Endodontic anaesthesia in the hot tooth: integrating mechanisms, clinical evidence, and practice-based clinical insights

Introduction

The main reason patients often postpone dental visits is due to the pain they might feel, which is also the main source of stress for dentists (1,2). Though anaesthetic techniques in routine endodontic therapy on asymptomatic teeth are usually easy to perform and extremely predictable, the situation changes drastically in teeth with symptomatic irreversible pulpitis. A single inferior alveolar nerve block (IANB), for example, can provide effective anaesthesia for restorative procedures for mandibular molars, but has a success rate of only 15–30% in case of symptomatic molars. This case with irreversible pulpitis is more commonly referred to as the “hot tooth” (2,3). The clinician might be able to achieve entry into the dentin or may reach near the pulp chamber, but often the pain is so bad that the patient just refuses to continue with the treatment. This results in a procedure that should have been routine and easy, and instead turns into a large source of stress for both the operator and the patient.

The inflammatory pathways create a unique mechanism for resisting anaesthetic action. In the inflamed soft tissues, the tissue pH is lower, resulting in fewer anaesthetic molecules in the lipid-soluble form (1,4). This, in turn, limits the anaesthetic’s ability to cross the neural membrane and impede the activity of sodium channels (for infiltration anaesthesia). Moreover, inflammatory mediators such as prostaglandins, cytokines, and bradykinin act to make nociceptors hyper-reactive and sensitized, that may fire in response to minimal stimuli (1,5).

However, the inflammatory response and tissue environment is only one piece of the puzzle. The anatomy also plays a critical role. The unique anatomical features of the mandibular posterior region, such as the presence of thick, cortical bone and unpredictable branching of the nerves, create challenges (6). Additionally, there are accessory innervations that may allow the peripheral tissues to bypass the blocked inferior alveolar nerve (7). Even when the anaesthetic has been deposited in the appropriate place, fascial barriers and vascular uptake may affect the distribution of anaesthetic solution before the solution has access to the nerve trunk.

In contrast to focusing solely on the biological part of the story, one must also consider the psychological aspect, which holds significant weight as well. Patients with a history of painful experiences in dentistry often arrive to their appointments anxious, with their sympathetic nervous system already activated (8). This subsequently becomes a self-fulfilling cycle in which fear of pain lowers pain thresholds and amplifies nociceptive input, thereby intensifying the patient’s pain experience (9-11). The anxiety drives the pain, and in the midst of this self-perpetuating system, the distress felt by the patient is amplified.

Over the years, this problem has been the target of multiple refinements, from changing anaesthetic formulation and buffering agents to the use of adjunct injection techniques such as intraligamentary or intraosseous injection (2,12,13). Preoperative non-steroidal anti-inflammatory drugs (NSAIDs) or the use of corticosteroids aim to alleviate the inflammation before anaesthesia (14). Unfortunately, none of these methods has given 100% success rates. Why anaesthesia fails and how to fix it must be viewed from the broadest angle possible. The “hot tooth” is a clinical problem. By recognising the intertwined biological and emotional dimensions of pain, the clinician can achieve some kind of predictability. The objective of this clinical practice review is to integrate mechanistic insights, clinical evidence, and practical strategies into a structured approach for managing anaesthetic failure in mandibular molars with symptomatic irreversible pulpitis. This review was designed as a narrative, clinically oriented synthesis rather than a systematic review or meta-analysis. The literature was selectively reviewed to integrate mechanistic evidence, randomized clinical trials, and practice-based insights relevant to the management of the hot tooth. Given the heterogeneity in study designs, outcome definitions, and anaesthetic protocols, pooled effect sizes, combined summary tables, and confidence intervals were not feasible.

Mechanisms of anaesthetic failure

The failure of anaesthesia in mandibular molars with symptomatic irreversible pulpitis is more than a simple factor event. Its failure is the end result of anatomical, physiological, biochemical, and psychological interactions that collectively compromise the effective action of local anaesthetics.

