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DENTAL ASPECTS OF MANIFESTATION OF ADVERSE DRUG REACTIONS
Teacher: Professor, Nithin Kumar
Musoxonov Axmadxon
23DS-02. ID:230404
Abstract
Background:
Drug-induced oral adverse reactions (ADRs) are frequently encountered in
dental practice but are often underrecognized or misdiagnosed due to their clinical
resemblance to primary oral diseases. As systemic drug use increases, particularly in aging
and polymerizate populations, awareness of these reactions becomes essential for timely
diagnosis and effective management.
Objective:
This review aims to synthesize current evidence on the range, frequency,
causative agents, and clinical implications of drug-induced oral ADRs, with an emphasis on
diagnostic relevance for dental professionals.
Methods:
A structured literature search was conducted across PubMed, Scopus, Cochrane
Library, and Google Scholar for articles published between January 2000 and March 2023.
From an initial pool of 20 studies, 8 met the inclusion criteria and were analysed. Data were
extracted on the type of oral ADRs, implicated drug classes, clinical presentation, and
management strategies. A narrative synthesis was used due to heterogeneity in study design
and outcome reporting.
Results:
The most frequently reported ADR was
xerostomia
, commonly induced by
antihypertensives, antidepressants, and diuretics.
Lichenoid reactions
,
oral ulcers
, and
mucositis
were frequently associated with NSAIDs, β-blockers, and methotrexate.
Gingival
enlargement
was commonly observed in patients taking calcium channel blockers,
phenytoin, or cyclosporine.
Medication-related osteonecrosis of the jaw (MRONJ)
was
reported with bisphosphonates and antiangiogenic agents.
Tongue disorders
, including
glossitis and burning tongue, were reported with nervous system and anti-infective
medications. Several studies highlighted
underreporting and diagnostic challenges
due to
lack of pharmacovigilance in dentistry.
Conclusion:
A wide range of systemic medications can induce clinically significant oral
ADRs. Dental professionals must be vigilant in recognizing these reactions, taking thorough
drug histories, and collaborating with medical teams for appropriate interventions. Increased
education, reporting practices, and awareness of pharmacogenomic variability are essential
for improving oral healthcare outcomes related to medication use.
Keywords:
Oral adverse drug reactions, xerostomia, gingival hyperplasia, lichenoid reaction,
osteonecrosis of jaw, drug-induced oral lesions, pharmacovigilance, dental pharmacology.
Introduction:-
The oral cavity, or buccal cavity, plays a vital role in systemic and local
health. It is also a frequent site of adverse drug reactions (ADRs), which can significantly
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affect oral functionality, aesthetics, and patient quality of life. Despite this, oral ADRs are
often underdiagnosed or misattributed, especially in polymerizate or systemically ill
individuals. Oral ADRs commonly manifest as xerostomia (dry mouth), mucosal ulcerations,
gingival overgrowth, pigmentation changes, and osteonecrosis. Prompt identification of
drug-related oral presentations is critical for preventing long-term complications.
Xerostomia, one of the most common drug-induced oral conditions, arises from reduced
salivary gland function and affects both comfort and oral microbiota. Drugs such as tricyclic
antidepressants, opioids, anticholinergics, and illicit substances like methamphetamine,
heroin, and cocaine are strongly linked to xerostomia and its sequelae—including rampant
caries, oral candidiasis, and halitosis (1). A cross-sectional study by Sakai et al. (2025)
found that 58.8% of cancer patients undergoing chemotherapy reported xerostomia, with
significant negative impact on daily life activities (3).
Other medications, including angiotensin-converting enzyme (ACE) inhibitors like lisinopril
and captopril, have been associated with oral ulcerations, angioedema, and dysgeusia. These
symptoms can mimic autoimmune diseases, complicating diagnosis (2). Clarithromycin,
terbinafine, and lansoprazole have also been reported to cause oral ulceration, mucosal
irritation, and altered taste perception in various patient populations (4).
More severe adverse events include mucocutaneous syndromes such as Stevens-Johnson
syndrome (SJS) and toxic epidermal necrolysis (TEN), linked to drugs such as phenytoin,
methadone, and hormonal agents (3). These conditions are life-threatening and present with
widespread oral and mucocutaneous erosions. Recent reviews have highlighted genetic
susceptibility—particularly specific HLA haplotypes—as critical risk factors in drug-
induced hypersensitivity syndromes (1).
