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Journal of Indian Society of Periodontology · 2026

Indian Society of Periodontology Good Clinical Practice Recommendations for dental pain management and use of analgesics.

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Grover V, Kumar A, Satpathy A, Jain A, Deshpande N, Grover HS, Khatri M, Nandkeoliar T, Nair A, Benjamin A, Nichani AS, Singh B, Dave BD, Bhutada G, Chahal GS, Sangha KS, Debnath T, Damera TK, Karemore V, Sheokand V, Bains VK

Аннотация

Pain is one of the most frequent reasons for seeking dental care and significantly influences patient comfort, treatment acceptance, and clinical outcomes. Effective management of dental pain requires accurate diagnosis, timely intervention, and the rational use of analgesics supported by evidence-based clinical decision-making. Recognizing the need for structured guidance for everyday dental practice, the Indian Society of Periodontology has developed Good Clinical Practice Recommendations on Pain Management and the Use of Analgesics in Dental Clinics. These recommendations were formulated by a panel of nineteen subject matter experts from across the country following a comprehensive review of the available literature and structured consensus discussions. The document is organized into three key sections: Dental Pain - Diagnosis and Assessment, focusing on the clinical evaluation and characterization of dental pain; Multimodal Strategies for Pain Management in Dentistry, outlining pharmacological and non-pharmacological approaches for optimal pain control; and Clinical Decision Making in Dental Pain Management, which provides practical guidance on the rational and safe use of analgesics in routine clinical scenarios. The recommendations aim to support clinicians in selecting appropriate pain management strategies, encourage responsible prescribing practices, and promote patient-centred care. This document is intended to serve as a concise reference for dental practitioners and contribute to improving the quality and consistency of pain management in dental practice.

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https://creativecommons.org/licenses/by-nc-sa/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

Pain remains a central concern in dental practice, often serving as both the primary motivator for patients to seek care and a key determinant of their overall treatment experience. Its effective management extends beyond mere symptom relief and encompasses accurate diagnosis, timely intervention, and the judicious use of analgesics within an evidence-based clinical framework. In contemporary practice, where patient expectations, safety considerations, and concerns regarding overuse or misuse of medications are increasingly relevant, there is a growing need for clear, structured, and clinically applicable guidance for dental practitioners.

In this context, the Indian Society of Periodontology presents these Good Clinical Practice Recommendations on Pain Management and the Use of Analgesics in Dental Clinics. Developed through a rigorous process involving comprehensive literature appraisal and expert consensus, this document seeks to bridge the gap between evidence and everyday clinical decision-making. The recommendations are designed to provide a pragmatic and structured approach to dental pain management, integrating diagnostic considerations, multimodal therapeutic strategies, and rational pharmacological interventions. By offering clear and concise guidance, this document aims to support clinicians in delivering safe, effective, and patient-centred care, while promoting consistency and excellence in pain management practices across diverse clinical settings.

SECTION I – DENTAL PAIN: DIAGNOSIS AND ASSESSMENT

According to the International Association for the Study of Pain (ISAP), the updated definition of pain reads as follows: “Pain is unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.” [1]

Orofacial pain (OFP) involves any pain that is felt in the mouth, jaws, and face. Dental pain is one of the most common pains felt in the orofacial region. This is described as pain originating from innervated dental tissues or tissues immediately adjacent to the teeth. Dental pain has also been characterized as pain originating from the teeth and supporting tissues as a result from disease or injury to the teeth. [2] The response to similar painful stimulation by different individuals differs in many ways. [3,4]

The reasons for dental pain are diverse, such as infections (reversible and irreversible pulpitis, periapical and periodontal abscess, and periodontitis) trauma, or any other intraoral pathologies. The pain an individual perceives is also subjective to fear, anxiety, and past experiences. Dental pain can negatively affect the quality of life and ultimately affect routine life functions and produce emotional concern. [5]

Although dental pain may be a common condition, the mechanisms that are involved in pain conduction and perception are intricate. The reasons are often inflammation of the tissues or nerve injury. [6,7] These reasons cannot explain the differences in perception of pain observed across populations.

The prevalence of dental pain is far and wide. Various factors such as age, socioeconomic status, gender, behavior, and psychology influence an individual’s well-being. [8]

The prevalence of pain can be linked to the increasing prevalence of oral diseases, especially in many low- and middle-income countries, due to various challenges faced by the population in these countries. [9,10]

Various studies have documented the prevalence of dental and OFP. In a study by Locker and Grushka, [11,12] 50% of the participants who reported dental pain considered their pain to be of moderately severe or severe intensity. Toothache was reported by 14.1% of the participants, whereas the most common dental and facial pain reported was pain in teeth exposed to hot and cold fluids (28.8%).

Lipton et al . in 1993 [13] reported that the most common type of OFP was dental pain (12.2%), whereas 22% of the general population in the USA had experienced OFP in the previous 6 months.

Although the dental pain was not specifically reported by Brattberg et al . in a study conducted in Sweden, the prevalence of head, neck, and mouth pain in Sweden was reported to be 14.6% among the general population. [14] They also mentioned that dental pain affects everyday life. Toothache was considered as the major reason for impairment of daily functioning by Adulyanon et al . [15]

In another study by Pau et al ., the prevalence of dental pain was reported for 5 case definitions: “pain in teeth with hot, cold or sweet things” – 25%–38%, “oral and facial pain” – 40%–44%, “toothache” – 7%–32%, “pain or discomfort in the mouth, teeth or gums” – 19%–66%, and “pain and discomfort needing medication or treatment” – 7%–9%. They stated that individuals belonging to lower socioeconomic groups and younger age groups were more likely to report pain. [16] Other studies have also found that the reasons associated with toothache are the younger age group, lower socioeconomic status, and the mother’s education. [17-19] Worse oral status, snacks consumption, [20] dental treatments, [21] with untreated decayed teeth, [22] anxiety, stress, [23] depression, [24] and homeless [25] were also found to be associated with toothache. Many other studies have reported that the prevalence of toothache ranged from 1.3% to 87.8% in different countries and populations. [26-34]

In a recent study in Chinese adults, the overall toothache prevalence among older adults was 15.3% (95% confidence interval [CI]: 14.9%–15.7%). They also reported the prevalence rates for toothache in 2011 (16.3%), 2014 (12.8%), and 2018 (16.0%), respectively. The 16.4% of males and 16.2% of females and 12.4% of males and 13.2% of females reported pain in 2011 and 2014, respectively. The prevalence of toothache among different age groups was significantly varied. Moreover, participants with more years of schooling, more natural teeth, and higher toothbrushing frequency suffered from a higher toothache prevalence ( P < 0.05). The dental pain reported among older Chinese adults aged ≥65 years in the last 6 months was 15.3%. [35]

The quality of life of the patients is significantly affected by pain. There are chances that the pain can become chronic in nature, thereby increasing healthcare costs and adversely affecting the health and mental status of the individual. [36]

The widespread occurrence and multifactorial etiology require a comprehensive approach to effectively manage pain. Pain management is a fundamental aspect of dental care. Effective pain management not only alleviates suffering but also plays a critical role in reducing psychological stress and anxiety and improving overall clinical outcomes. [37-39] The number of patients, the nature of dental pain, and the variability in pain management protocols can lead to discrepancies and limit assessment and management of pain. [40]

The pharmacologic and nonpharmacologic interventions are two major pain management methodologies. [41] Opioids, nonopioids, and adjuvants are the main pharmacologic interventions used to manage pain. Nonopioid analgesics, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen, are generally the first choice for managing mild-to-moderate pain compared to opioids. [42,43] Opioids are more commonly used for moderate-to-severe pain but have associated risks and require monitoring. [44]

Combination therapy that involves combining different categories of analgesics is based on the principle of multimodal analgesia. The principle of multimodal pain management is based on the usage of different classes of analgesic agents that target different pain pathways. Usage of combination therapy may provide superior pain relief while minimizing the adverse effects associated with higher doses of individual medications. When NSAIDs are used in combination with opioids for severe pain, the combination therapy allows usage of reduced dosages of opioid analgesics and significantly reduces the opioid-related adverse effects. [37,45] This approach may allow for personalization depending on the patient’s pain profile, clinical condition, and preferences, which in turn may result in improvement of treatment outcomes and eventually enhance patients’ satisfaction levels. [37,45]

This personalization approach to manage pain can be further bolstered by amalgamating pharmacologic and nonpharmacologic interventions to improve the efficacy of pain management. [37,45] Nonpharmacologic interventions and alternative therapies are also vital to pain management. Use of heat or cold can help in managing acute pain by reducing inflammation and improving blood circulation. [46] Physical therapies, cognitive behavioral therapy (CBT), [47] and alternative therapies, such as acupuncture, breathing exercises, massage, meditation, and relaxation techniques, can provide significant relief from pain stimuli.

Pain management has clinical, operational, and patient-related challenges. [48] Clinical challenges include variability in pain assessment and its management. This variability can lead to inadequate pain management for some and overmanagement for others. [49]

Operational challenges include making decisions regarding the choice of analgesic considering the requirement for rapid pain relief and keeping in mind the risks associated with certain analgesic drugs. [50] Expectation of immediate and fast pain relief, patients’ psychological circumstances, dogmas, and previous experiences with pain are the patient-related challenges that can affect pain management. [51]

Balancing the use of opioid, non-opioid, and non-pharmacologic methods can be difficult in pain management. [49] Combining pharmacologic and non-pharmacologic modalities can ensure a more holistic approach to pain management. Utilizing a combination of analgesics, such as acetaminophen and NSAIDs, with adjunct therapies such as physical therapy, cold therapy, CBT, or acupuncture can help in better pain management. [47]

Effective pain management should include the use of validated pain scales to gauge pain intensity accurately. [51] Standardized pain assessment tools, such as the Numerical Rating Scale or the Wong-Baker FACES Pain Rating Scale, should be adopted to ensure consistency and accuracy. Incorporation of pain assessment tools in electronic health records systems can help in evaluating, tracking, and documenting pain records. [51] Evidence-based optimized latest medication protocols on the use of non-opioid and opioid analgesics can improve pain management. [52]

INFLAMMATORY PAIN

Inflammatory pain is the type of pain that occurs during tissue injury and active inflammation. It is characterized by spontaneous pain in the absence of an external stimulus and is identified most prominently by pain hypersensitivity. In these situations, the stimulus that would normally not produce pain would do so.

It is the consequence of the activation and change of nociceptor function by immune signals and the signals arising from damaged cells. [53] Some of these signals activate nociceptors directly; however, many produce changes in sensitivity that reduce the threshold of the nociceptors so that they may then be activated by innocuous stimuli. This change is known as peripheral sensitization, which results from posttranslational changes in ion channels in the nociceptor peripheral terminal and promotes pain within the active site of inflammation. [54]

NEUROPATHIC PAIN

Neuropathic pain is that pain that follows an injury or disease of the somatosensory nervous system, invariably of the peripheral nervous system but may also involve the central nervous system (CNS). [55] The neural injury produces negative symptoms such as loss of sensation or sensitivity and positive symptoms such as spontaneous pain, allodynia (characteristically responses to cold and tactile stimuli), paresthesia, and hyperalgesia or hyperpathia, which are magnified responses to noxious stimuli. [56]

Unlike inflammatory pain, neuropathic pain, which is usually long-lasting, outlasts the initiating trigger, which may be nerve trauma, diabetic- or chemotherapy-induced neuropathy, stroke, or spinal cord injury. The pain arises both from alterations in injured neurons (such as the development of ectopic action potentials initiating from hyperexcitable membranes) and from structural and functional changes in CNS circuits due to a permanent facilitation of few excitatory synaptic connections and loss of other inhibitory synaptic connections, accompanied by variations in microglia and astrocytes. [57]

PROCEDURAL PAIN

Procedural pain is defined as pain resulting from a specific, limited, invasive procedure, i.e. an acute increase or sudden onset of pain in a short duration. [58] Dental procedures such as dental injections, restorative treatment, periodontal procedures, implant placement, tooth extraction, other surgical procedures, biopsies, root canal therapy, and orthodontic treatment are invariably associated with procedural pain.

Table 1 summarizes the differential features of inflammatory, neuropathic, and procedural pain.