Anatomical considerations

Successful administration of an anaesthetic relies on an accurate assessment of the anatomical structures involved. In the context of an IANB, the anaesthetic solution must be delivered at the inferior alveolar nerve of the pterygomandibular space (PMS) (6,15). This is a conformed, albeit narrow and variable, space bordered by the medial pterygoid muscle, ramus of the mandible, and the parapharyngeal fascia. Throughout this space, the nerve runs close to several arteries and veins, and other fascial septa, which can potentially impede the movement of the anaesthetic solution (6,15,16).

Inaccuracies with the angulation of the needle, its insertion point, and overall depth can result in the anaesthetic being deposited too anterior to the sphenomandibular ligament or, on the other hand, too medial to the bone. Consequently, as a result of this placement, there will be a poor contact near the nerve trunk. Additionally, anatomical variations, such as a high mandibular foramen, bifid mandibular canal, or those involving accessory innervation from the mylohyoid, lingual, or buccal nerves, can affect the anaesthesia (15-19).

The mandible’s dense cortical bone also constricts the lateral diffusion of anaesthetic molecules. This is a sharp contrast with the maxilla, which has a more porous trabecular bone. Therefore, while the same anaesthetic technique is more likely to be successful in the upper jaw, it is more likely to be unsuccessful in the lower posterior region (20,21).

Biochemical barriers in inflammation

The local tissue environment of a particular region is radically transformed by the process of inflammation. In the case of symptomatic irreversible pulpitis, the pulp and the surrounding tissue undergo increased metabolic processes, and, as a result, inflammation and the by-products are lactic acid. The pH of normal tissue is around 7.4, but in the case of severely inflamed pulps, it is essentially 6.0 or lower (1,22). Local anaesthetics, such as lidocaine, exist in equilibrium as both an ionised (charged) form and a non-ionised (uncharged) form. Only the non-ionised molecules are capable of crossing the membrane of a nerve. In an acidic environment, there is a shift in this equilibrium towards the ionized form, which results in the formation of a deficit of molecules that would be able to cross the membrane of the nerve (1).

Although some anaesthetics may reach a nerve, inflammation decreases their binding efficiency. Prostaglandins, bradykinin, and cytokines sensitize nociceptors and promote the upregulation of tetrodotoxin-resistant (TTX-R) sodium channels (2,5,23). These sodium channels, especially the subtypes Nav1.8 and Nav1.9, are resistant to anaesthetics. Hence, despite the deposition of a local anaesthetic solution, a constant concentration of Nav1.9 may still function (24), and the nerve remains capable of transmitting and propagating nociceptive signals. Failure is further compounded by the vascular changes that happen with the inflammation. There is a widening of the capillaries and a raised permeability that increases the uptake of anaesthetic solution.

Neural plasticity and central sensitization

The nervous system also adapts when there is persistent pain, and this is called central sensitization (25). From the inflamed pulp, there is persistent nociceptive input that leads to the hyperexcitability of the spinal trigeminal nucleus neurons (5). This means that stimuli such as light pressure or vibration can now be perceived as painful stimuli. This hypersensitivity is sustained by excitatory neurotransmitter release, such as glutamate and substance P, in the central pathways (25,26).

Psychological and emotional modulation of pain

Pain extends beyond physiology and represents a complex interaction between perception, anticipation, and memory (11,27). Patients that have had unpleasant dental experiences are more likely to be anxious about upcoming appointments due to learned anticipation of pain (8,9,28). This apprehension activates the sympathetic nervous system, resulting in an increase in adrenaline production, heart rate, and muscle tension. Moving from apprehensive to fully engaged fight-or-flight mode increases pain sensitivity and reduces the threshold necessary to trigger pain. Even a gentle dental drill, in the absence of analgesia, and below the pain threshold, may trigger a pain response.

