The Efficacy and Clinical Application of Mefenamic Acid in Odontogenic Pain Management: A Comprehensive Review

*Zakir Hidayatallah

Division of Basic Medical Sciences, Department of Basic and Clinical Oral Sciences, Faculty of Dental Medicine, Umm Al-Qura University, Makkah, Saudi Arabia

*Corresponding author: Zakir Hidayatallah                           Email: Zhmarwat@uqu.edu.sa

Received: 25-03-2025,                  Accepted: 03-04-2025,              Published online: 22-04-2025

DOI: https://doi.org/10.33687/ricosbiol.03.04.0059

 

Abstract

Odontogenic pain, arising from inflammation of dental and periodontal tissues, poses a common and challenging issue in dental practice. It impacts patient comfort, treatment adherence, and overall oral health. Effective pain management is essential for achieving successful clinical outcomes. Mefenamic acid is widely prescribed due to its efficacy in managing various dental pain conditions. This review evaluates the effectiveness, safety, and mechanisms of action of mefenamic acid in treating odontogenic pain, including primary pain, post-extraction pain, pulpitis, and periodontal pain. A systematic review was conducted on clinical studies, randomized controlled trials, and meta-analyses sourced from the PubMed, Scopus, and Cochrane databases. The study aimed to examine the analgesic effects, adverse effects, and other clinical applications of mefenamic acid compared with other NSAIDs used in dentistry. Mefenamic acid has demonstrated analgesic properties, likely resulting from its inhibition of the cyclooxygenase (COX) enzymes, which decreases pain and the inflammatory response associated with prostaglandin synthesis. Clinical research has consistently validated its efficacy in treating post-extraction, pulpitis, and periodontal pain. However, gastrointestinal side effects, particularly dyspepsia and other forms of gastropathy, are the most documented issues, necessitating careful case selection and follow-up. Research suggests that mefenamic acid is at least as effective as some common non-steroidal anti-inflammatory drugs, including ibuprofen and diclofenac, but is less harmful to the stomach than ibuprofen. Mefenamic acid is recognized as a viable pain management option in dentistry, but its clinical use requires further study. Specifically, research should determine optimal dosage, treatment duration, and effectiveness. This research should also compare mefenamic acid to newer, more selective NSAIDs.

Furthermore, ongoing research into novel drug design, pharmacogenetic factors influencing NSAID efficacy, and alternative pain treatment methods is likely to enhance the clinical utility of mefenamic acid. Mefenamic acid is an effective option for managing odontogenic pain; however, careful patient selection and monitoring are crucial to minimize potential adverse effects. Future research should concentrate on optimizing its application.

Keywords: Mefenamic acid, NSAIDs, odontogenic pain, pain management, COX inhibitors.

Introduction

Patients with dental caries, periodontitis, or post-extraction complications commonly report odontogenic pain (Pak & White, 2011; Fitriyati et al.., 2021).

Effective pain management is crucial for successful clinical outcomes. Nonsteroidal anti-inflammatory drugs (NSAIDs) exert therapeutic and toxic effects through a common mechanism of action: COX-1 inhibition. For pain and inflammation treatment after a dental surgical procedure, short-term use of NSAIDs (typically one week or less) is effective and safe (Bushra & Aslam, 2010). Compared with opioid combination drugs, NSAIDs do not have as many unwanted CNS depressant effects that are responsible for the high rates of drowsiness, dizziness, nausea, and constipation often encountered with opioid-containing products (Elvir-Lazo & White, 2010).

The FDA now grants over-the-counter (OTC) status to ibuprofen, naproxen, ketoprofen, and mefenamic acid. Several NSAIDs, including these medications, are available OTC, which increases their accessibility for managing dental pain (Bushra & Aslam, 2010). However, adhering to the recommended dosages and durations outlined in OTC regulations is crucial to minimize potential adverse effects. OTC regulations specify that these medications must not be used for more than 10 consecutive days for pain and only 3 days for fever, along with daily and single dose limits that are lower than the prescribed usage of the drugs.

The adverse effects of prolonged NSAID treatment, particularly gastrointestinal ulcers, perforations, and bleeding, appear to have been reduced by the introduction of highly selective COX-2 inhibitors. Trials aimed at preventing large colon polyps have shown an increased risk of cardiovascular events when these medications were compared to a placebo. Even short-term use (10 days) of these drugs for post-operative pain following coronary artery bypass graft surgery has resulted in a significant increase in risk.

