available for pain management belong to two postoperative pain. They are usually more effective when
major groups: the non-narcotic analgesics (NSAIDs and prescribed in adequate doses before the synthesis of PGs at
acetaminophen) and the opioids (or narcotics). The most the site of inflammation (within 2 hours of tissue injury).
commonly used non-narcotic analgesics in dentistry are Therefore, clinicians should consider an initial loading
available as over-the-counter medications. Unlike opioid dose, such as double the maintenance dose, which will
analgesics, NSAIDs exhibit the ceiling effect to analgesia, allow therapeutic levels to be reached more rapidly.12,13
with no tolerance or physical dependence and possess Another consideration for the use of NSAIDs is
both anti-inflammatory and analgesic actions.8 reduction of pain after surgery; therefore, NSAIDs are
NSAIDs are the mainstay therapy for acute dental prescribed on a regular basis for the first 1 to 2 days
pain. They have also been evaluated for treatment of following a surgical procedure, such as every 4 hours,
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266 Nagi et al. March 2015

Table I. Nonsteroidal anti-inflammatory drugs (NSAIDs) used in dentistry drug dosages have been verified. No
revisions necessary
Group Generic name Dosing form Adult dose Pediatric dose
Salicylic acid derivatives Aspirin Tablets 325-650 mg, q4h 10-15 mg/kg/dose q4-6h
Aryleacetic acid Diclofenac Tablets/suppositories/ 50 mg/8 h PO 2 to 3 mg/kg/d in divided
derivatives Aceclofenac injection 75 mg/24 h IM doses 2-4 times daily
Maximum daily dose
200 mg
Propionic acid derivatives Ibuprofen Tablets 200-400 mg/q4-6h 20 mg/kg/d in 3-4 doses
Liquid 20-40 mg/cc solution q4-
6h
Ketoprofen Tablets 25-50 mg q8-12h 1.5-2 mg/kg/d in 3-4 doses
Naproxen Tablets 250-500 mg/q8-12h 10 mg/kg/d in 2 doses
Liquid 125 mg/5 mL solution
q8-12h
Indole derivatives Indomethacin Capsules 200-400 mg/q6-8h Not recommended under
14 years (hepatotoxic)
Oxicam derivatives Piroxicam Tablets/suppositories 40 mg/d on first day 20 0.2 to 0.3 mg/kg/d
mg/d on following days Maximum daily dose
15 mg
Pyrazolones Metamizol Capsules, solution for 500-1000 mg/q6-8h 1-3 years 250 mg/q6-8h
injection, suppositories Maximum 6 g/d PO 3-11 years 250 mg/q6h
2 g/8 h IV
Pyrrolo-pyrrole derivative Ketorolac Tablets/IM injection 10 mg/q4-6h Not recommended under
IM: 30 mg q6h 16 years (nephrotoxic)
(limit 5 days)
Selective COX-2 Inhibitors Celecoxib Tablets 100-200 mg q12h Safety not evaluated in
children
Para-aminophenol Acetaminophen/ Tablets/intravenous 325-650 mg/q4-6h 10 mg/kg q4h
derivatives paracetamol infusion/suspension/ 1 g/8 h 15 mg/kg q6h
suppositories
q4-6h, every 4 to 6 hours; q8-12h, every 8 to 12 hours; mg/kg/d, milligrams per kilogram per day; PO, per oral; IV, intravenous; IM, intramuscular;
COX, cyclooxygenase.

as opposed to an “as needed” basis. The analgesic can endodontic therapy is usually controlled with local
be taken on an as-needed basis following this initial anesthesia, but post-treatment pain continues to be a
period.13 Table I provides the recommended doses of challenge for the dental clinician because of either
NSAIDs used in dentistry. One of the limitations of insufficient relief of pain or unacceptable side effects.
NSAIDs is that they have a ceiling effect; thus, after Ibuprofen (200-400 mg; every 4-6 hours), acetamino-
an analgesic ceiling has been reached, an increase in phen or paracetamol (325-650 mg; every 4-6 hours)
the dose only increases the side effects without are commonly prescribed by dentists to reduce pree
achieving additional analgesia. However, this problem and posteendodontic treatment pain (see Table I).
can be overcome by adding synergistic medications, Combination of ibuprofen and acetaminophen
for example, adding acetaminophen to ibuprofen or provides additive analgesia for treating intense
acetaminophen to diclofenac.8 endodontic pain.14
Although NSAIDs are effective analgesics, at times
nociceptive pain in the moderate to severe range may NSAIDs and orthodontic pain
require additional analgesia by combining an opioid NSAIDs are usually prescribed by orthodontists to
analgesic (hydrocodone, oxycodone) with an manage pain resulting from application of force to bio-
NSAID.12,13 Combination therapy has the advantages logic tissues during orthodontic treatment. NSAIDs
of the anti-inflammatory properties of NSAIDs and a block PG synthesis and result in slower tooth movement.
possible decrease in NSAID-induced adverse effects. Acetaminophen is the drug of choice for orthodontic
Table II lists the various NSAIDeopioid combination pain without affecting orthodontic tooth movement.15
analgesics used for treating dental pain.