Among the most debilitating oral ADRs is medication-related osteonecrosis of the jaw
(MRONJ), primarily caused by bisphosphonates like zoledronic acid and pamidronate.
These drugs, commonly used in oncology and osteoporosis treatment, compromise bone
remodelling and increase the risk of necrosis following minor trauma or dental surgery. A
13-year review by Zhong et al. (2025) based on FAERS data identified bisphosphonates and
RANKL inhibitors as the most common drug classes associated with MRONJ, with females
and older adults showing the highest prevalence (2).
Gingival overgrowth, or gingival hyperplasia, is most frequently seen with calcium channel
blockers (e.g., amlodipine), phenytoin, and cyclosporine. This condition can impair oral
hygiene, promote periodontal disease, and require surgical correction. Lichenoid drug
reactions—clinically similar to oral lichen planus—have also been associated with ACE
inhibitors, NSAIDs, and some antiepileptics (6).
In addition to structural lesions, sensory disturbances such as dysgeusia (distorted taste) and
burning mouth syndrome have been linked to drugs like metronidazole, lithium, and
chemotherapy agents. Discoloration of oral tissues and teeth is another concern. Agents such
as tetracycline, chlorhexidine, and iron salts can lead to pigmentation, while some
antimalarials and antipsychotics induce bluish or brown-black mucosal changes (5).
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Pharmacogenetics is increasingly recognized as a determinant of oral ADR susceptibility.
Genetic polymorphisms, particularly in the cytochrome P450 enzyme system (e.g., CYP2C9,
CYP2D6), modulate drug metabolism and can influence the likelihood and severity of
adverse reactions. Torpet et al. (2021) highlighted the importance of pharmacogenetic
screening in identifying high-risk patients, especially when multiple high-risk drugs are co-
administered (8).
To improve outcomes, clinical vigilance, early diagnosis, and interdisciplinary
management—including dental consultations—are vital. Oral adverse events are not just
cosmetic or minor; they can herald more serious systemic toxicity or serve as clues to
underlying hypersensitivity. Differential diagnosis should always include potential
iatrogenic aetiologies, particularly in patients with persistent or atypical oral lesions.
A recent innovation in managing drug-induced oral damage is the use of autologous platelet
lysate gel, especially in patients with chronic graft-versus-host disease (cGvHD). A study by
Rodríguez et al. (2025) showed significant symptom relief and improved healing in patients
with cGvHD-associated oral ulcers, pointing to regenerative therapies as a potential adjunct
in managing oral ADRs (4).
Ultimately, understanding drug-specific oral ADR profiles, along with patient-specific risk
factors (genetic, systemic disease, and concurrent therapies), can guide clinicians toward
safer prescribing practices and timely interventions.
Methodology:-
This review paper adopts a systematic and integrative approach to the
synthesis of current evidence on drug-induced oral adverse reactions or ADRs, specifically
those of significance to dental and oral healthcare practice. The overall objective was to
evaluate the nature of ADRs in the oral cavity, their corresponding drug classes, and the
clinical issues they present for dental practitioners. The approach taken was a systematic
search of the literature, selection and screening of studies, and narrative synthesis of findings.
Literature searching was conducted on four principal academic databases: PubMed, Scopus,
Google Scholar, and the Cochrane Library. These websites were selected to give
comprehensive coverage of clinical and pharmacological research on the topic. The
literature review searched publications from January 2000 to March 2023, representing more
than two decades of cumulative understanding of oral ADRs. To create the search string, a
mix of Medical Subject Headings (MeSH) keywords and free-text words was utilized. These
included: "oral adverse drug reactions," "drug-induced oral lesions," "oral mucosal
disorders," "oral lichen planus," "xerostomia," "oral pigmentation," "gingival hyperplasia,"
"osteonecrosis of the jaw," "oral aphthous ulcers," "drug-induced tongue disorders," and
"oral manifestations of systemic medications
The inclusion criteria for studies were determined a prior to these studies . The studies had
to be written in the English language, involve human subjects, and describe definite
documentation of adverse oral presentations resulting from systemic drug use. Research
articles and review articles were included, as well as high-level case reports if they provided
new or significant information on the clinical presentation or pathogenesis of oral ADRs.