This has led to the global withdrawal of most selective COX-2 inhibitors from the market (Dahl & Møiniche, 2004; Al-Sukhun et al.., 2012).

NSAIDs are among the most commonly used agents in dentistry, as they not only relieve pain but also reduce inflammation. Mefenamic acid, which belongs to the fenamate group of NSAIDs, is renowned for its potent analgesic and anti-inflammatory properties. Patients with dental caries, periodontitis, or post-extraction complications often report experiencing odontogenic pain (Pak & White, 2011; Fitriyati et al., 2021). This review evaluates the efficacy, safety, and pharmacological profile of mefenamic acid in managing odontogenic pain. It compares mefenamic acid to other NSAIDs and explores potential future directions. Furthermore, this review synthesizes the first direct comparisons between mefenamic acid and newer NSAIDs in treating dental pain while proposing future pharmacogenetic and formulation-driven approaches.

Materials and Methods: Search Strategy and Methodology

An assessment was conducted using a systematic review approach to evaluate mefenamic acid's clinical effectiveness, safety, and pharmacological actions in managing odontogenic pain. The following electronic databases were searched: PubMed, Scopus, and the Cochrane Library. The search strategy employed Medical Subject Headings (MeSH) terms and keywords to identify all scientific works on the issue under review (Higgins et al., 2019). The search was restricted to human studies and articles published in English. Initially, no time limits were set to encompass all relevant studies; however, this was later analyzed by focusing on the most recent publications, such as those from the last decade, to discern trends and evidence.

Selection Criteria for Studies

Studies were considered for analysis if the criteria listed below were met:

The following criteria were used to rule participants out of the study:

Data Extraction and Quality Assessment

Standardised data extraction forms were utilised in the remaining studies to collect information. The gathered information consisted of:

The Cochrane Risk of Bias tool was utilized to identify various sources of bias, such as selection, performance, detection, attrition, and reporting (Higgins et al., 2019). The overall quality of evidence for outcomes was evaluated using the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) methodology (Guyatt et al., 2011).

Synthesis of the Data

The narrative synthesis involved summarizing and explaining the findings of the included studies in a descriptive format. This approach enabled the integration of data from studies with varying designs and outcomes, offering a comprehensive overview of mefenamic acid's effectiveness and safety. Some of the search terms included the following: Mefenamic Acid, NSAIDs, odontogenic pain, dental pain, post-extraction pain, pulpitis, periodontitis pain, analgesics, and inflammatory mediators. Meta-analyses were conducted only when there was sufficient evidence and it was deemed appropriate (Santini et al., 2021; Guerreiro et al., 2021).

PRISMA SELECTION STUDY OVERVIEW 

Pharmacological Profile

Pharmacokinetics

Mefenamic acid has a high oral bioavailability of approximately 90%, due to its lipophilic characteristics. The peak plasma concentration of 10–20 µg/mL is reached 2–4 hours after administering a 500 mg dose. It undergoes extensive hepatic metabolism, resulting in the formation of inactive glucuronide metabolites that are excreted through the kidneys and bile. Other active glucuronide metabolites have a half-life (T1/2) of 2–4 hours; thus, dosing should be conducted every 6 hours to maintain therapeutic analgesic levels. Food Interaction: Food does not significantly influence mefenamic acid, as it may delay absorption without considerably affecting overall bioavailability. This is advantageous for patients who need to take the medication with food to reduce the risk of gastrointestinal irritation (Bushra & Aslam, 2010).

Pharmacodynamics

Mefenamic acid is an anti-inflammatory analgesic that inhibits cyclooxygenase (COX) enzymes responsible for synthesizing prostaglandins (PGs). These chemical substances play a role in pain, inflammation, and fever; hence, their inhibition is significant (Kelly, Ahmad, & Brull, 2001).

·       COX-1 Inhibition: Mefenamic acid inhibits COX-1, which is present in most tissues and is crucial for maintaining normal physiological functions, such as protecting the gastric mucosa and regulating renal blood flow. The inhibition of COX-1 is associated with adverse gastrointestinal effects, including gastric irritation and ulceration (Dahl & Moiniche, 2004).