NSAIDs in temporomandibular disorders

NSAIDs and endodontic pain Short-term use of oral (naproxen, ibuprofen) and topical
NSAIDs have been shown to be very effective for NSAIDs, such as ibuprofen and diclofenac, may provide
managing pulpal and periradicular pain. Pain during temporary relief from jaw discomfort in patients with
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Volume 119, Number 3 Nagi et al. 267

Table II. Nonsteroidal anti-inflammatory drugs (NSAIDs) and opioid combination dosing regimen for dental pain
NSAID þ opioid combination Dosing form Dosage
Acetaminopheneparacetamol þ codeine Tablets/liquid Acetaminophen 300 mg
Codeine: 30 mg q4-6h, as needed
2 tablets q4-6h, as needed
Acetaminopheneparacetamol þ hydrocodone Tablets/liquid Acetaminophen 500 mg
Hydrocodone 5 mg q4-6h, as needed
2 tablets q4-6h, as needed
Ibuprofen þ hydrocodone Tablets/liquid Ibuprofen 200 mg
Hydrocodone 7.5 mg q4-6h, as needed
2 tablets q4-6h, as needed
Ibuprofen þ oxycodone Tablets/liquid Ibuprofen 400 mg
Oxycodone 5 mg; 1 tablet qid, as needed PO
Acetaminopheneparacetamol þ oxycodone Tablets/liquid Acetaminophen 325-500 mg
Oxycodone 2.5-7.5 mg; 2 tablets q4-6h, as needed PO
Aspirin þ codeine Tablets/liquid Aspirin 325 mg
Codeine 30 mg; 1-2 tablets q4-6h, as needed PO
Acetaminopheneparacetamol þ tramadol hydrochloride Tablets Acetaminophen 325 mg
Tramadol 37.5 mg; 2 tablets q4-6h, as needed
q4-6h, every 4-6 hours; qid, four times a day; PO, per oral.