Trials were included if they described or investigated ADRs that occurred in the oral mucosa,
gingiva, tongue, salivary glands, jawbones, or perioral tissues, either as single events or as
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part of a broader systemic reaction. Exclusion criteria were also applied: non-English
publications, in vitro or animal research, editorials or commentaries without primary data,
and reports without evident association between oral findings and drug use were excluded.
20 articles were identified at first using the combined search strategy. These records were
screened independently by two reviewers in a two-stage process. During the first stage, the
title and abstract were screened for relevance and duplicates eliminated. In the second stage,
full-text articles were retrieved and screened in detail against inclusion and exclusion criteria.
Following assessment, 8 articles were eventually considered suitable to be included within
this review. These studies were chosen for their clinical relevance, scientific quality, clinical
utility to dental practice, and richness of data on unique ADRs, associated drug classes, and
to patient care relevance.
Relevant data points from each of these selected studies were extracted into a standardized
table for comparison and consolidation. These included the article title, authors, publication
year, journal, study design (e.g., review, case series, observational study), type of oral ADRs
reported, involved drugs, postulated mechanisms of action, and suggested diagnostic or
management strategies. The data were then tabulated to search for patterns of recurring drug
classes, common oral presentations, and reporting trends. Special attention was given to
drug classes that are high risk, such as cardiovascular medications, NSAIDs,
immunosuppressants, chemotherapeutic drugs, and bisphosphonates, all of which were
demonstrated to have an essential role to play in oral ADR causation.
Owing to study heterogeneity by study type, patient population, and reporting strategy, a
meta-analysis was not feasible. Rather, a narrative synthesis approach was utilized to
synthesize and put into context evidence across studies. This qualitative review of the
evidence would highlight the gaps in the literature and make practical suggestions for
improving the identification and reporting of ADRs among dental practitioners. It also
illustrates how underreporting, pharmacovigilance among dentists, and misdiagnosis of
ADRs as primary oral diseases like lichen planus or aphthous ulcers tend to cause issues.
Since the review was derived from secondary analysis of previously published data and
entailed no data from direct contact with patients, ethical approval was not required. All
information was derived from publicly available literature and the review accords with
approved guidelines for narrative reviews.
Overall, this method provides a reproducible and systematic approach to evaluate drug-
induced oral ADRs, increasingly significant in the context of the growing polypharmacy,
especially in elderly populations. Based on the consolidation of evidence from appropriate
literature, the present review aims to make ADRs better known, enhance diagnostic accuracy,
and enhance clinical management of oral ADRs in dentistry.
Results
This review synthesized findings from eight peer-reviewed articles published between 2004
and 2023, each detailing various manifestations of drug-induced adverse effects in the oral
cavity. The collected data revealed that a broad range of systemic medications are capable of
inducing oral adverse drug reactions (ADRs), spanning from relatively minor and reversible
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effects such as xerostomia to severe mucocutaneous and osseous complications, including
ulcerative lesions and osteonecrosis of the jaw.
Across nearly all studies, xerostomia, or dry mouth, emerged as the most commonly
documented oral ADR. This condition was predominantly linked to systemic medications
that impair salivary gland innervation or reduce glandular blood flow. Chief among these
were antihypertensives, antidepressants, and diuretics. Yousefi et al. noted that
cardiovascular drugs were also the most frequently implicated agents in the development of
ulcerative and vesicular-bullous lesions, followed closely by methotrexate and nonsteroidal
anti-inflammatory drugs (NSAIDs) [8]. Løkken and Skoglund further emphasized that
virtually all drug classes have the potential to trigger oral manifestations, but particularly
highlighted xerostomia, taste disturbances, and mucosal ulceration as recurring symptoms in
users of anticholinergic and psychoactive drugs [9]. Complementing these findings, Aziz et
al. analysed a Dutch drug database and reported that out of 1,645 systemically used drugs,
121 (7.4%) were associated with tongue-related ADRs, including glossitis, tongue burning,
and discoloration [10].