The PMS and the volume of anaesthetic solution

The PMS is a conical space having the medial pterygoid muscle and ramus of the mandible and parapharyngeal fascia as borders (18). Within the space, the inferior alveolar nerve and its accompanying structures (vessels, connective tissue, and fascial layers) traverse, and all of these structures contribute to the varying degrees of efficacy of an anaesthetic diffusion. It is common clinical practice to administer 1.8 mL of local anaesthetic; however, multiple studies have demonstrated that this volume may be insufficient in cases of symptomatic irreversible pulpitis (29,30). Anatomical and radiological research of the PMS has shown that it is able to accommodate just above 2 mL, and this volume can increase further (18). This clinical observation generated the so-called “volume hypothesis”, which posits that an appropriate volume of local anaesthesia can overcome the spatial and fascial boundaries of the anatomical area to achieve anaesthetic success. In the case of IANB for symptomatic irreversible pulpitis, clinical studies have shown that the success rates approximate doubled if the volume of anaesthetic injected is increased from 1.8 to 3.6 mL (31). It is hypothesized that the larger volume of local anaesthetic is able to achieve thorough diffuse-infiltration of the anaesthetic, resulting in blockade of more of the sodium channels adjacent to the nerve that are responsible for impulse transmission. Provided that an adequate and slow technique is used and proper aspiration is performed, this increased volume also does not carry the risk of increased systemic toxicity and/or complications. However, routine use of higher volumes should be individualized, especially in patients with low body weight, anatomical constraints, or heightened sensitivity to epinephrine.

Unpredictable diffusion: the speed of injection and the head position

The diffusion of local anaesthetic that has been deposited into the PMS is one of the most unpredictable factors. Even with accurate needle placement and volume of anaesthesia, factors such as tissue resistance, fascial compartmentalisation, and vascular uptake of the anaesthetic, which are all beyond the clinician’s direct control, may lead to incomplete or delayed anaesthesia.

Literature has shown that changing mechanical parameters, such as speed of injection or head orientation, provides little to no benefit in improving the diffusion of anaesthetic solution. For instance, the speed of injection, whether rapid or slow, did not differ with respect to the success of the IANB (32). With sufficient volumes of anaesthetic, changing the rate of delivery did not affect the diffusion of anaesthetic solution within the PMS. However, the study did point out that slow injection resulted in a reduction of the injection pain, thus improving patient comfort (32). Therefore, the clinical advantage of slow injection lies in the fact that it improves the patient’s tolerance of the procedure (or their comfort) rather than increasing the efficacy of anaesthesia.

Another study sought to determine if head position could affect the anaesthetic spread due to gravity (33). The hypothesis was that angling the head toward or away from the injected side would enhance control of the directional flow of anaesthetic. However, the results showed statistically insignificant outcomes of anaesthetic success across the positions, reinforcing that gravity has little/no effect on the diffusion of anaesthetic within the PMS. In this case, diffusion is much more determined by the internal fascial and vascular structures than the position of the patient.

In order to address barriers to diffusion, in addition to mechanical alterations, a wide variety of chemical methods have been attempted. Hyaluronidase (34-37), which is added to anaesthetic solutions, is able to break down the hyaluronic acid present in the connective tissue, lowering the viscosity of the tissue and allowing for an easier spread of the anaesthetic. Even though it has a higher and more rapid onset of numbness, the success of the IANB is still inconsistent. The addition of sodium bicarbonate to the anaesthetic solutions increases the pH of the solution, which increases the amount of non-ionized, active anaesthetic able to cross the membrane (38). Buffering of local anaesthetic solutions with sodium bicarbonate increases the proportion of the non-ionized base, thereby accelerating the onset of anaesthesia and potentially reducing injection discomfort. Even though it increases the onset of the numbness and reduces the pain of the injection, it does not rectify the mechanical issues of the dense connective tissue.