Table 1
Difference between inflammatory, neuropathic, and procedural pain

Inflammatory painNeuropathic pain[ 71 ]Procedural pain[ 72 ]
OriginPain associated with tissue injury or damage[ 70 ]Pain associated with injury or disease of nerve tissuePain triggered by medical procedures like injections, surgeries, or biopsies
SymptomsRedness (rubor), heat (calor), swelling (tumor), pain or hypersensitivity (dolor), and loss of function (functio lasea)May include spontaneous pain (pain without a clear cause), burning, stabbing, electric shock-like pain, tingling, numbness, or a “pins and needles” feelingStabbing, severe or excruciating, and distinct from the background pain associated with the underlying condition
OnsetGradualDelayedSudden and acute (short duration)
MechanismInvolves activation of immune cells and release of inflammatory substances that damage nerves and trigger nerve inflammation, leading to painInvolves sensitization of nerves, either at the peripheral level (increased stimulation of pain receptors) or centrally (increased signals to the brain)Related to the specific procedure and the body’s response to it

PREOPERATIVE/PREPROCEDURAL PAIN

Pain that the patient is experiencing before surgery can influence their perception and experience of postoperative pain. Preoperative assessment may disclose factors such as previous pain experiences, psychological distress (anxiety and depression), or outlooks about pain, which can influence the severity of postoperative pain. Using the preoperative evaluation visit to ratify preoperative optimization strategies, such as teaching new ways to cope with stress, handling perioperative expectations, and presenting mindfulness techniques, has noteworthy potential to improve health well beyond the postoperative period. The patient’s self-assessment of their preoperative psychological state offers important information about whether or not the subject is at high risk for poor postoperative pain control or disappointment with their overall hospital experience. [59]

In addition, high levels of depression or anxiety may foretell less successful rehabilitation and a delayed return to baseline recovery/function. [60]

PERIOPERATIVE PAIN

This refers to the pain experienced during the surgery and in the immediate postoperative period. Multiple studies have been conducted where local anesthetics such as articaine, lidocaine, mepivacaine, and prilocaine with a vasoconstrictor are preferred to be administered intraoperatively to minimize pain. [61] Local anesthesia (LA) results in a numbing effect to the area of operation and prevents pain signals from reaching the brain. The duration of soft tissue anesthesia after the administration of these intermediate duration drugs is stated to be between 3and 5 h. [62] Prolonged durations are observed when the drug is administered by nerve block rather than infiltration. [63]

When the comparison of maxillary and mandibular teeth was done in terms of pain management, studies infer that it was easier to control pain in the maxillary teeth by virtue of buccal infiltration near the apex of the teeth due to the porous nature of the maxillary bone, which allows for the easy diffusion of LA. However, due to the thicker and denser cortical plates in the mandible, it was extremely difficult to anesthetize the mandibular molars, followed by the mandibular premolar and incisors. [64,65]

POSTOPERATIVE PAIN

It is defined as an unpleasant physical and psychological experience associated with actual or potential tissue damage caused by the surgery itself. [66] Postoperative pain is a reason for delayed recovery and discharge after surgery, as well as amplified risk of respiratory and cardiovascular complications. [67] Clinical trials performed on pain intensity following dental surgical procedures have demonstrated that pain is most intense approximately 5–6 h postprocedure completion, reaching its peak levels during the 1 st postoperative day.

For the management of postsurgical pain, bupivacaine administered by an appropriate nerve block (inferior alveolar, Gow-Gates, anterior superior alveolar, and posterior superior alveolar) close to the conclusion of a surgical procedure can render the patient a pain-free period of up to 12 h. [68]

In addition, there might be a requirement for long-term pain management, as post-traumatic and postsurgical pain may continue with varying degrees of intensity (mild, moderate, and severe) for days or weeks. In these cases, NSAIDs represent the most effective drugs for the management of post-surgical pain. [69]

PERIODONTAL PAIN

Periodontal pain is defined as discomfort experienced in the gingival tissues, often associated with inflammation, swelling, and bleeding, typically arising from conditions such as gingivitis or chronic periodontitis. [73]

It is the result of acute inflammation of the gingiva, bone, and the PDL due to bacteria. The pain is easily localized, and the teeth affected are tender to pressure. The etiology could be the following:

The sequelae of pupal necrosis and pulpal infection that lead to periapical inflammation Periodontal infection with periodontal pocket formation due to a lateral periodontal abscess.

PULPAL PAIN

The dental pulp is richly innervated and vascularized, and when it is stimulated, there is a single sensory response: pain. The pupal tissues’ neural compartment contains sensory terminal afferent axons, and the sympathetic efferent fibres regulate the blood flow. Pulpal pain arises from exposed dentinal tubules, which transfer the information to the dental pulp via a dense network of trigeminal sensory axons intimately related to odontoblasts. [74]

Importance of differential diagnosis

The importance of differential diagnosis between periodontal and pulpal pain lies at the very core of effective dental care, as both conditions often present with overlapping clinical features yet require fundamentally different treatment approaches. Accurate differentiation between periodontal and pulpal pain is essential because it directly influences treatment decisions and clinical outcomes [ Table 2 ]. Misdiagnosis can lead to inappropriate therapy, such as performing periodontal treatment instead of required endodontic intervention, or vice versa, resulting in persistent symptoms and potential iatrogenic damage. Timely and correct identification helps prevent disease progression – whether it is advancing attachment loss in periodontitis or worsening pulpal pathology like pulpitis. It also aids in recognizing combined endo-perio lesions, where proper sequencing of treatment is crucial. Ultimately, precise diagnosis ensures effective pain relief, preserves tooth structure, and improves overall patient outcomes and satisfaction. [75-79]

Table 2
Differentiating periodontal versus pulpal pain
TMJ – Temporomandibular joint

Pulpal painPeriodontal pain
OriginInflammation/infection of pulpInflammation/infection of the periodontium
TypeReversible pulpitis - Sharp and shooting pain of short duration Irreversible pulpitis - Dull. throbbing pain, poorly localised or spontaneous pain Pain may be exacerbated by heat and relieved by cold stimuliIrritating pain, the affected teeth are extremely tender on chewing
LocalizationLocalization is poor (no proprioceptive fibres are present in pulp) and becomes poorer as pain severity increasesEasily localized (contains proprioceptive fibres)
Aggravating factorsReversible pulpitis - sensitivity to cold Irreversible pulpitis - sensitive to cold or hot or to biting pressureSensitive to biting pressure
Alleviating factorsReversible pulpitis - usually none Irreversible pulpitis - cold/ice waterWarm salt water rinses
SituationsDeep caries, tooth fractures, recent restorations, open restoration marginsPeriodontal disease, periodontal pockets
ReasonPain impulse is initiated due to stimulation of free nerve endings at the periphery of the pulp, leading to increased osmosis and fluid movement inside the pulp. The increased osmosis is generally credited to the extraction of tubular fluid outwards due to cold or compressed air, or the inward movement of tubular fluid due to heat, or applying biting pressure on loose fillingResults from an acute inflammatory process of the gingivae, the periodontal ligament, and the alveolar bone due to bacterial or viral infection
Diagnosisa. Application of ethyl chloride on a pellet of cotton wool usually induces a short and mild painful response from the intact teeth. The pulpal condition may be reversible or irreversible. In reversible pulpitis, the pain response is increased (hyperalgesia) and outlasts the stimulus, usually by<10 s. In irreversible pulpitis, application of ethyl chloride results in excruciating pain that outlasts the stimulus for more than 10 s b. Percussion helps in locating the tooth with painful pulpitis. 80% are tender to percussion. Nonvital pulps do not react to cold applicationPercussion Diagnosis is confirmed by a well-localized, painful tooth that is tender to percussion. There is increased mobility, radiographs show changes, and a painful or absence of response to sensibility testing
Differential diagnosisOdontogenic causes such as reversible pulpitis, irreversible pulpitis, and apical periodontitis Nonodontogenic causes such as TMJ disorders, pericoronitis, sialolithiasis, etca. Necrotizing Periodontal diseases b. Periapical abscess c. Periodontal-endodontic lesions d. Pericoronitis e. Aggressive periodontitis f. Nondental issues such as systemic diseases (leukemia), medication side effects, referred pain from headaches, and self-inflicted trauma

RECOGNIZING REFERRED OR NONODONTOGENIC PAIN

“Referred pain” occurs in an area far from the primary lesion and is sometimes associated with secondary hyperalgesia and trophic changes in the referred areas. [80] Dental pain can occur with the patient complaining of a toothache, even if the origin of the pain is a location other than the teeth. However, the etiology of the dental pain is masked, misleading the diagnosis. Information from the teeth and other sites, such as the blood vessels and muscles, is transmitted and bundled together at the synapses of trigeminal nerve neurons – both primary and second order – as well as at the spinal nucleus of the trigeminal nerve. For instance, pain in the masseter muscles is transmitted through the masseteric nerve before reaching these points. In addition, the inferior alveolar nerve also relays to these points from the molar region of the mandible. When masseteric pain continues, the pain-transmitting neurons become hypersensitive, a phenomenon known as “central sensitization” and the accelerator of pain transmission is pressed down. Further, the mildest stimulus broadcasts to the central nerves via neurotransmission, resulting in pain that originally developed in the masseter but felt as pain travelling through the inferior alveolar nerve, i.e. mandibular molar pain. The source of pain at the exact site in the masseter produces a referred pain at a different location, i.e. the mandibular molar region. [81]

Referred pain is not associated with muscles alone. Cluster headaches, migraine headaches, and other neurovascular headaches can also be referred to the teeth. In such cases, the terminology given to them is neurovascular toothaches. In the situation of neurovascular headaches, neuropeptides are released from trigeminal nerve endings in the intracranial blood vessels which dilate and stimulate the blood vessels. The inflammation, as a consequence, is thought to produce pain. The same mechanism produces dental pain. Migraine headaches, which lead to referred dental pain causes episodic, pulsating vascular pain, commonly in the maxillary and mandibular premolars and maxillary canines. In case it is accompanied by a headache, the diagnosis is comparatively straightforward as invariably patients do not visit the dentist for headaches. However, the examination and the diagnosis are more complicated in those with toothache alone, as the subjective symptoms of pulpitis are similar, and dentists must be cautious to avoid performing inappropriate pulpectomy. Finally, pain resulting from internal organs can cause a type of referred dental pain termed as visceral toothache. Visceral toothache comprises referred pain from the heart or the stomach. Another type of referred pain, termed as cardiac toothache, results when pain from angina pectoris is referred to the teeth. [81]

There are diagnostic dilemmas with dental pain, OFP, and conditions mimicking OFP. Systemic conditions that might affect the nerves, muscles, or bones in the head and neck region can manifest with OFP as a symptom. Examples include autoimmune diseases like lupus, which can have oral manifestations that include pain and ulcers.

Certain systemic conditions and diseases may present with symptoms similar to OFP and lead to misdiagnosis and delayed treatment. The pain associated with OFP can sometimes be difficult to distinguish from other conditions, leading to misdiagnosis and inappropriate treatment.

Myofascial pain: Trigger points in the jaw and neck muscles can cause referred pain that mimics toothache Trigeminal neuropathies: Conditions such as trigeminal neuralgia and painful posttraumatic trigeminal neuropathic pain can cause facial pain that is often mistaken for toothache Acute and chronic maxillary sinusitis: Congestion in the maxillary sinuses can put pressure on the roots of upper teeth, leading to a sensation of tooth pain Cardiac pain: Referred pain from heart conditions can manifest as jaw or tooth pain, causing diagnostic confusion Other neuralgic pains: Pain related to the glossopharyngeal nerve or other cranial nerves can also be mistaken for OFP Atypical facial pain and atypical odontalgia (PDAP), also known as “phantom tooth pain” or “dental migraine,” is characterized by persistent tooth pain without a clear dental cause Idiopathic OFP: This type of pain, with unknown cause, can present with symptoms that mimic toothache Temporomandibular joint (TMJ) disorders: Pain from TMJ problems can be felt in the jaw and surrounding areas, potentially being mistaken for a toothache.

CLINICAL ASSESSMENT OF DENTAL PAIN

The characterization of pain can be done on six features, which also form the basis for pain assessment. These features were added by the latest definition of “pain” from the IASP: [82]

Pain is a personal experience, shaped by biological, psychological, and social factors Pain and nociception are distinct concepts, with the former being notably more intricate People develop their understanding of pain throughout their lives When a patient communicates pain, their expression deserves maximum respect Despite its protective and adaptive roles, pain can negatively affect psychological and social well-being. Verbal description stands as just one method to portray pain. [1]

Two principal functions of clinical pain assessment are discriminative and evaluative. Discriminative function helps to evaluate a precise stage of pain and helps in coming to a diagnosis. Evaluative function assesses the progression of a patient’s medical or dental condition. [83] Pain assessment helps in determining the course of the disease and also the degree of disability that may be a consequence of this pain. It also helps in determining the choice of therapeutic aids, especially the usage of non-pharmacological therapeutic regimens (such as relaxation techniques and cognitive strategies), and the social, economic, and work-related consequences. [83,84]

There are pain assessment tools available, and their applicability is dependent on their validity, reliability, and sensitivity. Validity signifies the capability to measure the quantity. Reliability means that the chances of random error are minimal and the results are repeatable. [85] Sensitivity signifies the capacity of the tools to record clinically relevant change over time. [86]

Valid rating scales aid in collecting higher-quality data with greater comparability, reducing effort and increasing the credibility of the data. [4] There are several ways to assess the validity of a questionnaire, such as comparing the results obtained with biological monitoring, personal exposure monitoring, or historical records. [3]

Pain assessment tools can be classified as subjective and objective tools: subjective tools include rating scales, questionnaires, or pain diaries and objective tools include functional magnetic resonance imaging (MRI) and electroencephalography.

The subjective methods have been considered the “gold standard” for pain assessment for a long time. However, they may have limitations of reduced accuracy and underestimation of pain under certain conditions, like environmental factors, personality traits like feeling shame in showing vulnerability, psychological conditions, and the way the medical professional enquires about the pain may cause bias. [83,87]

Pain is an invisible symptom experienced by the patient and can only be communicated. The diagnosis is many times based on the patient’s communication with the clinician. Hence, communication skills are one of the most important tools for pain assessment, especially chronic pain. The patient must be heard carefully, and corroboration of information provided by the patient will help in elucidating important information about the patients’ experience. A careful history recording can be many times instrumental in arriving at the diagnosis and also the treatment plan.

Components of the pain history: Essential elements should include a detailed history of the current pain and, for those that suffer from chronic pain, their previous pain history [ Table 3 ] Pain-focused physical examination [ Table 4 ].