A consistent finding across the reviewed studies was the occurrence of lichenoid drug
reactions (LDRs), a form of delayed hypersensitivity reaction that closely resembles
idiopathic oral lichen planus. Teoh et al. extensively discussed these reactions, identifying β-
blockers, NSAIDs, and antihypertensives as the most frequent triggers [11]. Clinically,
LDRs present as bilateral white striations on the buccal mucosa and require detailed patient
history and diagnostic exclusion of autoimmune aetiologies. Additionally, Yousefi et al.
described the potential for methotrexate and NSAIDs to induce vesicular-bullous disorders
such as Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) [8]. Teoh et
al. corroborated these observations, warning that in rare cases, LDRs can escalate to severe
immune-mediated conditions such as pemphigus vulgaris or mucous membrane pemphigoid,
necessitating histopathological and immunofluorescence investigations to confirm diagnosis
[11].
Gingival enlargement, or drug-induced gingival hyperplasia, was also a recurring ADR,
most commonly associated with calcium channel blockers (e.g., nifedipine), the
anticonvulsant phenytoin, and the immunosuppressant cyclosporine. Glick et al. reported
that this fibrovascular overgrowth is generally dose-dependent and often exacerbated by
inadequate oral hygiene [12]. The affected gingiva typically becomes firm, lobulated, and
asymptomatic, although it can severely affect aesthetics, mastication, and hygiene practices.
Torpet et al. delved into the pathophysiology of this ADR, suggesting that these drugs
stimulate excessive fibroblast proliferation and extracellular matrix accumulation, especially
in genetically predisposed individuals [13].
The most severe oral ADR discussed in the included studies was medication-related
osteonecrosis of the jaw (MRONJ), primarily associated with long-term use of
bisphosphonates and, more recently, antiangiogenic agents. According to studies by Yuan et
al. and Glick et al., MRONJ typically presents as areas of exposed necrotic bone in the
maxillofacial region persisting for over eight weeks in patients with no history of radiation
therapy to the head or neck [14,12]. Patients who had undergone dental extractions or other
invasive procedures while on these medications were particularly vulnerable. Both studies
stressed the importance of preventive strategies such as pre-treatment dental evaluations,
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conservative surgical techniques, and prophylactic antibiotics to reduce the risk of MRONJ
development.
Aziz et al. dedicated their investigation to drug-induced tongue disorders, identifying a wide
range of symptoms including glossitis, burning tongue syndrome, macroglossia, and
discoloration [10]. The drugs most often responsible were from the nervous system, anti-
infective, and metabolic categories. For instance, antibiotics like tetracyclines were linked to
black hairy tongue, while central nervous system stimulants frequently resulted in burning
sensations and taste disturbances. These findings emphasize the need for clinicians to
evaluate tongue morphology and function during routine oral assessments, especially in
patients undergoing long-term pharmacotherapy.
In addition to structural and sensory disruptions, pigmentary and taste changes were also
frequently reported ADRs. These included bluish-black oral mucosal pigmentation
associated with drugs such as minocycline and chloroquine, as well as dysgeusia or metallic
taste induced by metronidazole [9,12]. While often benign and reversible, these
manifestations can cause psychological distress in patients and thus require appropriate
counselling and clinical explanation.
An important trend observed across the studies was the frequent association of specific drug
classes with distinct oral ADRs. Cardiovascular drugs were consistently linked to
xerostomia, lichenoid lesions, and taste alterations [8,13]. NSAIDs were responsible for
lichenoid lesions, oral ulcers, and mucositis [8,11], while antidepressants and antipsychotics
were associated with xerostomia and dysgeusia [9]. Immunosuppressants such as
cyclosporine were often implicated in gingival overgrowth [12], and bisphosphonates were
the leading cause of MRONJ [12,14]. Notably, mTOR inhibitors emerged as a newer class
linked to deep oral ulcerations that can mimic autoimmune lesions [14].
Finally, a critical issue highlighted in several studies was the underreporting of oral ADRs.