Inflammation, prostaglandins, and preoperative modulation

Upon inflammation, there is a reduced tissue pH and a reduced proportion of non-ionised anaesthetics. This blocks the effective movement of anaesthetic solution through the nerve membrane. Even when the solution is able to cross the nerve membrane, there is still the barrier of receptor modification and neural sensitization. The arachidonic acid pathway is the key trigger of biochemical inflammation, and in particular, inflammation from chemical mediators: the cytokines, leukotrienes, and prostaglandins (39-41). NSAIDs have been used to reduce the effects of inflammation. By blocking the cyclooxygenase (COX) enzymes, NSAIDs garner a reduction in the synthesis of prostaglandins and theoretically reduce the overall nociceptor sensitization (42,43). There are a number of studies that test and evaluate the use of ibuprofen, diclofenac, and ketorolac preoperatively to evaluate the efficacy of the IANB, and they have shown some success in the analgesic group when compared to the placebo (44-48). Unfortunately, though these studies have shown some benefit, the results were statistically insignificant. This may be due to timing, as patients have severe pulpitis and a significant amount of time has passed, where the inflammatory cascade is certainly advanced, and receptor sensitization has already occurred. Studies indicate that premedication with high doses of ibuprofen (400–600 mg) or diclofenac certainly has the potential to improve outcomes and does appear to be best if given prior to the inflammatory cascade peaking (13).

The corticosteroids have a strong effect due to the specific point of the system they act upon. Corticosteroids operate on the higher levels of the inflammatory cascade. These ease the activity of phospholipase A₂, thus inhibiting the pathways of COX and lipoxygenase as well as the release of arachidonic acid from the membranes of the cell (14,43). Among other corticosteroids, dexamethasone is the most examined and studied drug. Statistically significant higher levels of success were seen using preoperative doses of dexamethasone, both systemically and through intraligamentary injection (44,49,50).

The pain continuum: preoperative and intraoperative pain correlation

Patients that enter the procedure room with high preoperative pain scores are almost guaranteed to have high intraoperative pain scores as well. In a prospective study, over 170 patients quantified this relationship (51). Those with mild preoperative pain achieved 33% anaesthetic success, whereas those with severe pain achieved only 16%. The correlation between initial and operative pain scores was strongly positive. These results illustrate how inflammatory load and central sensitisation at presentation directly predict the clinical outcome. Preoperative counselling, therefore, becomes part of the anaesthetic plan. When patients understand that additional injections or supplemental methods may be needed, their anxiety decreases, and cooperation improves. Incorporating short-acting anxiolytics or nitrous oxide can further reduce sympathetic arousal and raise the pain threshold.

Strategies to improve anaesthetic success

In the field of endodontics, the ability to provide optimal anaesthesia for patients with symptomatic irreversible pulpitis of the mandibular molars remains one of the greatest challenges. Even with the use of the proper technique and sufficient volume of local anaesthesia, the IANB is often rendered ineffective due to the presence of inflammation, nerve changes, and alterations in innervation and anatomy. As the years have gone by, numerous techniques have been developed to improve the reliability of obtaining anaesthesia. These methodologies include, but are not limited to, supplemental infiltration, supplemental anaesthetic volume optimisation, adjustment of the anaesthetic agent, increase of the vasoconstrictor concentration, and the variation of the techniques for administering the nerve block, to name a few. When integrated, these techniques represent a more effective, multifaceted method for addressing the problem of the “hot tooth”.

Supplemental buccal infiltration with articaine

When IANB is insufficient to achieve the desired level of anaesthesia, adjunctive buccal infiltration with 4% articaine has demonstrated significant effectiveness (21,44,52). In practice, articaine infiltration following ineffective blocks has been shown to significantly increase rates of success. This is most likely due to the chemical structure of articaine, which contains a thiophene ring that increases the drug’s lipid solubility and, thus, enhances diffusion through the relatively dense cortical bone of the mandible (53).

Effects of volume of supplemental articaine infiltration

The next issue to be investigated is whether larger volumes of anaesthetic are associated with improved success. In one multicentre clinical study where success rates of infiltration with 1.8 vs. 3.6 mL of 4% supplemental buccal infiltration of articaine were evaluated, success rates were statistically comparable at 62% vs. 64% (52). This implies that after saturating the infiltration site, the addition of more anaesthetic is of little or no value. Thus, the limiting factor is not the quantity of anaesthetic deposited, but rather the infiltration, or the permeability of the bone and soft tissue in the inflamed area.