Table 3
Components of the pain history
NRS – Numeric Rating Scale; VAS – Visual Analogue Scale

Basic ElementsKey clinical questions/indicators
1. Onset of recent painWhen did the pain start?
What initiated the pain/what was the patient doing at the time?
Onset pattern: Sudden/gradual/flare-up of chronic pain
2. Aggravating and alleviating factorsWhat relieves the pain? (rest, medication, cold/warm application)
What worsens the pain? (chewing, temperature, posture, activity)
Response to nonpharmacological measures or analgesics
3. Quality of pain experienceAsk the patient to “describe the pain?” in terms of:
Nature: Sharp, dull, throbbing, burning, crushing, tearing
Pattern: Intermittent/constant/pulsating/episodic
4. Location of painExact site of pain
Does the pain radiate or spread to other areas?
Localized or diffuse?
5. Severity of painIntensity using pain scale (VAS/NRS)
Baseline pain level
Peak intensity during exacerbations
6. Circumstances of original painCircumstances at the onset of initial pain
Duration and frequency of episodes
Acute versus chronic pattern

Table 4
Physical examination for assessment of pain

Examination areaQuick clinical findings to assess
1. InspectionSkin changes (color, flushing, sweating)
Hair loss or goose bumps
Muscle atrophy/spasm
Edema
2. PalpationDefine the painful area
Change in pain on pressure
Trigger points
Altered sensation
3. Musculoskeletal systemWeakness/flaccidity
Abnormal movements
Reduced light touch or proprioception
Limited range of motion
4. Neurological examinationCranial nerve function
Motor strength
Reflexes and sensory testing (pinprick, proprioception)
Coordination

Basics

Onset of recent pain Aggravating and alleviating factors Quality of pain experience Location of pain Severity of pain Circumstances of original pain.

Functionality

How is pain affecting the current level of function? Is the patient working? How is the patient coping with pain?

Comorbidities

Significant past medical and/or surgical history Chronic diseases (obesity, hypertension, diabetes, etc.) Psychosocial and/or psychiatric comorbidities Family history of substance abuse.

Psychosocial and psychiatric

Depression Suicidal ideation or past suicide attempts Pastpsychiatricadmissions Physical, sexual, and/or emotional abuse.

History-taking remains of paramount importance in facilitating the diagnostic process. Blau [88] suggested fifteen questions to facilitate the history taking process in OFP, which cover the following aspects of the presenting pain:

Onset Frequency Duration Provoking factors Site of initiation of pain Radiation and referral of pain Is the pain deep or superficial Aggravating or exacerbating factors Relieving factors Characteristics of the pain Severity Other associated features, for example, lacrimation or other autonomic signs and symptoms Previous management strategies attempted Patient’s perceived cause (s) of pain.

PATIENT FACTORS TO CONSIDER WHEN ASSESSING PAIN

Assessing pain in certain special populations can be challenging and requires multiple considerations such as age, level of development, communication skills/language, cognitive skills, prior pain experiences, and associated beliefs.

Pain assessment scales

Pain is a multifactorial entity, but most of the pain scales assess pain intensity. There are different validated pain scales available for adult, pediatric, elderly, and nonverbal groups of patient populations [89-114] [ Table 5 ]. As there is no defined threshold of correlating score to actual pain and its intensity, so the interpretation of the score is not so direct. Pain intensity measurement using the same scale on two different patients does not mean that their scores are comparable for pain intensity.

Table 5
Pain assessment scales
VNS – Verbal Numeric Scale; NRS – Numeric Rating Scale; VAS – Visual Analogue Scale; DVPRS – Defense and Veterans Pain Rating Scale; NVPS – NonVerbal Pain Scale; PAINAD – Pain assessment in advanced dementia; BPS – Behavioral Pain Scale; CPOT: Critical-care observation tool; NIPS – Neonatal Infant Pain Scale; NPASS – Neonatal Pain Assessment and Sedation Scale; NFCS – Neonatal facial coding system; r-FLACC – Revised faces, legs, activity, cry, and consolability; NCCPC-R: Noncommunicating children’s pain checklist; CHEOPS – Children’s Hospital of Eastern Ontario Pain Scale

Pain scalesVerbal, alert, and orientedNonverbal or cognitive impairment
Adult1. VNS/NRS[ 89 90 ]1. Adult NVPS[ 95 ]
2. VAS[ 91 92 ]2. Scale PAINAD[ 96 97 ]
3. DVPRS 2.0[ 93 94 ]3. BPS[ 98 99 ]
4. CPOT[ 100 ]
Pediatric3 years and olderBirth-6 months
1. Wong Baker faces[ 101 ]1. NIPS[ 103 104 ]
2. Oucher (3–12 years)[ 102 ]2. N-PASS[105,106]
3. NRS (7–11 years)3. NFCS[107,108]
4.CRIES[109]
8 years and olderInfant and older
1. VAS1. r-FLACC[110,111]
2. VNS/NRS2. NCCPC-R[112]
3. CHEOPS (ages 1–7)[113,114]

Patient genetics, past experiences, comorbidities, or other pain-influencing factors are not accounted for in pain scales. Baseline pain level determination may become vital in subjects with preexisting pain. Because of the subjective nature of standardized pain scales, patient functionality may be the best indicator of pain intensity.

Fundamentally, pain must be assessed holistically. Dr. Sean Mackey [115] of Stanford University created the basis of interdisciplinary pain management called the Stanford Five. It is an augmented set of medical history obtained by the clinician during the medical interview for patients with pain and is designed to assess and present the pain experience as viewed from the patient’s primary belief system.

The following are the components of the Stanford Five:

Cause: What tissue abnormalities the patient believe to be the cause of the current problem?

Meaning: The presence of any sinister beliefs related to the pain, in terms of tissue damages, that preclude activities.

Impact: What impact does the primary problem have on the patient’s life, including interference on vocational, social, recreational activities, and in general the patient’s quality of life?

Goals: What the patient expects to achieve with further treatment?

Treatment: What the patient believes needs to be done now and in the future to help resolve the problem?

Patient examination with orofacial pain

The examination of a patient with OFP should include the following as a bare minimum, and more detailed examination of some tissues or systems may be added as the diagnostic process refines:

Inspection of the head and neck, skin, topographic anatomy, and swelling or other orofacial asymmetry Palpation of the TMJ and masticatory muscles, tests for strength, and provocation. With the assessment and measurement of the range of mandibular movement Palpation of soft tissue (including lymph nodes) Palpation of cervical muscles and assessment of cervical range of motion Cranial nerve examination General inspection of the ears, nose, and oropharyngeal areas Examination and palpation of intraoral soft tissue Examination of the teeth and periodontium (including occlusion).

Investigations

Investigations are needed to exclude some systemic diseases that may exacerbate OFP, and these must be excluded by history and blood tests.

Ongoing diseases that may worsen or initiate OFP systemic diseases associated with headache and OFP include hyperthyroidism, hypothyroidism, multiple myeloma, Vitamin B deficiencies, systemic lupus erythematosus, folic acid and iron deficiency anemias, Paget’s disease, and metastatic disease.

The various hematology investigations may be required including full blood count – predominately looking for anemias, hematinics: ferritin, B12, folate – looking for deficiency states causing secondary burning mouth syndrome, zinc levels, hypothyroidism – causing headache, diabetes (HBA1c), antibody screen ENAs ANAs, ESR or CRP if inflammatory condition suspected.

Diagnosing of pain may require additional use of radiographs (Intraoral periapical or orthopantomogram), computed tomography (CT) scans (cone beam CT), MRI (for space infections and lesions, demyelination and vascular compromise of the trigeminal nerve), ultrasounds, bone scans electromyogram and nerve conduction studies, angiograms or diagnostic nerve blocks can be used to assist in diagnosing the cause of pain.

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SECTION II – MULTIMODAL STRATEGIES FOR DENTAL PAIN MANAGEMENT

PRINCIPLES OF EVIDENCE-BASED PAIN MANAGEMENT

Evidence-based pain management in dentistry involves the integration of the best available clinical evidence, clinician expertise, and patient preferences to guide decisions related to pain control. [1,2] The objective is not only to alleviate discomfort but also to ensure safe, effective, and individualized care that enhances patient outcomes and satisfaction.

Pain is a multidimensional experience influenced by biological, psychological, and contextual factors, and its management must be guided by a structured, evidence-informed multimodal approach. This includes selecting appropriate pharmacologic and non-pharmacologic modalities based on the nature of the pain, the procedure involved, and the patient’s health status.

The foundation of evidence-based pain control rests on four pillars:

Accurate assessment of pain, including its intensity, duration, and source Selection of analgesics based on pharmacological efficacy, safety profile, and patient-specific factors Appropriate dosing and timing, aligned with clinical guidelines and individual needs Regular monitoring and reassessment to adjust therapy, manage side effects, and ensure continued efficacy.

Clinicians must also stay informed about emerging research on analgesics, updates to clinical guidelines, and pharmacovigilance data. [3] Emphasizing rational prescribing, avoiding unnecessary polypharmacy, and prioritizing patient education are all essential aspects of ethical and evidence-based practice. [4]

NONPHARMACOLOGICAL MANAGEMENT OF DENTAL PAIN

Cognitive behavioral therapy in the management of dental pain

Cognitive behavioral therapy (CBT) is a structured, evidence-based psychological treatment that focuses on the interconnection between thoughts, emotions, and behaviors. CBT has been extensively validated for a wide range of psychological conditions, including depression, anxiety disorders, substance use, chronic pain, and stress-related disorders. [5] In the context of dentistry, CBT offers a valuable adjunct to pharmacological treatment, particularly for managing odontogenic pain complicated by dental anxiety, procedural fear, and chronic orofacial pain syndromes. [6]

CBT is based on the following core principles:

Psychological distress is often influenced by maladaptive patterns of thinking These thought patterns are maintained by learned, unhelpful behaviors Individuals can be taught to identify, challenge, and replace these thoughts and behaviors with more adaptive coping strategies, leading to reduced emotional distress and improved functionality.

Relevance of cognitive behavioral therapy in dental pain management

Pain is not just a physiological experience; it is also shaped by psychological, emotional, and behavioral factors. In dentistry, odontogenic pain can be exacerbated by: (a) dental anxiety and fear, (b) catastrophic thinking (“This pain will never go away”), (c) anticipatory stress, and (d) negative past dental experiences. [7]

CBT helps manage pain by modifying these psychological responses, thereby: (a) reducing perceived pain intensity, (b) improving treatment compliance, (c) minimizing the need for excessive pharmacologic intervention. [8]

Table 6 summarizes foundational cognitive behavioral therapy techniques applicable in dental practice, highlighting their psychological foundations and relevance for managing dental pain and anxiety. These techniques equip dental professionals with structured approaches to modify maladaptive thoughts and behaviors. When used appropriately, they foster improved coping, enhance patient trust, and reduce the need for pharmacological interventions.

Table 6
Core cognitive behavioral therapy techniques used in dental pain
CBT – Cognitive behavioral therapy

CBT techniqueDescriptionApplication in dental pain
Cognitive restructuringIdentifying and challenging irrational or exaggerated beliefs about painHelps reduce fear of procedures and dental avoidance
Relaxation trainingTeaching deep breathing, progressive muscle relaxation, and mindfulnessUsed in waiting areas or chairside to lower anxiety
Distraction techniquesEncouraging patients to shift focus from pain to neutral/positive stimuliHelpful during procedures, especially in children
Graded exposureGradual exposure to feared dental stimuli (e.g., instruments, anesthesia)Builds tolerance in phobic patients
Positive self-talkReplacing negative internal dialogue with reassuring thoughtsEncourages a sense of control and self-efficacy
Pain coping skills trainingTeaching patients how to interpret and respond to pain constructivelyUseful for chronic or recurrent orofacial pain

Therapeutic process and collaboration

CBT is delivered in a collaborative format, where the dental professional (or behavioral specialist) and patient work together to: (a) understand the nature of the problem, (b) set achievable behavioral goals, and (c) develop personalized strategies tailored to the patient’s needs and readiness. [9-11] The focus is primarily on the present and future coping, rather than a detailed exploration of past experiences. A limited history may be relevant, but the therapeutic emphasis is on functional improvement and behavior change. CBT is best utilized in combination with patient education, local and systemic analgesia, behavioral reinforcement, and sedation where required (for severe dental phobia or surgical interventions).

Core cognitive behavioral therapy techniques

Cognitive restructuring

This technique involves identifying and challenging negative or irrational thoughts that lead to dental fear or avoidance. In dental settings, it helps patients replace anxious thoughts like “This is going to hurt” with more realistic and reassuring beliefs such as “The dentist will use anesthesia and monitor my comfort.” This shift in thinking reduces anticipatory anxiety and improves cooperation during treatment. [12]

Clinical application: If a patient believes, “Local anesthesia never works on me.” Gently question this belief by reviewing past experiences and educating the patient on modern anesthetics, setting realistic expectations: “Many patients feel anxious before injections , but most respond well to anesthesia . Let’s take it step by step.”

Relaxation training

Relaxation techniques aim to calm the body’s physical response to stress. Simple practices like deep diaphragmatic breathing or progressive muscle relaxation can be taught chairside to help patients manage symptoms such as rapid heartbeat, tense muscles, or shallow breathing. These exercises help create a sense of control and comfort, especially before or during procedures. [13]

Clinical application: Teaching of diaphragmatic breathing.

“Take a deep breath in through your nose for 4 counts, hold for 2, and exhale slowly through your mouth for 6.” This can be practiced in the waiting area or chairside before and during treatment.

Exposure and desensitization

This technique involves gradually and safely exposing the patient to feared dental stimuli (such as drills or needles) in a non-threatening way. Over time, repeated exposure reduces fear and avoidance. [7]

Clinical application: A patient fearful of the dental drill is first shown the instrument, then allowed to hear it without usage, and eventually undergoes a brief, noninvasive use (e.g. polishing), building tolerance over sessions.

Behavioral activation

Behavioral activation encourages patients to take positive, goal-directed actions despite fear or discomfort. [14]

Clinical application: A patient who missed multiple appointments due to fear is encouraged to schedule short, noninvasive visits first to build confidence, then gradually progress to full treatment. These small successes help break the avoidance cycle and build confidence over time.

Positive reinforcement and self-efficacy building

This technique focuses on boosting the patient’s confidence and motivation by acknowledging their efforts and progress. [15,16]

Clinical application: Positive comments like “ You did really well today ” or “ You were very calm during the injection ” reinforce the belief that they can handle dental procedures. This builds self-efficacy and reduces future anxiety.