TMDs. NSAIDs, such as ketoprofen, ibuprofen, and SIDE EFFECTS OF NSAIDS

piroxicam, can be incorporated into transdermal creams Gastrointestinal alterations
for application on the skin over the painful muscle or The link between gastroduodenal mucosal injury and
joint.16 The combination of NSAIDs and physical therapy NSAIDs is well recognized. PGs modulate virtually
administered for 4 weeks has been proven to be an every aspect of mucosal defense, and this is evident
effective primary treatment for disk displacement from the increased susceptibility of the GI mucosa to
without reduction and without osseous changes.17 injury following chronic use of an NSAID.23 Increasing
age, stress, Helicobacter pylori infection, smoking,
NSAIDs in oral cancer pain alcohol use, and a history of ulcer are some of the
PGs, especially PGE2, appear to have an important role predisposing factors for NSAID-induced gastro-
in the pathogenesis of cancer. Overexpression of COX-2 pathy.24 Studies have shown that a significant
is thought to contribute to carcinogenesis by stimulating proportion of patients experience upper GI symptoms,
cell proliferation, inhibiting apoptosis, and enhancing usually dyspepsia, and lesions ranging from petechial
angiogenesis. Therefore, nonselective NSAIDs and se- hemorrhages to bleeding peptic ulcers, as seen on
lective COX-2 inhibitors may prevent carcinogenesis by endoscopy.23,25 In dental practice, NSAIDs are pre-
decreasing cell proliferation and inducing apoptosis.18 scribed for a shorter duration in patients of all age
NSAIDs in combination with opioids have long been groups to treat acute pain or as a prophylactic measure.
part of the analgesic pharmacopoeia in the treatment of The most frequently experienced GI side effects are
mild to moderate pain from oral cancer. Benzydamine dyspepsia, diarrhea, and abdominal pain.26
hydrochloride oral rinse is used for prophylactic Mechanism of NSAID-induced gastropathy. There
treatment of radiation-induced oral mucositis.19 are two major components to the pathogenesis of
NSAID-induced gastropathy. NSAIDs cause direct
NSAIDs and periodontal bone loss damage through topical irritant effects and indirect
Numerous clinical studies have shown that PGE2 levels damage through systemic inhibition of PG synthesis.27
are elevated at the sites of ongoing attachment loss and PGs reduce gastric acid secretion and increase mucous
alveolar bone loss. PGE2 has been found to be a production, and thus, the ability of an NSAID to cause
potentially significant mediator of periodontal disease gastric damage correlates well with its ability to
progression, which suggests NSAIDs as a therapeutic suppress gastric PG synthesis.28
possibility for preventing alveolar bone resorption in Selective COX-2 inhibitors in gastroenterol-
progressive periodontitis.20,21 Dentifrices and mouth- ogy. Recently, high Gl risks have been reported with
washes that contain NSAIDs, such as flurbiprofen, chronic use of traditional NSAIDs, such as piroxicam,
naproxen, and ibuprofen, are available in some ketoprofen, and ketorolac; low-dose ibuprofen offers
markets.20 PGs have also been implicated in the peri- the lowest risk. Selective inhibitors of COX-2 were
implantitis, suggesting the role of NSAIDs in control- expeditiously developed with the notion that they
ling implant failure.22 would inhibit inflammatory PG synthesis (thus reducing
MEDICAL MANAGEMENT AND PHARMACOLOGY UPDATE OOOO
268 Nagi et al. March 2015

edema and pain) but not gastric PG synthesis (thus not Nonselective NSAIDs, such as diclofenac, sulindac,
causing ulceration). They are associated with reduction and aspirin, have been reported to be more commonly
in GI risks, associated with most NSAIDs at equivalent associated with hepatotoxicity.33 Aspirin-related hepa-
doses, and offer the opportunity for safe and effective totoxicity is a dose-related phenomenon associated with
treatment of patients who are at risk of developing GI intrinsic salicylate hepatotoxicity and generally only
complications.29 occurs when aspirin is used in full anti-inflammatory
doses (i.e., not 75-300 mg, as used in antiplatelet in-
dications). The United Kingdom Medicines Control
Cardiovascular adverse effects agency has recommended that children under 16 years
CV safety of NSAIDs is a highly controversial topic due