Anaesthetic solutions

The level of anaesthesia may be influenced by the choice of anaesthetic agent. Lidocaine, articaine, and bupivacaine are the likely primary agents for IANB and have been studied comparatively for their effectiveness in symptomatic irreversible pulpitis. Their success rates were about 23% for lidocaine, 33% for articaine, and 17% for bupivacaine when given as a primary IANB injection (54). This suggests that no single agent completely overcomes the anaesthetic resistance due to inflammation. Compared to its primary block use, articaine does have its own benefits when used as buccal infiltration.

Effect of epinephrine concentrations

While higher levels of epinephrine do in fact lead to a prolonged time of effect, it does not show as much benefit when we consider cases of irreversible pulpitis. In fact, research has shown no clear or significant improvement when comparing 1:80,000 to 1:200,000 when considering anaesthetic success or pulpal anaesthesia (55). Nociceptor sensitisation and an acidic tissue pH represent the principal contributors to anesthetic failure, rather than rapid vascular washout alone. Although soft tissue anaesthesia is prolonged via higher concentrations of epinephrine, it does not override the biochemical barriers of the pulp. In addition, higher epinephrine solutions are more acidic, which can lead to greater pain upon injection (1).

Alternative block techniques

When conventional IANB fails, alternative block techniques can be invaluable in extending anaesthetic coverage and improving reliability. The Gow-Gates mandibular nerve block is one such technique. By targeting the neck of the mandibular condyle and depositing the anaesthetic near the mandibular nerve trunk before its divisions, the Gow-Gates block anaesthetises a broader area, including accessory branches such as the mylohyoid, lingual, and buccal nerves (56-61). Clinical evaluations have shown that it achieves a higher success rate compared to the traditional Halstead technique, particularly in patients where accessory innervation contributes to anaesthetic failure (56).

Another valuable alternative is the Vazirani-Akinosi closed-mouth technique, which targets the mandibular nerve and its branches in the superior aspect of the PMS (56). This technique is especially useful in patients with limited mouth opening or trismus, where conventional access is restricted. Although its overall success rate is slightly lower than that of the Gow-Gates approach, it offers consistent soft tissue anaesthesia and is technically easier to perform in certain anatomical conditions.

Supplementary and rescue anaesthetic techniques

Intraosseous injection

Intraosseous anaesthesia involves perforation of the cortical plate and direct injection into the cancellous bone (62,63). It provides pulpal anaesthesia in an almost instant manner. The chief limitation of this method is the need for a special apparatus. The cost and the need for specialised equipment slightly limit this method from being used routinely worldwide.

Intrapulpal injection

Intrapulpal injection is the ultimate rescue technique when all other methods have failed. The anaesthesia is almost instant. The only limitation is the momentary pain during the administration of the injection. The type of the solution injected is not what determines the efficacy of the technique, but rather the back-pressure (64,65).

Intraligamentary injection

Intraligamentary injections (periodontal ligament injections) have become a pivotal adjunct to IANB when obtaining pulpal anaesthesia in some lower molars with symptomatic irreversible pulpitis. Historically viewed as a last resort, it has become a proven authoritative supplement with clinical history and documentation to support it. Intraligamentary injections consist of the delivery of anaesthetic solution, under pressure, into the gingival sulcus adjacent to the root of the tooth, usually at the mesiobuccal and distobuccal line angles. The anaesthetic solution is forced to flow through the cribriform plate into the cancellous bone surrounding the root apex to anaesthetize the terminal nerve endings (66-68). The periodontal ligament has been documented to help facilitate the solution as a conduit, and with this technique, the injection is a practical intraosseous without needing to perforate the cortical bone.