Tell-show-do technique

Commonly used in pediatric and anxious adult patients, the Tell-Show-Do method involves three steps: explaining the procedure in simple terms, demonstrating it on a model or finger, and then performing it gently. This structured approach helps reduce uncertainty and builds trust by letting the patient know what to expect. [17]

Clinical application:

Tell: “I’m going to use a small brush to clean your tooth.”

Show: Demonstrate brushing on a finger or a model.

Do: Gently perform the action in the mouth.

Table 7 outlines practical strategies for chairside application of CBT in dentistry, including examples of real-time use, patient communication, and engagement methods. This table serves as a quick guide for integrating psychological support into everyday care, especially for anxious or pain-sensitive patients. Systematic application enhances treatment outcomes, patient satisfaction, and adherence to dental care.

Table 7
Clinical Implementation of cognitive behavioral therapy in dental settings
CBT – Cognitive behavioral therapy

ModeDescription
Chairside interventionUse empathetic communication: Validate the patient’s pain without exaggerating it
Apply basic CBT techniques (e.g., breathing exercises) while administering local anesthesia or performing extractions
Incorporate preprocedure counseling for patients with a history of dental anxiety or poor pain tolerance
Referral to a psychologistFor patients with complex anxiety, chronic pain, or maladaptive behaviors that interfere with treatment
Digital CBT toolsOnline modules and mobile app-based mindfulness training/guided relaxation may support ongoing self-management

Cold and heat application in the management of dental pain

Cold and heat applications are simple, noninvasive, and cost-effective nonpharmacological methods used as adjuncts in the management of dental and orofacial pain. They play a supportive role in reducing discomfort, inflammation, and muscle-related tension and are particularly effective in the early stages of acute pain or postoperative care.

Cold application (cryotherapy)

Mechanism of action

Cold therapy works through: (a) vasoconstriction, which limits local blood flow and reduces edema, (b) decreased nerve conduction velocity, resulting in a numbing effect, and (c) suppression of inflammatory mediators, minimizing tissue damage and discomfort. [18,19]

Method of application

A cold pack or ice wrapped in a clean cloth should be applied externally to the affected area, over the skin corresponding to the site of dental pain or postoperative swelling. It should be applied for 15–20 min per session, with the skin resting for at least 20 min between applications to prevent cold injury. This can be repeated 2–3 times daily during the first 24–48 h after a dental procedure or acute trauma to help minimize swelling, numb the area, and reduce inflammatory pain.

Precautions

Direct contact of ice with the skin should be avoided to prevent frostbite or cold-induced skin damage. Cold therapy is contraindicated in individuals with known cold sensitivity, Raynaud’s phenomenon, or impaired peripheral circulation. During use, the skin should be monitored for any signs of irritation or adverse reaction, and prolonged application should be avoided to ensure tissue safety.

Heat application (thermotherapy)

Mechanism of action

Heat application: (a) increases local blood flow through vasodilation, (b) promotes muscle relaxation, reducing spasm and myofascial tension, (c) enhances tissue flexibility and healing, and (d) helps reduce referred pain from temporomandibular joint (TMJ) or masticatory muscle dysfunction. [20,21]

Method of application

Warm compresses or moist, heated towels should be applied over the affected muscle or joint to promote relaxation and alleviate discomfort. Each application should last 15–20 min per session and may be repeated 2–3 times per day, depending on the severity and chronicity of the symptoms. This approach supports muscle relief and enhances local circulation in conditions involving chronic orofacial pain or muscular tension.

Precautions

Heat application should be avoided in the presence of acute infections or active inflammation, as it may worsen swelling and facilitate the spread of infection. [22] The temperature of the compress should be comfortably warm, not hot, to prevent the risk of skin burns. In addition, heat therapy is contraindicated in individuals with reduced sensation, neuropathy, or open wounds, where the ability to detect excessive heat may be impaired, increasing the risk of thermal injury.

Table 8 presents a structured summary of cold and heat application in dental pain management, outlining their indications, application methods, frequency, and safety precautions. It offers clinicians a quick reference for integrating thermal modalities into care, particularly for postoperative and inflammatory conditions. Used correctly, these nonpharmacological interventions enhance comfort, reduce analgesic load, and support tissue healing.

Table 8
Cold and heat application in the management of dental pain
MPDS – Myofascial pain dysfunction syndrome; TMJ – Temporomandibular joint; RCT – Randomized controlled trial

Clinical scenarioRecommended thermal modalityTiming of applicationPurpose/expected benefit
Tooth extraction (simple/surgical)Cold → HeatCold: First 24–48 hCold: Reduces postoperative pain and swelling
Heat: After 48 h if no swellingHeat: Promotes healing, relieves stiffness
Minor oral surgical procedures (e.g., cyst removal, biopsies, implant placement)ColdFirst 24–48 hControls inflammation, minimizes bruising, and edema
Periodontal surgery (e.g., flap surgery, osseous resection, grafting)Cold → HeatCold: 24–48 h postoperativeCold: Controls the inflammatory response
Heat: From day 3 onwardHeat: Enhances tissue healing and comfort
Subgingival debridement in inflamed periodontitis casesColdImmediately posttreatmentSoothes inflamed tissues, reduces discomfort
Acute periapical conditions (e.g., apical abscess, symptomatic apical periodontitis)ColdBefore or shortly after drainage or RCT initiationTemporarily alleviates throbbing pain and decreases the inflammatory response
Acute pulpitis (symptomatic irreversible)ColdEarly phaseTransient pulpal relief and pain reduction
Gingival trauma (e.g., from instrumentation, food impaction, or brushing injury)ColdImmediately posttraumaReduces tissue damage, pain, and bleeding
Lip/cheek/tongue trauma due to local anesthesia or accidental bitingColdImmediately postinjuryMinimizes swelling and secondary discomfort
Chronic apical periodontitis (low-grade pain, postobturation soreness)HeatAfter the acute phase subsidesImproves blood flow, reduces deep tissue discomfort
MPDSHeatAs needed, 2–3 times dailyRelieves muscle spasm, improves mobility
TMJ discomfort or bruxism-related painHeatAs neededReduces joint stiffness, relaxes masticatory muscles
Muscle fatigue or tightness after lengthy dental proceduresHeat48–72 h posttreatmentEases jaw fatigue and improves circulation

These thermal therapies are safe, well-tolerated, and patient-friendly interventions that should be incorporated into routine pain management protocols in dental practice. When applied appropriately and timed according to the stage of injury or inflammation, cold and heat applications can significantly enhance patient comfort, reduce the dependence on pharmacological analgesics, support the natural healing of tissues, and ultimately improve patient compliance and overall satisfaction with treatment outcomes.

Low-level laser therapy/photobiomodulation

Low-level laser therapy (LLLT), also referred to as photobiomodulation (PBM), is a non-invasive therapeutic modality that uses low-intensity laser or light-emitting diode sources to stimulate biological tissues and promote healing. It induces photochemical and photobiological changes within tissues that help reduce pain, inflammation, and tissue damage. In dental practice, PBM is increasingly used as an adjunctive nonpharmacological method for managing pain associated with inflammatory oral conditions and postoperative healing.

Mechanism of action

The therapeutic effects of PBM are attributed to the absorption of light energy by cellular chromophores, particularly cytochrome c oxidase in mitochondria. This leads to an increased mitochondrial activity and ATP production, enhancing cellular metabolism and tissue repair. [23] Modulation of nerve conduction, which reduces nociceptive signaling and provides analgesic effects. [24] LLLT increases nitric oxide, a powerful vasodilator, thereby increasing blood flow and augmenting healing. [25] There is also a well-described anti-inflammatory effect [26] and, following use of LLLT, a decrease in prostaglandin E2 concentrations has been documented. [27] This anti-inflammatory action suggests a potential role for LLLT in conditions involving inflammation and pain. Together, these mechanisms contribute to pain relief, reduced inflammation, and accelerated healing.

LLLT has shown potential benefits for reducing postoperative dental pain and inflammation in selected procedures, such as third molar extraction, [28] postendodontic pain [29] and periodontal surgery. [30] However, due to variability in treatment protocols and limited standardization, it should be considered an adjunctive modality rather than a primary pain management strategy.

Preprocedural anxiety reduction

Preprocedural anxiety is a common barrier to effective dental care. It can amplify the perception of pain, hinder cooperation during treatment, and result in avoidance behaviors that delay essential interventions. Recognizing and addressing patient anxiety as part of comprehensive pain management not only improves procedural outcomes but also fosters long-term patient trust and satisfaction.

Anxiety can lead to various adverse outcomes during medical procedures by altering physiological responses and affecting patient comfort. An increased sympathetic nervous activity can elevate heart rate and reduce heart rate variability, increasing the risk of sudden cardiac events. [31] Furthermore, elevated anxiety levels result in a notable elevation in respiratory rate and its pattern. [32] It can heighten pain perception and muscle tension, making cooperation difficult. [33]

Patient education

Patient education is the first-line strategy in managing dental anxiety. Fear often stems from a lack of understanding, fear of the unknown, or past negative experiences. Clear, empathetic communication can significantly reduce anticipatory stress and improve pain tolerance.

Patient education offers several psychological benefits that contribute significantly to the overall success of dental treatment. [34] It helps reduce uncertainty and fear related to pain or treatment failure by clarifying expectations and addressing misconception. [35] This, in turn, improves patient cooperation and builds confidence, especially in those with prior negative dental experiences. Furthermore, by lowering physiological arousal and anxiety levels, patient education enhances the effectiveness of local anesthesia and analgesic measures, leading to better pain control and procedural outcomes.

Clinical counselling aids for anxiety reduction

Use simple, reassuring language to explain the procedure Set realistic expectations regarding duration, sensations, and recovery Enhance understanding with visual aids, models, or videos Provide a step-by-step overview of what to expect before, during, and after treatment Encourage patients to ask questions and share concerns or past experiences Give clear written instructions for pre- and postprocedure care Apply the “Tell-Show-Do” method, especially in pediatric and anxious patients. [7]

Chairside sedation in dentistry (conscious sedation)

Chairside sedation, also known as in-office conscious sedation, involves administering sedative agents in the dental clinic to alleviate anxiety, enhance patient cooperation, and improve comfort during dental procedures. It is particularly beneficial for patients with mild-to-moderate dental anxiety, low pain threshold, strong gag reflex, or those undergoing minor oral surgical or extended procedures. [36]

Commonly used modalities

Inhalation sedation with nitrous oxide-oxygen (N 2 O-O 2 ): This method is safe, well-tolerated, and offers rapid onset and recovery. It is especially suitable for both adults and pediatric patients Oral sedation using benzodiazepines (e.g. diazepam, midazolam, and alprazolam): Convenient and effective for anxiety reduction, but requires prior planning regarding dosage and timing Despite its sedative effects, conscious sedation preserves patient responsiveness, protective reflexes, and the ability to communicate. When used appropriately, it significantly reduces procedural stress and enhances the overall patient experience.

Indications

Dental anxiety or phobia: For patients experiencing excessive fear that interferes with dental treatment Exaggerated gag reflex: To facilitate tolerance during intraoral procedures Difficulty with local anesthesia alone: To increase patient comfort in those requiring enhanced pain control Patients with special healthcare needs or disabilities: To improve cooperation and safety during treatment Long or complex procedures: To maintain comfort and minimize fatigue during extended appointments.

Safety and clinical considerations

Monitoring: Continuous monitoring of vital signs, level of consciousness, and oxygen saturation is mandatory during and after the procedure to ensure patient safety. [37,38]

Trained personnel: Sedation must be administered only by dental professionals trained and certified in conscious sedation techniques, airway management, and emergency response.

Contraindications: Sedation may be unsuitable in patients with certain medical conditions (e.g. uncontrolled cardiovascular disease, respiratory compromise, and pregnancy) or when contraindicated medications are in use. A thorough medical evaluation must precede its use.

Emergency preparedness : The dental office should be equipped with emergency drugs, oxygen supply, and resuscitation equipment, and staff should be trained in basic life support (BLS) or advanced cardiac life support (ACLS), as appropriate.

PHARMACOLOGICAL MANAGEMENT OF DENTAL PAIN

Nonsteroidal anti-inflammatory drugs

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the cornerstone of pharmacological pain management in dentistry, particularly for odontogenic pain, which is predominantly inflammatory in origin. Their dual properties, analgesic (pain-relieving) and anti-inflammatory, make them especially effective for managing most dental pain presentations’ symptoms and underlying cause.

Mechanism of action

Dental pain often results from tissue injury, bacterial infection, or surgical trauma, which releases inflammatory mediators such as prostaglandins, bradykinin, and cytokines. Prostaglandins sensitize nociceptors (pain receptors) and amplify pain perception at the inflammation site. NSAIDs exert their pharmacological action by inhibiting cyclooxygenase (COX) enzymes, specifically COX-1 and COX-2, responsible for the biosynthesis of prostaglandins from arachidonic acid. By blocking COX activity, NSAIDs not only reduce the intensity of pain but also limit vasodilation, edema, and other inflammatory responses. [39]

Pharmacokinetics

NSAIDs are rapidly absorbed when administered orally, with most agents achieving peak plasma concentrations within 1–2 h. Their onset of action generally begins within 30–60 min, making them suitable for managing acute dental pain where timely relief is essential. The pharmacokinetic profiles of NSAIDs vary depending on the specific drug. Short-acting NSAIDs, such as ibuprofen, have a plasma half-life of approximately 2–4 h, requiring dosing every 6–8 h. In contrast, longer-acting agents like naproxen have a half-life of 12–17 h, allowing for dosing every 8–12 h. Potent agents like ketorolac have a moderate half-life of 5–6 h but are recommended for short-term use only due to their higher risk of adverse effects. [40,41]

NSAIDs are primarily metabolized in the liver via cytochrome P450 enzymes and are excreted by the kidneys. Therefore, dose adjustments or caution are warranted in patients with hepatic or renal impairment. In elderly individuals or those with cardiovascular comorbidities, careful monitoring is advised due to the increased risk of gastrointestinal bleeding, renal dysfunction, and hypertension.