should not be given aspirin because of its linkage with
to past research suggesting an increased CV risk with all
Reye syndrome, the rare but potentially fatal disorder
nonselective NSAIDs and selective COX-2 inhibitors
found almost exclusively in children and adolescents.35
except naproxen (1000 mg daily) and low-dose
The newer selective COX-2 inhibitors (e.g., cele-
ibuprofen (1200 mg daily).30 Clinical trials have
coxib, nimesulide) are also associated with hepatotox-
found that ibuprofen and naproxen may attenuate the
icity.36,37 although celecoxib is said to have lesser
antiplatelet effects of low-dose aspirin, which is used
potential for hepatotoxicity.38 Patients who develop
for prevention of myocardial infarction and other CV NSAID-induced hepatotoxicity must be advised to
diseases.31 It is an important consideration in patients
stop taking NSAIDs permanently. Acetaminophen re-
with a high risk of CV disease, but the clinical
mains the analgesic of choice for these patients, even in
implication of the interference by NSAIDs on the
the presence of jaundice.35
antiplatelet effect of aspirin is still unclear. Therefore,
further studies are required to characterize the CV
effects of aspirin in people taking NSAIDs. Renal effects and hypertension
Adverse cardiovascular events with selective COX-2 Studies have confirmed the relationship between anal-
inhibitors. PGs are thought to play an important role in gesic use and renal damage. Regular use of NSAIDs
normal CV homeostasis. The development of imbal- increases the risk of kidney disorders. Acute deterio-
ance between PGI2 and TXA2 may be a key factor in ration of kidney function occurs in 0.5% to 1% of pa-
the genesis or progression of myocardial ischemia. tients who regularly take NSAIDs.39 Phenacetin was
Selective COX-2 inhibitors are not an acceptable sub- proven to cause “analgesic nephropathy,” and was
stitute for aspirin in patients who need antiplatelet banned in the United States and has been replaced by
therapy for cardioprotection because these agents do acetaminophen.40
not inhibit TXA2 production. By selectively decreasing Nearly all NSAIDs have been found to increase
PGI2 production without inhibiting TXA2 production, blood pressure in normotensive and hypertensive in-
selective COX-2 inhibitors, theoretically, might dividuals and could also attenuate the antihypertensive
decrease the vasodilatory and platelet antiaggregatory effects of diuretics and angiotensin-converting enzyme
effects of PGI2 without inhibiting the vasoconstrictor inhibitors. The pathogenesis is believed to be renal
and platelet aggregatory effects of TXA2.32 In response vasoconstriction secondary to the inhibition of vaso-
to findings of increased risk of thrombotic CV events, dilatory PGs, thus increasing peripheral resistance and
rofecoxib was taken off the market in September blood pressure.41 COX-2 expression has also been
2004, valdecoxib was withdrawn in April 2005, and a found to be upregulated in the salt depletion status in
black box warning was designated for celecoxib.5,32 renal ischemia. Some evidence indicates that specific
COX-2 inhibition may induce electrolyte imbalance,
and abnormal blood pressure in renal ischemia, ulti-
Hepatotoxicity
mately leading to fluid and sodium retention.40
The hepatotoxicity of NSAIDs was identified nearly 70
years ago, leading to the withdrawal of several drugs
from clinical use.33,34 There are two main clinical pat- Dermatologic adverse effects
terns of hepatotoxicity from NSAIDs.34 The first is NSAIDs are among the most commonly prescribed
acute hepatitis with jaundice, fever, nausea, and drugs in medical practice due to its ability to inhibit
greatly elevated transaminases and sometimes both lipoxygenase (LOX) and COX pathways. Chronic
eosinophilia. The alternative pattern is with serologic use of NSAIDs has been found to result in various
(antinuclear factorepositive) and histologic (periportal adverse cutaneous reactions. Photosensitivity is a
inflammation with plasma and lymphocyte infiltration commonly overlooked adverse effect associated with
and fibrosis extending into the lobule) features of benaxoprofen, piroxicam, diclofenac, and benzyd-
chronic active hepatitis. amine.42 Among the currently marketed NSAIDs,
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Volume 119, Number 3 Nagi et al. 269