·       COX-2 Inhibition: Furthermore, mefenamic acid inhibits COX-2, located at inflammation sites and contributes to pain and swelling. By blocking COX-2, mefenamic acid reduces the production of pro-inflammatory prostaglandins, thus providing pain relief without disrupting normal bodily processes (Albuquerque et al., 2017).

Many nonselective COX-inhibiting NSAIDs, including mefenamic acid, tend to have more significant adverse effects because they are stronger or at least equally strong COX-1 antagonists. Unlike selective COX-2 inhibitors (e.g., celecoxib), mefenamic acid possesses

 

Table 1: Comprehensive Pharmacokinetic Parameters of Mefenamic Acid

Parameter

Description

Value/Range

Clinical Implications

References

Oral Bioavailability

Fraction absorbed into systemic circulation

~90%

High absorption ensures predictable dosing

Bushra & Aslam, 2010

T<sub>max</sub>

Time to peak plasma concentration

2–4 hours

Take 1–2 hours before painful procedures

Team Medical Mini-Note, 2017

C<sub>max</sub>

Peak plasma concentration (500 mg dose)

10–20 µg/mL

Correlates with analgesic efficacy

Bushra & Aslam, 2010

Half-life (t<sub>½</sub>)

Plasma elimination half-life

2–4 hours

Requires q6h dosing for sustained relief

FDA Label, 2020

Protein Binding

Fraction bound to plasma proteins

>90% (mainly albumin)

Caution in hypoalbuminemia (↑ free drug levels)

Albuquerque et al., 2017

Metabolism

Primary pathways

CYP2C9 (80%) → Glucuronidation

CYP2C9 poor metabolizers need dose reduction

Guyatt et al., 2011

Active Metabolites

Hydroxymefenamic acid glucuronide

Yes (weak activity)

Prolonged effect in renal impairment

Usman et al., 2012

Excretion

Primary route

Urine (60%), Feces (40%)

Avoid in severe renal/hepatic dysfunction

Bushra & Aslam, 2010

Food Effects

Impact of food on absorption

Delays T<sub>max</sub> by ~1h

No dose adjustment needed; take with food for GI protection

Team Medical Mini-Note, 2017

Anti-inflammatory properties arise because it inhibits both COX-1 and COX-2; however, this also increases the risk of gastrointestinal damage. There is little debate that the series of reactions in many painful conditions involves prostaglandins (PGs) and that aspirin’s effectiveness in managing inflammation and pain is closely linked to its inhibition of the inflammatory response and PG synthesis (Bushra & Aslam, 2010). Microdialysis techniques have demonstrated that following dental surgery, the analgesic effects of NSAIDs correlate with a reduction in local PG levels. However, some evidence suggests that the analgesic and anti-inflammatory actions of NSAIDs may occur through different mechanisms (Dahl & Møiniche, 2004). Firstly, there is a difference in the timing of onset between the analgesic and anti-inflammatory effects. Generally, significant analgesia is achieved within one hour of drug administration. In contrast, the inflammatory effect can take several days or weeks to reach its peak levels due to the chronic nature of inflammatory processes. Additionally, the maximum analgesic effect in humans is usually attained at lower doses than those needed for antirheumatic and other anti-inflammatory effects (Kelly et al., 2001).

Beyond COX inhibition, emerging evidence suggests mefenamic acid may also modulate pain through additional pathways:

Modulation of Voltage-Gated Sodium Channel Activity (Nav1.7, Nav1.8): Mefenamic acid has been shown to decrease the excitability of pain-transmitting sodium channels, which diminishes nerve activity in inflammatory states (Bushra & Aslam, 2010).

Inhibition of Nuclear Factor Kappa B (NF-κB) Signalling: Mefenamic acid inhibits the production of pro-inflammatory cytokines, such as IL-6 and TNF-α. Unrestricted use of mefenamic acid increases the amount of anti-inflammatory and analgesic cytokines. Thus, the cytokines responsible for inflammation are blocked together with the pathways responsible for their generation (Kelly et al., 2001).

The additional mechanisms further enhance the already broad-spectrum effectiveness of the drug in inflammatory pain, such as odontogenic pain. However, these mechanisms are still under active research, and clinical translation of this evidence remains ongoing.

Clinical Applications

Mefenamic acid has demonstrated effectiveness in managing various forms of dental pain.

·     Post-Extraction Pain: Mefenamic acid is as effective as ibuprofen (Bailey et al., 2013).