Best practices for use of nonsteroidal anti-inflammatory drugs for dental pain

Use NSAIDs as first-line agents : Prefer NSAIDs over opioids for managing mild to moderate dental pain, especially of inflammatory origin [42,43] Select the appropriate NSAID : Choose based on efficacy, patient tolerance, and risk factors Prescribe the lowest effective dose : Always start with the lowest dose that provides adequate relief. Avoid high doses unless clinically justified and for a short duration Limit duration of use : NSAIDs should be prescribed for the shortest possible duration, typically 3–5 days in acute dental settings Avoid NSAID duplication : Do not combine two NSAIDs concurrently. Use fixed-dose combinations like NSAID + paracetamol judiciously Assess patient risk factors : Evaluate for gastric ulcer, renal dysfunction, hypertension, asthma, and cardiovascular disease before prescribing. Avoid in pregnancy (especially the 3 rd trimester) and uncontrolled comorbidities Co-prescribe gastroprotection when indicated : In high-risk patients, add a proton pump inhibitor (PPI) such as pantoprazole to reduce the risk of gastrointestinal complications Educate the patient : Instruct patients on correct dosing intervals, maximum daily dose, and the importance of not using over-the-counter (OTC) NSAIDs simultaneously Monitor for adverse effects : Watch for signs of GI distress, allergy, edema, or renal dysfunction, especially in elderly or medically compromised patients Review medication history for interactions : Be cautious if the patient is on antihypertensives, anticoagulants, or nephrotoxic drugs Document and reassess : Record indication, dose, and duration in the clinical notes. Reassess pain relief and discontinue as soon as not needed.

Opioids

Opioids are a class of centrally acting analgesics that provide relief from moderate to severe pain by binding to specific opioid receptors in the central nervous system (CNS). While they can be effective in managing acute, intense dental pain, their use in routine dental practice is highly restricted and selective, due to concerns regarding adverse effects, dependency, misuse, and regulatory control. [44]

In dentistry, opioids are not considered first-line analgesics and should only be prescribed when NSAIDs and paracetamol (acetaminophen) fail to control pain or are contraindicated. Their role is generally reserved for short-term relief of severe acute pain, such as post-surgical pain following complex oral surgeries, fractures, or infections with significant systemic involvement. [45]

Opioids may be useful as:

Adjunctive therapy for severe acute pain: Opioids may be used in conjunction with NSAIDs or paracetamol for short-term relief in cases of: [46,47] Complex surgical extractions (e.g. impacted third molars) Facial trauma involving bone or soft tissue Severe periapical abscess with spreading infection Pain in patients who cannot tolerate NSAIDs or high-dose paracetamol. Bridging analgesia In rare cases, opioids may serve as a temporary bridge until definitive dental treatment (e.g. endodontic therapy or surgical drainage) can be performed. Postoperative pain in special populations

For patients with NSAID contraindications (e.g. gastric ulcer, kidney disease, and bleeding disorders), short-term use of weak opioids such as tramadol may be considered.

Clinical limitations, adverse effects, and regulatory considerations

The use of opioids in dental pain management should be strictly limited to cases of severe pain that is unresponsive to first-line analgesics such as NSAIDs and paracetamol. These agents should be prescribed only when clearly indicated and for the shortest effective duration, typically not exceeding three to five days. Opioids are not recommended for routine dental pain and must be approached with caution due to their potential for side effects and dependency.

Common adverse effects of opioids include nausea, vomiting, dizziness, constipation, sedation, and dry mouth. [48] Prolonged or high-dose use significantly increases the risk of respiratory depression, [49] opioid dependence, [50] and opioid-induced hyperalgesia, [51] a paradoxical condition where patients become more sensitive to pain.

From a legal standpoint, opioid prescribing in India is governed by Schedule H1 of the Drugs and Cosmetics Rules and, in some cases, the Narcotic Drugs and Psychotropic Substances (NDPS) Act. [52] Drugs such as tramadol and codeine are regulated substances requiring documented prescriptions, and their OTC sale is prohibited. Dental surgeons are expected to maintain detailed records of opioid prescriptions, including patient history, indication, dosage, and duration. Misuse, overprescription, or failure to comply with regulatory protocols can lead to professional disciplinary action or legal consequences.

Before initiating opioid therapy, clinicians must perform a thorough risk assessment, including evaluating any history of substance use disorder, psychiatric illness, or chronic pain syndromes. A risk–benefit approach should guide decision-making, particularly in patients with multiple comorbidities or those on concurrent medications that may increase the risk of adverse effects or drug interactions.

Best practices for safe opioid prescribing for dental pain

Use the lowest effective dose for the shortest appropriate duration Avoid long-acting formulations or combination opioids with sedatives Avoid concurrent use with alcohol, benzodiazepines, or CNS depressants Provide clear instructions on dosage, duration, and potential side effects Educate patients on safe storage and disposal of unused opioids.

Matching analgesic strategy to severity and source of pain

Effective pain management in dental care depends on accurately matching the type and intensity of pain to the appropriate analgesic strategy. Odontogenic pain arises from various sources, pulpal, periodontal, periapical, or post-surgical, and each has distinct characteristics that influence therapeutic choices.

Matching severity

To guide this graded approach, the World Health Organization Analgesic Ladder, [53] originally designed for cancer pain, can be adapted for dental pain:

Step 1: Nonopioids or NSAIDs for mild pain.

Step 2: Add weak opioids for moderate pain unrelieved by Step 1.

Step 3: Stronger opioids (rarely required in dentistry) may be added for short durations in select cases of severe pain.

This stepwise model promotes rational prescribing, minimizes drug overuse, and enhances patient safety, making it a valuable tool in evidence-based dental pain management [ Figure 1 ].

Figure 1 Adapted World Health Organization ladder for dental pain
Figure 1 Adapted World Health Organization ladder for dental pain

Mild pain: Mild dental pain, such as that associated with reversible pulpitis, early gingivitis, or minor soft tissue irritation, is best managed with non-opioid analgesics. Paracetamol is the agent of choice due to its favorable safety profile, especially in elderly patients, pregnant women, and those with contraindications to NSAIDs. [54] Mild NSAIDs, such as ibuprofen at lower doses, can also be effective where inflammation is evident Moderate pain: Moderate pain, commonly seen in conditions such as symptomatic irreversible pulpitis, acute apical periodontitis, periodontal abscess, or minor surgical procedures, requires anti-inflammatory intervention. NSAIDs such as ibuprofen, diclofenac, or aceclofenac are effective in reducing both pain and inflammation. Where additional analgesic synergy is required, combination therapy using NSAID + paracetamol may be prescribed. This dual approach provides better pain control than monotherapy and reduces the need for higher NSAID doses Severe pain: Severe dental pain, often seen in cases such as acute apical abscess with swelling, surgical extractions, bone impaction, or postoperative complications, may require more potent analgesia. In such cases, short-term use of ketorolac (oral or injectable) can be effective due to its strong analgesic properties. If pain remains uncontrolled, especially in patients with heightened anxiety or low pain tolerance, weak opioids such as tramadol, used judiciously and for the shortest necessary duration, may be added. Importantly, analgesics must always be part of a comprehensive treatment plan, such as drainage, debridement, or endodontic therapy, rather than a substitute for definitive care.

Matching source

The origin of the pain must also guide the choice of analgesic:

Pulpal pain typically responds well to anti-inflammatories; early dental intervention is definitive Periapical pain may require stronger NSAID combinations and drainage Periodontal pain often benefits from NSAIDs alongside mechanical therapy Muscular or TMJ pain responds best to long-acting NSAIDs or muscle relaxants, along with heat therapy or behavioral interventions Postoperative pain management should begin pre-emptively and continue with scheduled analgesia in the early healing phase In all cases, analgesic choice should be tailored to the patient’s age, medical history, drug tolerance, and comorbidities, avoiding unnecessary opioid use and minimizing side effects.

Table 9 provides a comprehensive overview of commonly used analgesics in dental practice, detailing their dosages, routes of administration, and typical indications based on pain severity and source. It serves as a practical guide to selecting appropriate pharmacological agents based on the clinical presentation. Proper application of these strategies ensures effective, safe, and patient-centered pain management.

Table 9
Summary of analgesic agents used in the management of dental pain
*Maximum 40 mg/day; do not exceed 5 days of total treatment, NSAIDs – Nonsteroidal anti-inflammatory drugs

Pain sourceSeverityRecommended analgesics with dosages and routes[ 54 55 56 57 58 59 60 ]
Pulpal pain
Reversible pulpitisMildParacetamol 500–650 mg oral every 6 h
Ibuprofen 200–400 mg oral every 6–8 h
Aceclofenac 100 mg oral twice daily
Irreversible pulpitisMild to moderateIbuprofen 400–600 mg oral every 6–8 h
Aceclofenac 100 mg+Paracetamol 325 mg oral twice daily
SevereIbuprofen 400–600 mg oral every 6–8 h
Aceclofenac 100 mg+Paracetamol 325 mg oral twice daily
Ketorolac: Standard (Ages 17–64) - 20 mg once, then 10 mg every 4–6 h*; reduced (ages 65+, <50 kg, or renal impairment) - 10 mg every 4–6 h*
Periapical pain
Apical periodontitisModerateIbuprofen 400–600 mg oral every 6–8 h
Aceclofenac+Paracetamol oral twice daily
Paracetamol 650 mg oral every 6 h (if NSAIDs contraindicated)
Acute apical abscessSevereIbuprofen 600–800 mg oral every 6–8 h
Aceclofenac+paracetamol oral twice daily
Ketorolac: Standard (ages 17–64) - 20 mg once, then 10 mg every 4–6 h*; reduced (ages 65+, <50 kg, or renal impairment) - 10 mg every 4–6 h*
Tramadol 50 mg oral or parenteral every 6–8 h if needed
Periodontal pain
GingivitisMildParacetamol 500–650 mg oral every 6 h
Mild NSAID orally if discomfort is present
Chlorhexidine mouthwash 10–15 mL topical rinse twice daily
PeriodontitisMild to moderateIbuprofen 200–400 mg oral every 6–8 h
Aceclofenac 100 mg oral twice daily
Paracetamol 650 mg oral every 6 h if NSAID intolerance
Periodontal abscessMild to moderateIbuprofen 400–600 mg oral every 6–8 h
Aceclofenac 100 mg oral twice daily
Paracetamol oral adjunct if needed
SevereIbuprofen 400–600 mg oral every 6–8 h
Aceclofenac 100 mg oral twice daily
Paracetamol oral adjunct if needed
Ketorolac: Standard (ages 17–64) - 20 mg once, then 10 mg every 4–6 h*; reduced (ages 65+, <50 kg, or renal impairment) - 10 mg every 4–6 h*
PericoronitisMild to moderateIbuprofen 400 mg oral every 6 h
Aceclofenac 100 mg oral twice daily
Paracetamol 500–650 mg oral every 6 h
SevereIbuprofen 400 mg oral every 6 h
Aceclofenac 100 mg oral twice daily
Paracetamol 500–650 mg oral every 6 h
Ketorolac: Standard (ages 17–64) - 20 mg once, then 10 mg every 4–6 h*; reduced (ages 65+, <50 kg, or renal impairment) - 10 mg every 4–6 h*
Cracked tooth syndromeMild to moderateIbuprofen 400–600 mg oral every 6–8 h
Aceclofenac + paracetamol oral twice daily
SevereIbuprofen 400–600 mg oral every 6–8 h
Aceclofenac + paracetamol oral twice daily
Ketorolac: Standard (ages 17–64) - 20 mg once, then 10 mg every 4–6 h*; reduced (ages 65+, <50 kg, or renal impairment) - 10 mg every 4–6 h*
Postsurgical/procedural pain (dental extraction, periodontal surgery)Mild to moderate (routine)Ibuprofen 400–600 mg oral every 6 h (routine)
Aceclofenac+paracetamol oral twice daily (surgical)
Severe (surgical)Ibuprofen 400–600 mg oral every 6 h (routine)
Aceclofenac+paracetamol oral twice daily (surgical)
Ketorolac: Standard (ages 17–64) - 20 mg once, then 10 mg every 4–6 h*; reduced (ages 65+, <50 kg, or renal impairment) - 10 mg every 4–6 h*
Oral ulcers (traumatic, aphthous, etc)Mild to moderateParacetamol 500–650 mg oral every 6 h (systemic control)
Benzocaine gel application 3–4 times per day topically
Topical corticosteroids paste application 2 times per day topically
SevereParacetamol 500–650 mg oral every 6 h (systemic control)
Benzocaine gel application 3–4 times per day topically
Topical corticosteroids paste application 2 times per day topically
Ketorolac: Standard (Ages 17–64) - 20 mg once, then 10 mg every 4–6 h*; reduced (ages 65+, <50 kg, or renal impairment) - 10 mg every 4–6 h*

ROLE OF ANTIMICROBIALS IN THE MANAGEMENT OF DENTAL PAIN

Dental pain is often associated with inflammatory or infectious conditions involving the pulp, periapical tissues, or periodontium. While analgesics target symptoms of pain and inflammation, antimicrobials (antibiotics) are indicated only when there is a confirmed or suspected bacterial infection with signs of systemic involvement. [61] Inappropriate or overuse of antibiotics in cases of dental pain, particularly when pain is not infection-related, contributes to the growing global challenge of antimicrobial resistance. [62]

It is important to note that antibiotics do not relieve pain directly; their role is to control or eliminate the infection that may be contributing to the pain. Therefore, antibiotic use should always be used as an adjunct to definitive dental treatment, such as drainage, extraction, or endodontic therapy.