piroxicam appeared to have the greatest association COX-2 inhibitors are appropriate for prolonged treat-
with serious adverse reactions, such as Stevens- ment of chronic pain associated with TMDs and orofa-
Johnson syndrome (SJS) and toxic epidermal necrol- cial pain; however, their high cost and CV toxicity limit
ysis (TEN), which can affect the oral health of patients. the routine use of these pharmacotherapeutics.11
Thus, health care providers should be aware of the signs Dental management of cardiac patients on aspirin
and symptoms of SJS and TEN.43 therapy remains a challenging issue for dental pro-
fessionals. Low-dose aspirin (75-300 mg daily) is
routinely used as a prophylactic clotting inhibitor in
NSAID use in pregnancy cardiac patients to prevent CV disease outcomes.
Removal of the source of pain using local anesthesia is
However, it has been found to increase the risk of
the optimal management of dental pain during preg-
bleeding after dental extractions and also appears to
nancy. The U.S. Food and Drug Administration (FDA)
affect periodontal assessments by prolonging bleeding
includes most NSAIDs in Category C (drugs that can be
on probing.48,49 Earlier recommendations suggested
used before 30 weeks of pregnancy) and Category D
discontinuation of aspirin use for 7 to 10 days, but the
(drugs that can be used starting at 30 weeks of preg-
current recommendation is up to 3 days of discontinu-
nancy). Starting at 30 weeks of pregnancy, NSAIDs
ation before invasive dental procedures.49 However,
should be avoided by pregnant women as ineffective recent studies have reported that the riskebenefit
contractions during labor and premature closure of the
analysis favors continuing aspirin anticoagulant
ductus arteriosus may occur due to inhibition of PG
therapy even during dental extractions, as bleeding
synthesis.26 If, however, postoperative pain is present,
can be safely controlled with local homeostatic
an analgesic may be necessary and should be
measures except in a small number of patients in
prescribed. Acetaminophen at recommended doses
whom embolic events may prove fatal.50,51
(maximum allowed dose 4000 mg per day) is
Mucosal lesions can occur with any of the NSAIDs.
considered safe and well tolerated during all stages of
They can occur alone (e.g., aphthous ulcers) or in as-
pregnancy; however, due to the risk of kidney sociation with nonmucosal disorders (e.g., SJS and
damage or liver toxicity with overdose, it is avoided,
TEN). Use of NSAIDs (diflunisal, fenclofenac, and
if possible.26,44
indomethacin) can result in lichenoid reactions of the
oral mucosa, and diclofenac and piroxicam can cause
Miscellaneous adverse reactions pemphigus vulgaris. Prolonged contact of the muco-
Systemic effects observed with NSAID use are fever, buccal area with aspirin for relief of dental pain has
increased susceptibility to infection, and lymphadenopa- been found to be associated with epithelial necrosis and
thy. 45 Aspirin has complex effects on the blood sugar and ulceration.52
can give rise to both hypoglycemia and hyperglycemia.
Diclofenac prolongs diabetes mellitus with long-term ADVERSE DRUG INTERACTIONS IN DENTAL
use. Salicylates may reduce hyperglycemia in some pa- PRACTICE
tients with diabetes, independently of insulin.46 Drug interactions with use of NSAIDs have been well
documented. Concurrent use of NSAIDs and cortico-
steroids could increase the risk of GI bleeding, which is
DENTAL IMPLICATIONS OF NSAID USE a potential concern for dentists, particularly with long-
Most pain in the dental setting is acute pain arising from term utilization of these pharmacotherapeutics.53
preoperative conditions (infection, inflammation) or Sufficient evidence exists to support the occurrence of
from a dental procedure (surgery, inflammation). An interactions among NSAIDs, antihypertensives, and
effective model for assessing the efficacy of analgesics diuretics. Antihypertensives and diuretics stimulate
to treat acute pain is third molar extraction.9 Combining the release of the vasodilator PGI2. NSAIDs may
ibuprofen with acetaminophen provides dentists with an potentially reduce the efficacy of antihypertensive
additional therapeutic strategy for managing acute drugs. In patients taking diuretics, nephrotoxicity is
postoperative dental pain. This combination has been increased, which is likely to be the result of reduced
reported to provide greater analgesia without extracellular fluid.41
significantly increasing the adverse effects.47 Health care professionals should advise patients
Studies have found that selective COX-2 inhibitors regarding the appropriate concomitant use of aspirin
are as efficacious as nonselective NSAIDs in treating and ibuprofen, which might render aspirin less effective
acute dental pain with less GI toxicity.10 It has also been when used for its antiplatelet cardioprotective effect.30
suggested that for this short period, the risk of High-dose aspirin, mephenamic acid, and ketoprofen
developing serious upper-GI toxicity with nonselective increase the hypoprothrombinemic effects of warfarin
NSAIDs is very low and the currently available selective by displacing it from the protein-binding site. Levels of
MEDICAL MANAGEMENT AND PHARMACOLOGY UPDATE OOOO
270 Nagi et al. March 2015

methotrexate, which is used in cancer chemotherapy, We would like to thank our Principal, Dr B.N. Sreenivas
can be increased due to the direct competition for renal Murthy, BDS, MDS, Faculty of Dental Sciences, MS Ram-
excretion between methotrexate and NSAIDs.53 aiah University of Applied Sciences, MSRIT Post, Mathekere,
Serotonin reuptake inhibitors are indicated for the Bangalore, Karnataka for his support and guidance.
treatment of depression, and they impair the ability of
platelets to obtain serotonin from the bloodstream
thereby inhibiting platelet aggregation independent of
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38. Maddrey WC, Maurath CJ, Verburg KM, et al. The hepatic safety Ravleen Nagi, BDS, MDS
and tolerability of the novel cyclo-oxygenase-2 inhibitor cele- Senior Lecturer
coxib. Am J Ther. 2000;7:153-158. Department of Oral Medicine and Radiology
39. Blantz RC. Acetaminophen: acute and chronic effects on renal D.J. College of Dental Sciences & Research
function. Am J kidney Dis. 1998;28:S3-S6. Niwari Road
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and chronic renal failure. N Engl J Med. 2001;345:1801-1808. Ghaziabad, U.P.
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2013;17:171-173. [email protected]