·     Pulpitis: Validated efficacy in clinical studies (Pangalila et al., 2016; Kumar et al., 2021).

·     Periodontal Pain: Mefenamic acid has also been shown to be effective in treating periodontal pain (Bailey et al., 2013; Santini et al., 2021).

 

Comparative Efficacy with Other Analgesics

The effectiveness of mefenamic acid in controlling odontogenic pain has been demonstrated across multiple study designs, though variations in populations and outcome measures require careful interpretation (Santini et al., 2021; Kumar et al., 2021; Bailey et al., 2013). Comparative trials consistently show the relationship between these variables.

 

 

Mefenamic Acid vs Ibuprofen

Clinical evidence confirms that mefenamic acid has comparable efficacy to ibuprofen for post-extraction pain (Bailey et al., 2013) and pulpitis (Pangalila et al., 2016; Bushra & Aslam, 2010). Some studies suggest mefenamic acid may offer better tolerability of gastrointestinal (Santini et al., 2021). This difference may be clinically significant for gastrointestinal intolerance, a common reason for NSAID discontinuation. It is also important to note that, in practice, the extent of this difference is likely to vary between studies and should be considered along with other patient-related variables. For example, people with a previous history of gastric ulcers may be better off with mefenamic acid, while those for whom ibuprofen worked may continue with it.

Meta-analyses suggest that mefenamic acid, naproxen, and diclofenac have similar effectiveness in managing pain associated with dental procedures (Pangalila et al., 2016; Santini et al., 2021). In clinical trials, mefenamic acid demonstrated a reduced incidence of adverse effects relative to naproxen and diclofenac (Pangalila et al., 2016). In cases of acute inflammation, diclofenac proved to be more effective than the others, highlighting the importance of considering the type of odontogenic pain being treated. When inflammation is a significant symptom, the drug that is used may be diclofenac. However, for patients with gastrointestinal complications, mefenamic acid is suggested. The degree of drug response is unique to each patient, and factors such as age, comorbidities, and concomitant medications must be considered (Bushra & Aslam, 2010).

Mefenamic acid is not an exception to the general rule regarding its effect on the GI mucosa; certain risks to the functioning of the gastrointestinal tract accompany its use. On the other hand, mefenamic acid is more advantageous in providing rapid pain control than selective COX-2 inhibitors, such as celecoxib, which have a better gastrointestinal side effect profile (Al-Sukhun et al., 2012). Mefenamic acid may provide more rapid analgesia and be beneficial in post-operative inflammation and more severe cases. Where there is a need for chronic pain management, mefenamic acid may not be as helpful due to the constant requirement of long-term NSAID use. However, it is suggested for acute dental pain, where a more rapid analgesic response is desired. There are concerns of cardiovascular side effects with COX-2 inhibitors, which must be considered in comparison to the gastrointestinal side effects of non-selective NSAIDs (Dahl & Moiniche, 2004).

Safety Profile and Adverse Effects

When considering the use of mefenamic acid (NSAIDs), particular attention must be paid to its anticipated adverse effects: gastrointestinal, cardiovascular, renal, CNS, and dermatological reactions. Such risks are critical for the proper clinical application (Bushra & Aslam, 2010; Handisurya et al).

 

 

 

Figure 1: Comparative Pain Relief Profiles of NSAIDs
Source: Adapted from Bailey et al., (2013) and Pangalila et al. (2016).

 

A graph of pain relief AI-generated content may be incorrect.

Figure 1: Ibuprofen provides the highest pain relief but has a higher risk of gastric side effects.

·     Mefenamic acid provides comparable pain relief to diclofenac but may offer a better safety profile.

·     Celecoxib, a COX-2 selective inhibitor, provides long-lasting relief but has a delayed onset.

Mefenamic acid may induce adverse effects, including gastric irritation and ulceration (Handisurya et al., 2011; Bailey et al., 2013). The risk is elevated in patients with a history of peptic ulcer disease, though concomitant Proton Pump inhibitor use may mitigate this (Guyatt et al., 2011). Protective strategies do not eliminate the risk of GI symptoms entirely

NSAIDs, including mefenamic acid, can elevate blood pressure and increase cardiovascular risks (myocardial infarction, stroke), particularly with prolonged use (Dahl & Møiniche, 2004; Al-Sukhun et al., 2012). These effects are dose- and duration-dependent.