Indications

Antimicrobials are not indicated for routine dental pain, such as pulpitis or mechanical trauma. Instead, they are reserved for cases such as: [63]

Acute odontogenic infections with systemic signs (fever, malaise, and lymphadenopathy) Cellulitis or diffuse facial swelling Trismus, dysphagia, or respiratory compromise (suggesting deep space involvement) Spreading infections not amenable to immediate surgical intervention Postoperative infections (e.g. dry socket with secondary infection) Immunocompromised patients, even in localized infections, to prevent rapid progression.

CONSIDERATIONS AND BEST PRACTICES

Definitive dental treatment (e.g. drainage, extraction, RCT) must not be delayed or replaced by antibiotic therapy [64,65] Antibiotics should be chosen based on likely pathogens, local resistance patterns, and patient factors such as allergy or comorbidities In pregnant or lactating women, agents such as amoxicillin and clindamycin are preferred, while tetracyclines and quinolones should be avoided Patient education is crucial; patients should be advised to complete the full course of antibiotics and understand that antibiotics are not painkillers Dentists should maintain records and follow national antimicrobial stewardship guidelines, such as those recommended by the Indian Council of Medical Research (ICMR). [66]

ROLE IN PREVENTIVE AND PROPHYLACTIC SETTINGS

In addition to therapeutic use, antimicrobials may occasionally be prescribed prophylactically in high-risk patients undergoing dental procedures that may result in bacteremia. [67,68] This includes:

Patients with prosthetic heart valves, previous infective endocarditis, or congenital heart defects Patients on immunosuppressive therapy or with poorly controlled diabetes.

Prophylactic antibiotic regimens should be followed based on current evidence-based guidelines, such as those from the American Heart Association (AHA) [69] or the National Centre for Disease Control (NCDC-India). [70]

Table 10 provides a summary of antimicrobials commonly used in dental practice in India, detailing their spectrum, recommended dosages, and specific indications. It serves as a practical reference for rational antibiotic prescribing. Appropriate use supports effective infection control while reducing unnecessary antimicrobial exposure.

Table 10
Summary of antimicrobial agents commonly used in dental practice in India

AntimicrobialTypical adult doseCommon dental indicationsGuidelines/considerations
Amoxicillin500 mg every 8 h for 5 daysOdontogenic infections, acute apical abscess, and pericoronitisFirst-line unless contraindicated; increase to 875 mg every 12 h in severe infections
Amoxicillin + clavulanic acid625 mg every 8 h for 5–7 daysβ-lactamase-producing or refractory infectionsMore GI side effects; preferred after failed plain amoxicillin
Metronidazole400 mg every 8h for 5 daysAnaerobic infections, necrotizing gingivitis, adjunct to amoxicillinAvoid alcohol; often combined with amoxicillin for broader coverage
Cefixime200 mg every 12 h for 5 daysAlternative to nonanaphylactic penicillin allergyGood for soft tissue involvement; not first-line
Ciprofloxacin500 mg every 12 h for 3–5 daysPeriodontal infections, aggressive periodontitisUse with caution; contraindicated in children and pregnant women
Azithromycin500 mg once daily for 3 daysPenicillin-allergic patients; periodontal infectionsShort course aids compliance; safe in mild allergies
Clindamycin300 mg every 6 h for 5 daysAnaerobic or deep-seated infections in penicillin allergyEffective against anaerobes; risk of pseudomembranous colitis
Doxycycline100 mg every 12 h on day 1, then 100 mg once daily for 7–14 daysChronic or aggressive periodontitis, adjunct in refractory casesAnti-collagenase effect; avoid in children <8 years, pregnancy; photosensitivity risk

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SECTION III – CLINICAL DECISION-MAKING IN DENTAL PAIN MANAGEMENT

TRENDS OF ANALGESIC USE IN DENTISTRY

Pain management is a cornerstone of dental practice, critical to patient comfort, compliance, and recovery. Analgesics – particularly nonopioid and opioid medications – play a pivotal role. Over the years, clinical preferences and prescribing patterns have evolved, influenced by new evidence, drug safety profiles, regulatory changes, and public health concerns like the opioid crisis.

Ibuprofen remains the most widely prescribed nonsteroidal anti-inflammatory drug (NSAID) for mild to moderate dental pain. Naproxen and diclofenac are alternatives with longer half-lives but increased gastrointestinal (GI) risks. Ketorolac tromethamine is a potent NSAID indicated for short-term, moderate-to-severe acute pain, often used postoperatively in dentistry. Administered orally, intramuscularly, or intravenously, Ketorolac 10 mg PO q4-6h is equivalent in efficacy to low-dose opioids, without the addiction risk. A randomized clinical trial by Dionne et al . found ketorolac superior to codeine and equianalgesic to ibuprofen in third molar surgery.[ 1 ] Laskin et al . reported that ketorolac significantly reduced postextraction pain scores compared to placebo and even tramadol.[ 2 ] Warnick and Wahl concluded in a systematic review that short-term use of oral ketorolac is effective in acute dental pain, particularly in surgical patients.[ 3 ] Often used for moderate-to-severe pain, particularly after third molar extractions, implant surgeries, and periodontal procedures, where conventional NSAIDs are insufficient.

A Cochrane review concluded that ibuprofen 400 mg is more effective than paracetamol (acetaminophen) and superior to many opioids for acute dental pain.[ 4 ] A combination of ibuprofen + paracetamol offers synergistic effects, with fewer side effects than opioids.[ 5 ] Acetaminophen (paracetamol) is preferred for patients with NSAID contraindications (e.g. GI ulcers and asthma). Often used in combination with NSAIDs or opioids for additive pain relief. Opioid analgesics, previously common (e.g. codeine, hydrocodone, and tramadol), especially in North America use has declined significantly due to addiction risk, adverse effects, and regulatory tightening. A landmark 2018 study showed that NSAID-acetaminophen combinations are more effective than opioid-based regimens for most dental pain.[ 6 ] The American Dental Association (ADA) in 2018 recommended that dentists limit opioid prescriptions to no more than 3 days and favor NSAIDs.[ 7 ] Rapid decline in dental opioid prescriptions post-2016, driven by state-level mandates and ADA guidelines.[ 8 ] In Europe and India: Greater reliance on NSAIDs; opioids used sparingly and primarily in hospital settings. Australia and Canada: Similar to the US, opioids are used more cautiously in recent years.

Third molar extraction and periodontal surgery are the most common reasons for analgesic use. NSAIDs remain first-line unless contraindicated. Pre-emptive analgesia and multimodal approaches (e.g. long-acting local anesthesia [LA] + NSAID + paracetamol) are growing in popularity for effective pain control and faster recovery.[ 9 ]

EMERGING TRENDS AND FUTURE DIRECTIONS

Multimodal analgesia

Combining different drug classes with complementary mechanisms (e.g. LA + NSAID + paracetamol) for opioid-sparing effects.

Long-acting local anesthetics

Bupivacaine, articaine, and newer formulations (e.g. liposomal bupivacaine) are used to reduce the need for systemic analgesics.

Pharmacogenomics and personalized pain management

Genetic testing to tailor analgesic choice, especially for opioids and NSAIDs metabolism, is an area of future exploration.

Nonpharmacologic adjuncts

Cold therapy, low-level laser therapy, acupuncture, and behavioral techniques are gaining interest for mild postoperative discomfort.

The use of analgesics in dentistry has steadily shifted toward evidence-based, opioid-sparing strategies. NSAIDs, especially Ketorolac, ibuprofen, and its combinations with acetaminophen, remain the cornerstone of dental pain relief.[ 9 ] Regulatory awareness, growing opioid concerns, and enhanced understanding of drug efficacy continue to shape safer and more effective prescribing practices.

COMMONLY USED ANALGESICS IN DENTAL PAIN MANAGEMENT

Effective pain management is a cornerstone of dental care, particularly in operative and postoperative settings. Pain control not only alleviates patient suffering but also improves compliance and treatment outcomes. Among the pharmacological options available, NSAIDs, acetaminophen (paracetamol), and opioids constitute the most commonly used classes of analgesics.[ 7 9 ] This section provides an expanded summary of these medications, emphasizing their mechanism of action, efficacy, safety profile, dosing, indications, and limitations, supported by current literature.

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS: THE FIRST-LINE ANALGESICS

Ibuprofen

Ibuprofen remains the most widely used NSAID in dentistry. It acts by non-selectively inhibiting cyclooxygenase (COX) enzymes – COX-1 and COX-2 – leading to decreased synthesis of prostaglandins responsible for inflammation and pain. Its analgesic and anti-inflammatory properties make it suitable for both acute and chronic dental pain. Ibuprofen 400 mg was more effective than acetaminophen and placebo in reducing post-operative pain after third molar extractions.[ 10 ]

Dosage: 400–600 mg every 6 h, not exceeding 2400 mg/day Onset: 30–60 min Duration: 4–6 h Adverse effects: GI upset, renal toxicity, increased bleeding tendency Contraindications: Peptic ulcer, renal impairment, third-trimester pregnancy.

Ketorolac

Ketorolac is a potent NSAID indicated for moderate to severe dental pain conditions. It should only be used short-term due to its high potency and associated risk of GI and renal side effects on long-term usage. Ketorolac provided analgesia comparable to morphine in post-operative dental pain.[ 1 ]

Dosage: Ketorol 20 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (Adult Age 17–64 years) not more than 5 days, or 10 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age ≥65 years, renally impaired, and/or weight <50 kg) not more than 5 days Onset: 30 min (oral), 10 min (IM) Duration: 4–6 h Adverse effects: GI ulceration, renal impairment, bleeding.

Diclofenac

Diclofenac exhibits slightly preferential COX-2 inhibition, providing strong anti-inflammatory effects, particularly useful in pericoronitis and post-extraction inflammation. Its efficacy in acute dental settings is well established.[ 11 ]

Dosage: 50 mg every 8 h; maximum 150 mg/day Onset: 30–60 min Duration: 6–8 h Adverse Effects: Hepatotoxicity, cardiovascular risk, GI effects

Naproxen

Naproxen has a longer half-life, allowing for twice-daily dosing, making it advantageous for sustained pain relief. Naproxen demonstrated superior efficacy over acetaminophen in dental extraction pain.[ 12 ]

Dosage: 250–500 mg every 12 h; maximum 1000 mg/day Onset: 60–90 min Duration: 8–12 h Adverse Effects: GI irritation, renal impairment Contraindications: Same as other NSAIDs.

ACETAMINOPHEN (PARACETAMOL): A SAFE NON-NONSTEROIDAL ANTI-INFLAMMATORY DRUG OPTION

Acetaminophen acts primarily in the central nervous system, inhibiting COX enzymes to a lesser extent and lacking anti-inflammatory activity. It is preferred in cases where NSAIDs are contraindicated, such as patients with GI ulcers, bleeding risks, or during pregnancy. Paracetamol alone is effective for mild-to-moderate dental pain and when combined with ibuprofen offers superior analgesia.[ 13 ]

Dosage: 500–1000 mg every 6 h; maximum 4000 mg/day Onset: 30–60 min Duration: 4–6 h Adverse effects: Hepatotoxicity in overdose.

COMBINATION ANALGESICS: ENHANCED PAIN CONTROL

Ibuprofen + paracetamol

The combination of ibuprofen and acetaminophen has been extensively studied and is shown to provide superior analgesic effects compared to either drug alone. The synergistic effect addresses both central and peripheral pain mechanisms. The ibuprofen–paracetamol combination provided the best balance of efficacy and safety for third molar surgery pain.[ 14 ]

Dosage: Ibuprofen 200 mg + paracetamol 500 mg every 6–8 h Advantages: Enhanced pain relief, opioid-sparing effect.

OPIOID ANALGESICS: RESERVED FOR REFRACTORY CASES

Tramadol

Tramadol is a weak μ-opioid receptor agonist with additional inhibition of norepinephrine and serotonin reuptake. It is used for moderate-to-severe dental pain unresponsive to NSAIDs. Tramadol is less effective than NSAIDs for dental pain but useful as adjunctive therapy.[ 15 ]

Dosage: 50–100 mg every 6 h; ma × 400 mg/day Onset: ~1 h Duration: 6–8 h Adverse Effects: Nausea, dizziness, constipation, dependency, serotonin syndrome Contraindications: Concurrent use of SSRIs, history of seizures.

Codeine (± paracetamol)

Codeine is a prodrug metabolized into morphine by CYP2D6. It is frequently combined with paracetamol to enhance efficacy. Codeine combinations offer limited additional analgesia over NSAIDs for dental pain.[ 16 ]

Dosage: 30 mg codeine + 500 mg paracetamol every 6 h Adverse effects: Sedation, constipation, respiratory depression, and dependency Genetic considerations: Ultrarapid metabolizers may experience toxicity; poor metabolizers may see no benefit.

Selective COX-2 inhibitors

Celecoxib:

Celecoxib selectively inhibits COX-2, offering anti-inflammatory and analgesic effects with reduced GI toxicity. However, it is associated with increased cardiovascular risk. Celecoxib shows improved GI safety compared to non-selective NSAIDs.[ 17 ]

Dosage: 200 mg once or twice daily Onset: 1–2 h Duration: 12–24 h Adverse effects: Cardiovascular events, dyspepsia Indications: Patients with GI risk but low cardiovascular risk.