The level of intraligamentary injection anaesthesia depends on several clinical factors, which result in a success range of 48% to 92% for intraligamentary anaesthesia, according to clinical literature (66,69). The factors are anaesthetic type, dose/volume, and concentration of epinephrine in the solution. In a randomised controlled trial, patients received 4% articaine (1:100,000 epinephrine) or 2% lidocaine (1:80,000 epinephrine) as a supplementary intraligamentary injection after failed IANB, and success rates were documented (70). The success rates in the two groups were 66% and 78%, respectively, which were not statistically significant, and thus the conclusion is contrary to the assumptions that are often made, where articaine is considered better. Similar studies have strengthened this conclusion, observing that both articaine and lidocaine yield satisfactory results when adequate technique and injection pressure are employed. Another clinical study investigated increasing the volume of 2% lidocaine from 0.2 to 0.6 mL per root as a method to improve anaesthetic success. The higher volume group showed a significant rise in success rate from 64% to 84% (71). This finding was in contradiction to earlier recommendations that limited the intraligamentary injection volume to 0.2 mL per root and demonstrated that a moderate increase in volume was able to enhance the distribution of the solution within the cancellous bone, thereby optimizing the pulpal tissue desensitization. Other literature (72,73) supported that higher per-root volumes of up to 0.7–0.9 mL did enhance the success rates to above 80% when computer-controlled delivery systems were used. A randomised control trial investigated the 2% lidocaine formulations with either 1:80,000 or 1:200,000 epinephrine administered as supplemental intraligamentary injection (74). The results indicated a clear advantage for the higher concentration, with anaesthetic success of 82% compared to 57% in the lower concentration group. These data underscore that a stronger vasoconstrictor concentration enhances local drug retention and depth of anaesthesia.

Supplemental techniques such as intraligamentary and intraosseous injections may be associated with transient tachycardia, palpitations, and discomfort, particularly when epinephrine-containing solutions are used intraosseously. These effects are typically short-lived but warrant caution in patients with cardiovascular disease. Mitigation strategies include slow injection, aspiration, dose limitation, and avoidance of intraosseous delivery in high-risk individuals. When multiple anaesthetic techniques are combined during a single appointment, clinicians must remain within recommended maximum doses. For lidocaine, the maximum dose should not exceed 4.4 mg/kg (up to 300 mg), and for articaine, 7 mg/kg. Cumulative epinephrine should generally be limited to 0.04 mg in cardiovascular-compromised patients and 0.2 mg in healthy adults. Particular caution is advised with intraosseous injections due to rapid systemic uptake and transient cardiovascular effects.

Management of the hot tooth must be individualized in special patient populations where pharmacologic limits, systemic safety, and physiologic considerations influence anaesthetic choice and delivery. In pregnant patients, lidocaine with low concentrations of epinephrine remains the preferred local anaesthetic due to its favourable safety profile. Articaine and other agents should be used cautiously, and elective escalation to multiple supplemental injections should be avoided unless absolutely necessary. Emphasis should be placed on achieving adequate anaesthesia through optimized primary techniques, minimal effective volumes, and careful aspiration. In paediatric patients, strict adherence to weight-based maximum dosage limits is essential. Higher anaesthetic volumes and repeated supplemental injections may rapidly approach toxic thresholds. Consequently, the stepwise protocol should prioritize technique accuracy and behavioural management rather than volume escalation. Intraligamentary injections may be used judiciously, while intraosseous techniques are generally discouraged due to limited safety data in children. In patients receiving anti-coagulants, IANB is generally considered safe when international normalized ratio values are within therapeutic range; however, deep needle penetration and multiple punctures should be minimized. Supplemental intraligamentary injections may be preferred over intraosseous techniques, as the latter may increase bleeding risk. Careful aspiration and slow injection are mandatory. In patients with cardiovascular disease, cumulative epinephrine dosage should be strictly limited, and anaesthetic escalation should proceed cautiously. Intraosseous injections containing epinephrine may cause transient tachycardia and should be avoided or used only when the benefits clearly outweigh the risks. In such patients, emphasis should be placed on reducing inflammatory mediators preoperatively, optimizing anaesthetic technique, and using the lowest effective vasoconstrictor dose.

Integrating clinical evidence into a stepwise protocol

The following stepwise clinical protocol is recommended for the effective anaesthetic management of mandibular molars diagnosed with symptomatic irreversible pulpitis. The process begins with accurate identification of a “hot tooth”, which is typically characterized by spontaneous, lingering pain and a positive response to thermal testing. Radiographic assessment often reveals deep carious lesions in proximity to the pulp and, in some cases, signs of apical periodontitis.