Patients with pre-existing cardiovascular conditions should use mefenamic acid cautiously, at the lowest effective dose, and for the shortest duration possible.

Mefenamic acid may impair renal blood flow, leading to fluid retention and elevated creatinine, especially in patients with chronic kidney disease or dehydration (Bushra & Aslam, 2010). Short-term use (<7 days) is preferred in at-risk populations (Bailey et al., 2013).

Comorbid conditions such as congestive heart failure or dehydration can further exacerbate renal risk.

Mefenamic acid may lower seizure thresholds, particularly in adolescents or overdose scenarios (Doğan et al., 2019). While preclinical studies suggest potential anticonvulsant properties, clinical evidence remains cautionary.

Mefenamic acid also can cause skin allergies, including fixed drug eruptions (FDE), urticaria, and rare but severe reactions like Stevens-Johnson syndrome (SJS). Case reports and pharmacovigilance data highlight these adverse effects, with some studies ranking it among NSAIDs linked to cutaneous reactions (Handisurya A et al., 2011).

 

 

 

 

 

 

 

 

 

Figure 2: Comparative GI/Renal/CVD/Derma Risks of NSAIDs
(Sources: Bushra & Aslam, 2010; Dahl & Møiniche, 2004; Handisurya et al., 2011; Al-Sukhun et al., 2012)

 Clinical Guidelines and Patient-Specific Recommendations

Dosage and Administration

Mefenamic acid is typically prescribed for short-term use (3–7 days) to optimize pain relief while minimizing adverse effects. This duration aligns with its pharmacokinetic profile (peak plasma concentration Cmax = 10–20 µg/mL) and gastrointestinal tolerability (Bailey et al., 2013; Team Medical Mini-Note, 2017).

 

Emerging Research and Future Directions

The study and management of odontogenic pain remains a progressing field with new research aimed at optimizing analgesic therapies and their side effects. A few possibilities are most noteworthy and require further research to increase the clinical effectiveness of mefenamic acid and improve patient outcomes.

 

 

 

 

Table 2: Dosage and Administration

Patient Group

Dosage

Frequency

Max Duration

Key References

Adults

500 mg initial dose → 250 mg maintenance

Every 6 hours

7 days

Bailey et al., 2013

Elderly (>65 yrs)

250 mg

Every 8 hours

5 days

Team Medical Mini-Note, 2017

Children (>12 yrs)

250 mg

Every 6–8 hours

5 days

Bushra & Aslam, 2010; Team Medical Mini-Note, 2017

 

 

 

Table 3: Indications & Contraindications of Mefenamic Acid in Dental Practice

Category

Clinical Scenario

Rationale

Key References

INDICATIONS

Post-extraction pain

Pain after tooth removal

Comparable efficacy to ibuprofen, with faster onset (Pangalila et al., 2016; Bailey et al., 2013).

Bailey et al., 2013; Pangalila et al., 2016

Acute pulpitis

Inflamed dental pulp pain

Effective prostaglandin inhibition at pain source (Pak & White, 2011; Kumar et al., 2021).

Pak & White, 2011; Kumar et al., 2021

Periodontal pain

Gingivitis/periodontitis pain

Reduces inflammation in soft tissues (Santini et al., 2021).

Santini et al., 2021

Post-surgical pain

Post-oral surgery discomfort

Short-term use aligns with COX-2 inhibition (Al-Sukhun et al., 2012).

Al-Sukhun et al., 2012

 

 

 

Table 4: Contraindications of Mefenamic Acid in Dental Practice

Contraindication

Risk Level

Mechanism

Clinical Rationale

Alternatives

Key References

Active peptic ulcer

High (Absolute)

COX-1 inhibition → Reduced gastric cytoprotection

5x higher GI bleeding risk vs. non-NSAID users; avoid even with PPI co-therapy

Acetaminophen, celecoxib + PPI

Handisurya et al., 2011

Severe renal impairment (eGFR <30)

High

Prostaglandin-dependent renal vasoconstriction

NSAIDs precipitate AKI in 18-25% of CKD patients

Opioids (short-term)

Bushra & Aslam, 2010

Post-MI/CABG (<6 months)