According to the ADA and World Health Organization (WHO) guidelines, NSAIDs are recommended as the first-line therapy for acute dental pain.[ 7 ] The use of combination analgesics like ibuprofen with paracetamol is increasingly preferred due to their synergistic action and opioid-sparing potential. Opioids should be reserved for short-term use in severe cases and avoided when possible due to risks of dependency. Multimodal analgesia – the use of two or more analgesics with different mechanisms – provides superior pain control and minimizes the risk of side effects from any single drug. In addition, clinicians should assess patient-specific factors such as comorbidities, medication history, age, and genetic metabolism profiles before selecting an analgesic regimen.[ 7 9 ]

LOCAL ANESTHESIA

LA is critical for the successful execution of periodontal and peri-implant surgical procedures, ensuring effective pain control, minimal patient discomfort, and optimized surgical outcomes. The efficacy of LA in these contexts depends on the appropriate selection of agents, understanding of pharmacological dynamics, and precise administration techniques.[ 18 ] This section highlights the most suitable LA choices and approaches tailored specifically for periodontal and peri-implant surgeries, drawing on contemporary literature [ Table 11 ].

Table 11
Duration of action and surgical relevance of commonly used local anesthetic agents in dental clinics
SRP – Scaling and root planing

AgentPulpal durationSoft tissue duration (h)Relevance in periodontology/implantology
Lidocaine60–90 min3–5Ideal for moderate-length flap or regenerative surgeries
Articaine60–75 min3–6Best for infiltration in maxilla, anterior mandible
Mepivacaine20–40 min (plain)2–3Suitable for gingivectomy or SRP in cardiac patients
Bupivacaine3–9 h6–12Recommended for extensive surgical and implant procedures
Prilocaine60–90 min3–5Flap surgeries in systemically compromised patients

Choice of local anesthetic agents

Lidocaine (lignocaine)

Lidocaine has consistent reliability in periodontal flap surgeries and scaling and root planning.[ 18 ]

Suitability: Gold standard for most periodontal procedures Duration: Adequate for moderate-length flap surgeries.

Articaine

Articaine infiltration demonstrated higher success rates in dense cortical bone areas for periodontal procedures.[ 19 ]

Suitability: Preferred in dense bone areas, such as the anterior mandible or maxilla, often encountered in implant placements and flap access surgeries Advantages: Superior bone penetration, especially effective for palatal/lingual infiltrations in periodontal plastic surgery Caution: Used cautiously for nerve blocks during implant surgeries in the posterior mandible

Mepivacaine

Mepivacaine is useful for initial periodontal debridement or gingivectomy procedures.[ 20 ]

Suitability: Short-duration procedures and patients contraindicated for vasoconstrictors (e.g. those with cardiovascular issues undergoing periodontal debridement).

Bupivacaine

Advocated for osseous periodontal surgery where postoperative pain is anticipated.[ 21 ]

Suitability: Long-duration periodontal surgeries or full-mouth implant placements requiring post-operative pain control Caution: Cardiovascular monitoring advised due to increased cardiotoxicity risk.

Prilocaine

Found appropriate in periodontal surgeries with minimal cardiovascular load.[ 22 ]

Suitability: Recommended for flap surgeries in medically compromised patients.

Techniques of local anesthetic administration

Infiltration anesthesia

Maxillary Periodontal and Peri-Implant Surgeries: Articaine is preferred for its diffusion in dense palatal bone, essential for palatal flaps and ridge augmentations Mandibular Anterior Zone: Infiltration with articaine or lidocaine is effective for frenectomy, gingivoplasty, and anterior implant procedures.

Nerve block anesthesia

Nerve blocks significantly reduce the LA volume required for full-arch periodontal procedures.[ 23 ]

Inferior alveolar nerve block: Primary approach for mandibular quadrant surgeries, for example, periodontal flap surgeries and implant placements Long buccal and mental nerve blocks: Supplemental for mucogingival procedures and vertical ridge augmentations Maxillary nerve block: Useful for full arch or posterior maxillary surgeries.

Intra-ligamentary and intraosseous injections

Intraosseous articaine provided effective anesthesia during regenerative periodontal procedures.[ 24 ]

Periodontal applications: Effective in localized deep pockets or isolated defects Peri-implant use: Adjunctive for flapless implant placements.

Factors influencing anesthetic success in periodontal and implant surgery

Inflammation and infection: A common issue in periodontitis; lowers tissue pH, reducing LA effectiveness Injection site accuracy: Crucial for flap surgeries involving posterior or interproximal areas Tissue density and anatomy: Thicker gingiva or cortical bone around implants necessitates the use of articaine or intraosseous techniques Patient factors: Anxiety and previous negative experiences affect pain perception; pre-operative reassurance and topical anesthetics help.

Buffering agents such as sodium bicarbonate can be considered before mucogingival surgeries to improve onset and reduce injection discomfort.[ 25 ]

Effective local anesthesia in periodontal and peri-implant surgical procedures requires a strategic blend of agent selection, anatomical precision, and awareness of procedure-specific demands. Articaine’s superior bone penetration makes it invaluable in flap and implant surgeries, while lidocaine remains a consistent standard. Bupivacaine’s extended duration is advantageous for procedures requiring prolonged pain relief. Mastery of injection techniques – including nerve blocks and intraosseous injections – is essential for complete anesthesia in complex periodontal contexts. Evidence-based customization enhances patient comfort, clinical efficiency, and treatment outcomes.[ 18 23 25 ]

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS IN THE MANAGEMENT OF PERIODONTAL AND PERI-IMPLANT PAIN

NSAIDs are central to the pharmacological management of dental pain due to their dual action of analgesia and inflammation control. Their mechanism involves inhibition of cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis, which mediates both pain and inflammation in periodontal and peri-implant conditions.[ 11 ]

Role in periodontal and peri-implant surgeries

Postoperative pain following flap surgeries, regenerative procedures, and implant placement is often managed with NSAIDs. Ibuprofen remains the most widely prescribed first-line drug because of its efficacy, safety profile, and synergistic effect when combined with paracetamol.[ 26 ] Naproxen, Ketorol and diclofenac offer better, sometimes longer analgesic duration but with comparatively higher GI and other side effects.[ 27 ] Selective COX-2 inhibitors (e.g. celecoxib, etoricoxib) are considered for patients at higher risk of GI irritation but require caution in those with cardiovascular disease[ 28 ] [Refer Table 9 in Section II].

Management of acute periodontal and oral infections

Periodontal abscess: NSAIDs provide effective symptomatic relief, reducing inflammatory swelling and pain until definitive treatment (drainage and debridement) is performed[ 29 ] Necrotizing ulcerative gingivitis: NSAIDs help alleviate acute pain and improve patient comfort, though antimicrobial therapy and debridement remain the primary treatment[ 30 ] Pericoronitis: Often presenting with significant inflammatory pain, short courses of NSAIDs (ibuprofen or diclofenac) are recommended to manage symptoms before or after operculectomy or extraction[ 31 ] Herpetic gingivostomatitis: Pain control with NSAIDs is essential to allow fluid intake and oral hygiene; topical anesthetics may be used adjunctively[ 32 ] [Refer Table 9 in Section II].

Considerations in periodontal and implant patients

Drug interactions: Caution in patients taking anticoagulants or antihypertensives, as NSAIDs may potentiate bleeding or reduce antihypertensive efficacy[ 17 ] Systemic conditions: Alternative analgesics may be preferred in patients with peptic ulcer disease, renal impairment, or cardiovascular risk Combination therapy: Evidence supports combining NSAIDs with paracetamol for superior pain control after implant and periodontal surgeries compared to monotherapy.[ 26 33 ]

Clinical recommendations

First choice: Ibuprofen 400–600 mg every 6–8 h/ketorol 20 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age 17–64 years) not more than 5 days, or 10 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age ≥65 years, renally impaired, and/or weight <50 kg) not more than 5 days For prolonged analgesia: Naproxen 250–500 mg twice daily For severe cases or intolerance: COX-2 inhibitors (e.g. celecoxib 200 mg once daily) in selected patients Combination therapy: Ibuprofen (400 mg) with paracetamol (1 g) provides enhanced analgesia and reduces the need for opioids.[ 33 ]

NSAIDs, when used judiciously, provide predictable analgesia in periodontal and peri-implant practice. Their integration into pain management protocols enhances patient comfort, reduces reliance on opioids, and supports better surgical outcomes.[ 7 9 33 ]

MANAGEMENT OF PRE-, PERI-, AND POST-OPERATIVE DENTAL PAIN

Preoperative pain management

Assessing baseline pain levels

Effective preoperative pain assessment is crucial in dental practice to anticipate and manage postoperative discomfort. Validated tools such as the Visual Analog Scale (VAS), Numeric Rating Scale (NRS), and McGill Pain Questionnaire (MPQ) allow clinicians to quantify pain intensity and understand its qualitative aspects.[ 34 35 ] The VAS and NRS measure intensity, while the MPQ offers a multidimensional evaluation, capturing sensory, affective, and evaluative components.[ 36 ]

Beyond numerical scores, exploring pain history, including previous dental procedures, current analgesic use, and chronic orofacial pain, helps predict postoperative experience.[ 37 ] Patients with high baseline or chronic pain often exhibit greater postoperative pain and prolonged recovery.[ 38 ] Identifying such risk factors enables tailored pain strategies to improve patient comfort and outcomes.

Recommendation: Evaluate the patient’s pain level using VAS or NRS before endodontic, periodontal, or surgical cases.

Clinical context: Acute pulpitis, abscess, or periodontal inflammation may alter anesthetic effectiveness and recovery.

Action: Record pain score and review chronic pain history.

Treating existing inflammation or infection

Patients with active infections should not undergo elective procedures until stabilization is achieved.[ 29 ] An untreated infection may compromise anesthesia, prolong healing, and increase postoperative pain.

NSAIDs such as ibuprofen 400–600 mg every 6–8 h/ketorol 20 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age 17–64 years) not more than 5 days, or 10 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age ≥65 years, renally impaired, and/or weight <50 kg) not more than 5 days effectively control pain and inflammation.[ 39 ] If infection is present, antibiotics (e.g. amoxicillin or metronidazole) may be prescribed according to clinical presentation and systemic involvement.[ 40 41 ]

Recommendations:

Drain acute abscesses, initiate periodontal therapy, or perform debridement in endodontic infections before surgery.

Use NSAIDs (ibuprofen 600 mg q6h)/ketorol 20 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age 17–64 years) not more than 5 days, or 10 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age ≥65 years, renally impaired, and/or weight <50 kg) not more than 5 days for inflammation.

Prescribe antibiotics only with systemic involvement or immunocompromised status.

Use of pre-emptive analgesia

Pre-emptive analgesia aims to prevent central sensitization and reduce postoperative pain by giving analgesics before surgical trauma.[ 42 ] NSAIDs (ibuprofen 400–600 mg or ketorol 10 mg) administered 30–60 min preoperatively reduce prostaglandin synthesis and subsequent pain.[ 43 ] For NSAID-intolerant patients, acetaminophen 500–1000 mg may be used.[ 14 ] Selective COX-2 inhibitors (celecoxib 200 mg) provide effective alternatives with reduced GI toxicity.[ 28 ]

Clinical studies show that preoperative NSAIDs significantly lower postoperative pain and rescue analgesic need.[ 44 45 ] Oral ketorolac 10 mg has demonstrated superior short-term analgesia over ibuprofen in dental surgeries.[ 46 ]

Recommendations:

Ibuprofen 400–600 mg or ketorolac 10 mg, 30–60 min before extractions, flap, or implant surgery. Ibuprofen, while also capable of causing GI irritation, renal effects, and platelet inhibition, generally shows a lower relative risk of serious GI and bleeding complications at standard analgesic doses Avoid ketorolac in patients with peptic ulcer, renal impairment, or anticoagulant therapy Acetaminophen 500–1000 mg for NSAID-intolerant patients.

Managing patient anxiety and expectations

Anxiety amplifies pain perception and can complicate recovery.[ 47 ] Clear communication of procedure, pain expectations, and recovery reduces stress.[ 48 ] Adjunctive measures such as music distraction, guided relaxation, or anxiolytics (diazepam 5–10 mg) may be used.[ 49 ] Conscious sedation is an option in highly anxious patients.[ 50 ]

Peri-operative pain management

Local anesthesia selection and technique

Local anesthetic choice is critical. Lidocaine 2% with epinephrine 1:100,000 is standard for most procedures; articaine 4% is superior for mandibular infiltration due to bone penetration.[ 51 ] Bupivacaine 0.5% provides long-acting anesthesia for complex surgeries.[ 52 ]

Comfort can be improved by warming anesthetic to body temperature, injecting slowly (1 ml/min), and aspirating to avoid intravascular injection.[ 53 ]

Considerations for special populations

Cardiovascular disease: minimize epinephrine concentration and dose[ 54 ] Hepatic/renal impairment: adjust dosing to avoid toxicity[ 55 ] Pediatric patients: use weight-based dosing, shorter-acting agents[ 18 ] Geriatrics: monitor closely for polypharmacy and central nervous system effects[ 56 ] Diabetics: schedule early in day, monitor glucose, anticipate delayed healing.[ 57 ]

Role of conscious sedation

Conscious sedation improves patient comfort in anxious or special-needs patients. Nitrous oxide offers rapid anxiolysis; oral benzodiazepines provide moderate sedation, and IV sedation allows deeper control.[ 58 ]

Patient safety requires adherence to ADA and ASA guidelines with continuous vital monitoring and emergency preparedness.[ 59 ]

Preventing intraoperative trauma

Gentle tissue handling, adequate irrigation, and minimally invasive approaches (e.g. piezoelectric surgery) reduce trauma.[ 60 ] Systematic reviews show piezoelectric techniques reduce pain and swelling postoperatively.[ 61 ]

Post-operative pain management

Tailored analgesic prescription

Analgesics should be matched to the procedure invasiveness:

Mild: acetaminophen 500–1000 mg or ibuprofen 400 mg[ 6 ] Moderate: ibuprofen 600 mg q6h, optionally combined with acetaminophen[ 33 ] Severe: ibuprofen + low-dose opioid for ≤3 days, ketorol 20 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age: 17–64 years) not more than 5 days, or 10 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age: ≥65 years, renally impaired, and/or weight <50 kg) not more than 5 days or NSAID–acetaminophen combination preferred over opioids.[ 14 ]

Ketorolac 10 mg q4–6h provides potent relief for severe cases but should be limited to ≤5 days and ≤40 mg/day.[ 62 ] Sustained-release NSAIDs (etoricoxib) may provide 24-h coverage in select patients.[ 63 ]

Nonpharmacologic adjuncts

Incorporating nonpharmacologic strategies into postoperative dental care is essential for enhancing patient comfort, reducing reliance on medications, and promoting optimal healing.[ 14 64 ]

Cryotherapy, or the application of cold packs, is particularly effective within the first 24 h following dental surgery. Applying cold intermittently – typically for 15–20 min every hour – helps constrict blood vessels, thereby reducing swelling and numbing the affected area to alleviate discomfort.[ 65 ]

Activity restriction is another vital component. Patients are advised to rest for 24–48 h postsurgery, avoiding strenuous activities that could elevate blood pressure and disrupt the healing process.[ 66 ] Gradual reintroduction of normal activities should follow, based on individual recovery progress.