Once diagnosis is confirmed, the first line of anaesthetic management involves the administration of a standard IANB using 3.6 mL of 2% lidocaine with 1:80,000 or 1:100,000 epinephrine. After a waiting period of 5 to 7 minutes, the presence of lip numbness must be verified. If lip numbness is absent, the IANB should be repeated, or an alternative block technique, such as Gow-Gates or Akinosi, may be considered.

If lip numbness is present, the next step involves supplemental buccal infiltration with 1.0 to 1.8 mL of 4% articaine with 1:100,000 epinephrine in the buccal vestibule adjacent to the affected tooth. Following a 5-minute waiting period, a cold test should be performed again to assess pulpal response.

If the tooth no longer responds to cold, access cavity preparation may be initiated. If the tooth remains responsive or if the patient experiences pain upon access, a second IANB should be administered using 2% lidocaine. Following this, access preparation should be reattempted.

If pain persists during access, a supplemental intraligamentary (periodontal ligament) injection should be employed. This involves administering 0.2 to 0.6 mL of 2% lidocaine with 1:80,000 epinephrine per root using a high-pressure or dedicated periodontal ligament syringe. An onset of anaesthesia is typically achieved within 1 to 2 minutes. If the patient is now comfortable, treatment should proceed.

In the event that pain continues despite intraligamentary anaesthesia, intrapulpal anaesthesia becomes the final and definitive technique. The anaesthetic solution—any available local anaesthetic—must be delivered directly into the pulp chamber with firm back pressure, which is the primary determinant of success for this technique. The recommended stepwise anaesthetic protocol is illustrated in Figure 1.

Figure 1 Stepwise clinical protocol for anaesthetic management of mandibular molars with symptomatic irreversible pulpitis. +ve: positive; -ve: negative. IANB, inferior alveolar nerve block; IL, intraligamentary; infil, infiltration.

Following treatment, appropriate postoperative analgesics, such as NSAIDs or corticosteroids, should be prescribed based on the severity of inflammation and patient discomfort. Adverse events should be monitored, and all steps taken, including anaesthetic techniques used, volumes administered, and patient responses, must be documented thoroughly.

This protocol emphasizes a rational, escalatory approach, incorporating both pharmacological and technical strategies. By following this structured guideline, clinicians can improve their success in achieving profound pulpal anaesthesia in challenging endodontic cases and enhance patient comfort throughout the procedure.

The human element in pain control

Technology alone cannot guarantee comfort. The clinician’s voice, confidence, and empathy shape the patient’s pain perception as much as the pharmacology does. Explaining each step, acknowledging fear, and maintaining steady communication activate cognitive reassurance that dampens limbic anxiety circuits. Patients who feel understood exhibit lower physiological arousal and higher tolerance for discomfort (27).

For anxious individuals, pre-appointment relaxation, music therapy, or guided breathing can complement pharmacologic sedation. Even small gestures, such as maintaining eye contact and checking comfort before instrumentation, strengthen trust and reduce the subjective intensity of pain. In managing the hot tooth, empathy is as critical as epinephrine (28).

Conclusions

The “hot tooth” embodies the intersection of biology, technique, and human perception. Anaesthetic failure is rarely due to a single cause; it reflects the combined influence of anatomy, inflammation, neural sensitisation, and emotion. Understanding these layers allows clinicians to plan methodically rather than react defensively.

Effective management begins with acknowledging the challenge, pre-empting inflammation pharmacologically, and applying a sequence of escalating techniques—each grounded in evidence rather than routine. Among these, preoperative dexamethasone, adequate anaesthetic volume, articaine infiltration, and intraligamentary injection stand out as the most reliable allies.

Ultimately, success is measured not only in the absence of pain but in the restoration of patient trust. When science and empathy converge, even the most resistant tooth can be rendered painless, reaffirming the essence of endodontics: to heal without hurting.

Acknowledgments

None.

Footnote

Peer Review File: Available at https://joma.amegroups.com/article/view/10.21037/joma-2025-1-38/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://joma.amegroups.com/article/view/10.21037/joma-2025-1-38/coif). V.A. serves as an unpaid editorial board member of Journal of Oral and Maxillofacial Anesthesia from January 2026 to December 2027. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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