Authors such as Padayachee and Teoh et al. emphasized that many dental practitioners may
fail to recognize or report drug-induced lesions due to inadequate training in
pharmacovigilance and diagnostic uncertainty [11,15]. This often results in misdiagnosis—
treating drug-induced lesions as idiopathic conditions such as aphthous ulcers, candidiasis,
or lichen planus—and can delay appropriate management. These findings underscore the
urgent need for improved education, better drug history documentation, and interdisciplinary
collaboration in identifying and managing ADRs in the oral cavity.
Discussion:-
The findings of this systematic review reaffirm the fact that drug-induced oral ADRs are an
undoubtedly significant, but often overlooked, subset of clinical dental and general practice
systemic drug side effects. Oral cavity, being part of the gastrointestinal and immune system,
is routinely left out of systemic pharmacovigilance. However, as demonstrated in this review,
most pharmaceutical drugs in routine practice have the potential to cause oral manifestations
mimicking or obscuring primary oral pathology.
The spectrum of ADRs varies from harmless xerostomia to potentially life-threatening
lichenoid mucositis, mucosal ulceration, pigmentation, burning mouth syndrome, and
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medication-related osteonecrosis of the jaw (MRONJ), as well as from initial, sometimes
asymptomatic changes to irreversible damage. ADRs may imitate idiopathic or autoimmune
mucosal illnesses and, therefore, may cause misdiagnosis, overtreatment, and unwarranted
surgery. ADRs may significantly worsen the quality of life, oral function, and overall health
of the patient
The most frequently occurring ADR to be regularly reported in the studies under
consideration was Xerostomia due to antihypertensives, antidepressants, and anticholinergic
agents.
1–2,6. Xerostomia is relatively harmless in nature but significantly compromises oral
homeostasis through reduced salivary secretion and increased risk of dental caries, oral
infections (particularly candidiasis), halitosis, dysphagia, and intolerance to prosthesis.
Xerostomia is also responsible for interfering with speech and taste and social discomfort
and reduced nutritional intake. Treatment involves saliva substitutes, sugar-free gum,
systemic sialagogues, and fluoride rinses to prevent long-term oral morbidity.
More complex is NSAID, β-blocker, and methotrexate-induced lichenoid reactions and
mucosal ulcerations, which have been reported due to clinical similarity to lichen planus and
pemphigus. 1,4. Inevitably, misdiagnosis of these lesions will lead to unnecessary biopsies
and prolonged corticosteroid treatment. Bilaterality, temporal association with onset of drug,
resolution on withdrawal of drug, and supportive histopathology are emphasized in the
literature as requirements. Recognition of such characteristics will allow misdiagnosis to be
avoided and early conservative treatment to take place. Lesions typically resolve weeks after
withdrawal of the causative drug, stressing the importance of meticulous drug history in
dental clinical examination.
The most serious ADR in this report is Medication-Related Osteonecrosis of the Jaw
(MRONJ), which is typically caused by bisphosphonates and antiangiogenic agents
5,7. MRONJ is uncovered necrotic bone within the maxillofacial area unhealed after eight
weeks. It is most commonly caused by invasive dental treatment or spontaneous
development in patients undergoing high-dose intravenous antiresorptive or antiangiogenic
treatment. MRONJ requires complicated multidisciplinary treatment by specialists from
dentistry, medicine, and pharmacy. Pre-treatment dental assessment, risk classification,
patient education, and elective extractions during treatment aversion are critical to
preventing irreversible complications.
Gingival hyperplasia resulting from phenytoin, cyclosporine, and calcium channel
antagonists is one of those adverse drug reactions that are penned in black and white pages
however very little is spoken on the subject, either in professional literature or in clinical
practice. It impacts dental aesthetics, makes practicing oral hygiene more challenging, and
causes inflammation in the area of the gums. Usually, the patient does not feel pain, but the
disease can become so extensive or resistant to treatment that surgical intervention will be
required. Non-surgical therapy, elimination of the etiology, and a strict patient-centred
approach are among the conservative treatment options. It is a case in point of the
significance of regular oral checks in patients on chronic systemic medications.