Dietary modifications play a significant role in postoperative care. Consuming soft, cool to lukewarm, and non-spicy foods for the first 2–3 days minimizes irritation at the surgical site.[ 67 ] Maintaining adequate hydration is crucial; however, patients should avoid using straws, as the suction can dislodge blood clots and increase the risk of dry socket.[ 68 ]

Maintaining oral hygiene is essential to prevent infection and promote healing. Patients should gently brush their teeth, avoiding the surgical area, and may use antiseptic mouth rinses, such as chlorhexidine, starting 24 h after the procedure.[ 69 ] These practices help maintain cleanliness without disturbing the healing tissues.

Integrating these nonpharmacologic approaches into postoperative care not only enhances patient comfort but also supports faster recovery and reduces the need for additional medications.[ 70 ]

Cold therapy: Ice packs to reduce facial swelling (15–20 min per hour for the first 24 h) Rest and activity restriction: Avoid strenuous activity for 24–48 h postsurgery Dietary instructions: Soft, nonirritating foods Avoid hot, spicy, or hard foods for 2–3 days No use of straws to prevent dislodgement of blood clots.

Patient education

Effective postoperative pain management extends beyond pharmacologic interventions, emphasizing comprehensive patient education to ensure optimal recovery and minimize complications.[ 71 ]

Providing patients with a clear, written medication schedule detailing dosages and timing is essential. This approach helps prevent missed doses or accidental overdoses, ensuring consistent pain control and promoting adherence to the prescribed regimen.[ 72 ]

Educating patients about potential warning signs of complications is equally important. They should be informed to monitor for persistent bleeding beyond 24 h, foul odors, increased swelling, or fever, as these symptoms may indicate infection or other issues requiring prompt medical attention.[ 51 ] Recognizing these signs early allows for timely intervention, reducing the risk of more severe complications.

Scheduling follow-up appointments within 48–72 h postsurgery is recommended to assess healing progress and address any concerns.[ 73 ] Patients should also be encouraged to contact their healthcare provider sooner if they experience any alarming symptoms.

To reinforce understanding and retention of postoperative care instructions, utilizing multiple communication formats is beneficial. Providing information both verbally and through written materials, visual aids, or digital resources caters to different learning preferences and enhances patient comprehension.[ 74 ]

By integrating these educational strategies into postoperative care, healthcare providers can empower patients to actively participate in their recovery, leading to improved outcomes and reduced incidence of postoperative complications.[ 38 ]

Written and verbal instructions: Dosing schedule and medication adherence What to expect in terms of pain, swelling, and recovery. Signs requiring immediate attention: Fever, excessive bleeding, pus, severe swelling, or pain worsening after 3 days. Follow-up: Ensure 48–72-h review for surgical cases, especially periodontal or implant procedures.

Monitoring and managing complications

Effective postoperative pain management in dental care necessitates vigilant monitoring and prompt intervention to address potential complications, ensuring optimal patient outcomes.[ 75 ]

One common postoperative complication is dry socket (alveolar osteitis), typically manifesting 2–4 days after tooth extraction, particularly in cases involving smokers or traumatic extractions.[ 76 ] Patients often experience severe, radiating pain due to the loss of the protective blood clot, exposing the underlying bone. Management involves gentle irrigation of the socket with saline to remove debris, followed by the application of a medicated dressing such as Alvogyl, which provides analgesic and antiseptic effects, facilitating pain relief and promoting healing.[ 77 ]

Postoperative infections may present with escalating pain beyond 48 h postsurgery, accompanied by signs such as purulent discharge, swelling, or fever. Initial management includes thorough clinical evaluation and, if necessary, drainage of the affected area.[ 78 ] Empiric antibiotic therapy should be guided by clinical judgment and, when possible, tailored based on culture and sensitivity results to effectively target the causative pathogens.[ 79 ]

In instances where patients report persistent burning or shooting pain, neuropathic pain due to nerve injury should be considered.[ 80 ] Such cases warrant referral to a specialist for comprehensive assessment. Pharmacologic interventions may include the use of gabapentinoids, such as gabapentin or low-dose tricyclic antidepressants, which have demonstrated efficacy in managing neuropathic pain syndromes.[ 81 ]

Continuous documentation of postoperative pain patterns and patient responses to interventions is crucial. This practice enables clinicians to adjust analgesic regimens appropriately and identify early signs of complications, thereby enhancing patient care and recovery trajectories.[ 82 ]

Dry socket (postextraction alveolar osteitis): More likely after mandibular molar extractions Treat with gentle irrigation and intrasocket medicated dressing (e.g. Alvogyl). Infection: Monitor for signs 2–4 days postprocedure Manage with antibiotics (e.g. amoxicillin–clavulanate or clindamycin) and debridement as necessary. Prolonged / postoperative neuropathic pain: May follow nerve injury during extraction or implant placement Consider referral for specialized pain management and use of medications like gabapentin in chronic cases.

As a dental practitioner, effective pain management must begin before the procedure, be actively maintained during, and continue after treatment with a combination of pharmacologic and nonpharmacologic strategies. Personalized care, patient education, and awareness of complications are key to minimizing discomfort and improving treatment outcomes in oral and periodontal care.[ 83 ]

SELECTION OF ANALGESIC AGENTS AND REGIMENS

Anticipated pain levels based on intervention

The choice of analgesic regimen in dentistry should be tailored to the anticipated severity of postoperative pain based on the type of procedure performed [ Figure 2 ]. Mild discomfort, such as that following scaling and root planing or simple extractions, is usually managed effectively with paracetamol or low-dose NSAIDs (e.g. ibuprofen 200–400 mg every 6–8 h).[ 72 ] For moderate-to-severe pain – as commonly encountered after periodontal flap surgery, implant placement, or surgical extractions – higher-dose or different class (ketorol 20 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age: 17–64 years) not more than 5 days, or 10 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age: ≥65 years, renally impaired, and/or weight <50 kg) not more than 5 days) NSAIDs or combination therapy may be required.[ 26 ] In rare cases of severe surgical trauma, a short course of an NSAID–opioid combination may be justified for rescue analgesia.[ 14 ]

Figure 2 Clinical decision-making flow chart for the management of dental pain
Figure 2 Clinical decision-making flow chart for the management of dental pain

Combination analgesic drug therapy

Combining agents with different mechanisms of action enhances analgesic efficacy while reducing the required dose of each drug. The most evidence-based combination in dentistry is ibuprofen plus paracetamol, which has demonstrated superior pain control compared to either drug alone.[ 33 ] For patients who cannot tolerate NSAIDs, paracetamol combined with a weak opioid (e.g. codeine or tramadol) may be considered, although risks of sedation, dependency, and GI side effects limit routine use.[ 83 ]

Systemic versus local use of analgesics

Systemic administration (oral or parenteral) remains the standard for most dental pain scenarios. However, local delivery systems, such as intrapocket NSAID gels (diclofenac, ketorolac) or local anesthetic infiltration with long-acting agents (bupivacaine), may offer targeted pain relief with reduced systemic exposure.[ 84 ] Sustained-release local drug delivery systems in periodontal pockets have shown adjunctive benefits in reducing inflammation and discomfort following surgical or non-surgical therapy.[ 85 ]

Antibiotics (only if infection present or risk exists)

Antibiotics should not be prescribed solely for pain control, as they have no intrinsic analgesic properties.[ 86 ] Their use is indicated only when clinical evidence of infection exists (e.g. acute abscess, spreading cellulitis, and pericoronitis with systemic involvement) or when the risk of infection is high due to patient-related or procedure-related factors.[ 87 ] Overuse contributes to antimicrobial resistance and adverse events; hence, antibiotic stewardship must be observed.[ 41 ]

Adjunctive drugs – Corticosteroids and enzymes

Corticosteroids (e.g. dexamethasone and prednisolone) have strong anti-inflammatory properties and can be used as adjuncts to reduce postoperative pain, swelling, and trismus, particularly after third molar surgery and implant placement.[ 65 ] A single perioperative dose of dexamethasone has been shown to significantly improve patient comfort without notable adverse effects.[ 88 ]

Proteolytic enzymes such as serratiopeptidase and trypsin–chymotrypsin combinations have also been employed to reduce edema and accelerate resolution of inflammatory symptoms, though evidence supporting their routine use is less robust compared to corticosteroids.[ 89 ]

Special considerations

Children: Age-appropriate analgesics and behavioral approaches

Pain control in children requires consideration of developmental, pharmacological, and psychological aspects. Paracetamol (10–15 mg/kg every 4–6 h, not exceeding 60 mg/kg/day) and ibuprofen (5–10 mg/kg every 6–8 h, not exceeding 30 mg/kg/day or Ketorol 20 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age 17–64 years) not more than 5 days, or 10 mg once, then 10 mg q4–6 h, as needed, not >40 mg/day (adult age ≥65 years, renally impaired, and/or weight <50 kg) not more than 5 days remain the most recommended first-line analgesics for dental pain in children.[ 90 91 ] Aspirin should be avoided due to the risk of Reye’s syndrome.[ 92 ]

Non-pharmacologic strategies – including behavior management techniques, distraction, and parental involvement – play a critical role in reducing anxiety and improving pain tolerance.[ 93 ] Early use of local anesthesia and age-appropriate explanations further reduces the need for systemic medication.

Pregnancy: Safe medications and minimal interventions

Pregnancy demands a cautious approach to analgesic use. Paracetamol is considered the safest option throughout all trimesters when used at therapeutic doses.[ 94 ] NSAIDs may be used with caution in the second trimester but are generally contraindicated in the third trimester due to risks of premature closure of the ductus arteriosus, oligohydramnios, and prolonged labor.[ 95 ] Opioids should be avoided unless absolutely necessary and then only under medical supervision due to the potential for neonatal respiratory depression.[ 96 ] Nonpharmacologic methods, including reassurance and short appointments, should be prioritized, and elective invasive procedures are best deferred until after delivery.[ 97 ]

Medically compromised patients: Drug interactions and organ considerations

In patients with hepatic or renal impairment, analgesic prescribing requires dose modification and close monitoring. Paracetamol should be avoided or strictly limited in advanced liver disease, while NSAIDs should be avoided in chronic kidney disease due to risks of nephrotoxicity and GI bleeding.[ 98 99 ]

Drug interactions are another concern: NSAIDs may antagonize antihypertensives and potentiate anticoagulants, while opioids can interact with sedatives or antidepressants, enhancing central nervous system depression.[ 100 ] A detailed medical history and consultation with the patient’s physician are essential before initiating therapy.

Neuropathic pain: Role of antidepressants, anticonvulsants, and referral

Dental pain of neuropathic origin, such as atypical odontalgia, burning mouth syndrome, or post-traumatic trigeminal neuropathy, requires a different therapeutic approach. Conventional NSAIDs or opioids are usually ineffective.[ 101 ] Antidepressants (tricyclics like amitriptyline or SNRIs like duloxetine) and anticonvulsants (gabapentin, pregabalin, and carbamazepine) are considered first-line agents for neuropathic pain.[ 102 103 ] These drugs should be prescribed cautiously, ideally by or in consultation with a specialist in oral medicine, neurology, or pain management. Early recognition and referral are critical to prevent chronicity and improve quality of life.[ 104 ]

CONCLUSION

Effective pain management in dentistry requires a proactive and individualized approach, tailored to the patient’s condition, medical background, and the anticipated level of pain. Modern guidelines emphasize that no single analgesic regimen is universally applicable; rather, clinicians should assess patient-specific factors – including age, comorbidities, ongoing medications, and psychological profile – before prescribing.[ 7 9 14 ] A balanced strategy, integrating pharmacological and nonpharmacological measures, ensures optimal outcomes and minimizes adverse effects.

Communication and patient education are equally critical. Studies show that when patients are given clear explanations about the cause of their pain, expected course, and rationale for treatment, they report reduced anxiety, higher satisfaction, and improved compliance with prescribed regimens. Simple interventions such as explaining the importance of adherence to dosing schedules, warning about potential side effects, and setting realistic expectations can significantly improve pain management outcomes.

Finally, the importance of continuous professional development cannot be overstated. With evolving evidence on analgesics, combination therapy, and adjunctive measures, dentists must remain updated with international guidelines and consensus statements. Regular participation in continuing education programs, critical appraisal of new research, and interdisciplinary collaboration strengthen the clinician’s ability to provide safe, effective, and evidence-based care.

In summary, individualized pain management – grounded in scientific evidence, effective communication, and continuous learning – forms the cornerstone of modern dental practice. Such an approach not only alleviates pain but also fosters patient trust, improves long-term oral health outcomes, and enhances overall quality of care.

Conflicts of interest

There are no conflicts of interest.

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ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

Реквизиты и контакты