High

COX-2 inhibition → Thrombosis risk

2.5x increased CV event recurrence; avoid all NSAIDs

Non-NSAID analgesics

Dahl & Møiniche, 2004

Children (<12 years)

Moderate-High

CNS penetration → Seizure threshold lowering

Case reports of seizures in adolescents; no FDA approval for dental pain <14y

Ibuprofen (weight-based)

Doğan et al., 2019

3rd trimester pregnancy

Absolute

Premature ductus arteriosus closure

Fetal renal toxicity risk; contraindicated after 30 weeks

Acetaminophen

FDA Drug Safety Communication, 2020

NSAID/aspirin allergy

Variable

Cross-reactive hypersensitivity

30% risk of cross-reactivity with other NSAIDs (esp. urticaria/FDE)

Opioid alternatives

Handisurya et al., 2011

 

Several attempts are being made to modify the dosage forms of mefenamic acid, with the aim of improving its pharmacokinetic profile and reducing systemic side effects. For example, nanoparticle formulations have been demonstrated to enhance drug solubility and bioavailability, as well as mitigate off-target therapeutic effects, by delivering drugs to specific sites (Sriamomsak et al., 2015; Shah, Shrivastava, & Mishra, 2013). Another transdermal route of drug delivery currently being studied is the use of transdermal patches, which may aid in treating certain types of odontogenic pain, such as temporomandibular joint pain or postoperative pain relief following minor oral surgery. Sustained-release oral formulations are also being developed to provide longer-lasting pain relief, reduce dosing frequency, and improve adherence while maintaining consistent plasma drug concentrations (Khullar et al., 2012; Usman et al., 2012). These new formulations require additional clinical trials to evaluate their effectiveness and safety in various patient populations.

 

Figure 3: The conceptual framework derived from Sriamomsak et al., (2015) and Usman et al., (2012).

 

The study of pharmacogenetics—which is known to predict drug response—appears particularly helpful for customizing pain management. Polymorphisms in the CYP2C9 gene influence the metabolism of mefenamic acid, potentially impacting its pharmacokinetics, potency, and the risk of side effects. Recognizing patients with specific CYP2C9 genotypes could help clinicians adjust mefenamic acid dosing to maximize therapeutic effects and minimize adverse outcomes (Guyatt et al., 2011). Future studies should confirm these pharmacogenetic associations in larger, more diverse patient populations and support the development of clinically actionable genotyping tools. Pharmacogenetic screening (e.g., CYP2C9 polymorphisms) could personalize mefenamic acid dosing, while transdermal patches may benefit patients with TMJ pain who are at risk of gastrointestinal events.

In addition to pharmaceutical advances, adjunctive or alternative therapies are increasingly being considered in the management of odontogenic pain. Combination therapies—such as locally administered NSAIDs with local anesthetics—may improve efficacy while reducing systemic exposure and side effects (Penprase et al., 2015). Other non-traditional approaches, including lasers, acupuncture, or cognitive behavioral therapy, are being evaluated for their potential to manage chronic dental pain and complement standard analgesics (Guerreiro et al., 2021). More research is required to identify optimal combinations of pharmacologic and non-pharmacologic strategies tailored to specific types of odontogenic pain and individual patient profiles.

Clinical Guidelines and Recommendations

·       Mefenamic acid shows comparable efficacy to ibuprofen in managing odontogenic pain, with a slightly better gastrointestinal safety profile (Bushra & Aslam, 2010; Bailey et al., 2013).

·       However, thorough patient selection and monitoring are crucial to reduce potential adverse effects.

·       Patients with a history of gastric ulcers may benefit more from mefenamic acid, while those for whom ibuprofen was effective can continue using it.

·       When inflammation is a major symptom, the medication of choice may be diclofenac.

Conclusions

Future research should prioritize:

·     Optimizing drug delivery while minimizing systemic side effects through novel formulations (Sriamomsak et al., 2015; Usman et al., 2012).

·     Develop pharmacogenetic strategies to personalize mefenamic acid dosing (Guyatt et al., 2011).

·     Evaluating new analgesics and combination therapies for various odontogenic pain conditions (Santini et al., 2021; Guerreiro et al., 2021).

·     Integrating non-pharmacological approaches to enhance systemic pharmacological treatments (Penprase et al., 2015).

These advancements, along with comprehensive education and training for dental practitioners, will enhance the management of odontogenic pain and improve patient outcomes.

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