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A group of drug-induced tongue disorders can also cause a patient discomfort, yet that
section is not dwelled upon, if at all. The disorders can range from glossitis to taste
aberration and to burning tongue syndrome, and a relevant example is the report listed in
Aziz et al. 3. Most of these symptoms are not specific to drug toxicity and are thus mixed up
with other conditions particularly in the elderly and the timing of the coincident use of
multiple drugs. Broader pharmacovigilance studies continue to document the side-by-side
occurrence of such incidents. Early detection of the tongue pathology will decrease the
likelihood of unnecessary exams and allow the discontinuation of treatment or dose
modification of the incriminated drug.
One of the more concerning issues found in this research is the significant under declaration
of symptoms resulting from oral drug consumption in every case, but in dental care settings,
in particular
4,8. A majority of practitioners either do not recognize or just ignore the fact that oral
dysfunctions are a medium for the side effects of systemic drugs. Moreover, lack of
awareness of the symptoms leads to misdiagnosis, which is attributed to systemic causes,
and psychiatric aetiology. Multiple overlapping factors like the popularity of conservative
management, having a good doctor-patient relationship, and the lack of doctor's experience
may lead to such underreporting. Thus, efforts to establish a compulsory teaching of ADR
detection, reporting and also interprofessional relation in would be most enlightening into
dental curricula, that even cross-professional cooperation within the field of oral care can
prove effective.
Before undergoing dental treatment, the continuous checking whether the medication is
consistent or not should be an act.
The future role of pharmacogenomics in oral ADR prevention is one of the advanced topics
discussed in this review. The interindividual variability in cytochrome P450 enzymes,
especially in the genes like CYP2D6 and CYP3A4, is the main factor causing the
differences in drug metabolism 666. Thus, it is possible that one group of patients can
develop severe reactions despite the standard therapeutic dose, while others may not be
affected. Genetic screening technologies, when available, might facilitate the identification
of individuals' risks for ADRs before they even initiate drug therapy, bringing precision
medicine into dental practice.
Among the things I can also mention is the power of interprofessional collaboration. Dental
practitioners who are treating patients that are on immunosuppressants, antineoplastic drugs,
or antiepileptics must be in constant contact with doctors, pharmacists, and nurses. Such a
partnership enables better treatment protocols, especially when it comes to dental
interventions that might cause extra systemic problems.
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Limitations:
In spite of the clinical applicability of these findings, some methodological
weaknesses exist. The synthesis is founded mainly on narrative reviews, as well as case
reports, without the statistical power and generalizability of randomized controlled trials.
The lack of meta-analysis further prevents the determination of quantitative risk estimates or
prevalence. Inconsistent reporting practices, differences in diagnostic criteria, and
geographical bias (e.g., overrepresentation of Turkish and Iranian studies) could also
influence the external validity of the findings. In addition, rare but serious ADRs could be
overreported and mild ADRs could be underreported because of reporting bias. However,
qualitative synthesis of these patterns across different studies provides valuable information
on oral ADRs that deserve heightened clinical awareness and systematic study. Future
research must be aimed at prospective cohort studies with the use of standardized diagnostic
criteria for confirming findings and more accurately estimating the prevalence and risk
factors for particular oral ADRs.
Conclusion
: Harmful oral manifestations of drugs are among the most neglected yet
significant areas of systemic pharmacotherapy and dental diagnosis. Here in this article, in
comprehensive detail, we cover how commonly prescribed medications such as
cardiovascular
medications,
NSAIDs,
bisphosphonates,
antidepressants,
immunosuppressants, and anticonvulsants induce a vast range of oral pathologies from
xerostomia and lichenoid lesions to osteonecrosis, pigmentation, gingival overgrowth, and
tongue lesions. Identification of these patterns is the key to correct diagnosis, proper
treatment planning, and the prevention of unwarranted procedures. Dental professionals
need to be active participants in pharmacovigilance, obtaining thorough medication histories
as a matter of course and being ever vigilant for the occurrence of oral ADRs, particularly
when standard therapies fail. Incorporating ADR monitoring into daily dental practice and
training in pharmacogenomics will significantly contribute to patient safety and quality of
care. Finally, the results of this review emphasize the importance of increased clinical
vigilance, ongoing education, and interprofessional dialogue to optimally manage and
attenuate the burden of drug-induced oral ADRs. Through this, dentists can aid in decreasing
avoidable complications, reduce patient morbidity, and help achieve a safer, more informed
pharmacologic treatment.
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