Atypical odontalgia - pathophysiology and clinical management.

Atypical odontalgia (AO) is a chronic form of dental pain without signs of pathology. Several hypotheses have been put forward regarding the pathophysiology. AO has been proposed to be psychogenic, vascular, neuropathic or idiopathic. The scientific evidence supporting or rejecting these hypotheses are reviewed in this paper. At this time, the best supported hypothesis is that AO is a neuropathic pain condition. Relevant differential diagnoses, such as odontogenic pain, sinusitis, trigeminal neuralgia among others, are presented and the evidence regarding possible management strategies is reviewed. A treatment algorithm for AO is proposed based on the rather scarce scientific evidence available and inspired by a similar treatment algorithm for peripheral neuropathic pain. The proposed strategy involves an interdisciplinary approach including patient education, psychological counselling, topical and systemic medication and, importantly, avoidance of invasive treatments like surgery and endodontics. Two illustrative cases are presented.     

Atypical odontalgia – pathophysiology and clinical management

Summary  Atypical odontalgia (AO) is a chronic form of dental pain without signs of pathology. Several hypotheses have been put forward regarding the pathophysiology. AO has been proposed to be psychogenic, vascular, neuropathic or idiopathic. The scientific evidence supporting or rejecting these hypotheses are reviewed in this paper. At this time, the best supported hypothesis is that AO is a neuropathic pain condition. Relevant differential diagnoses, such as odontogenic pain, sinusitis, trigeminal neuralgia among others, are presented and the evidence regarding possible management strategies is reviewed. A treatment algorithm for AO is proposed based on the rather scarce scientific evidence available and inspired by a similar treatment algorithm for peripheral neuropathic pain. The proposed strategy involves an interdisciplinary approach including patient education, psychological counselling, topical and systemic medication and, importantly, avoidance of invasive treatments like surgery and endodontics. Two illustrative cases are presented.     

Atypical odontalgia: a review

Since persistent and chronic pain is more common in the head and neck region than in any other part of the body, dentists are more likely to encounter these rather complex cases in their practices. This article is a review and update on atypical odontalgia (AO). AO is a persistent neuropathic pain which may be initiated after deafferentiation of trigeminal nerve fibers following root canal treatment, apicectomy, or tooth extraction, or it may be of idiopathic origin. Details concerning its characteristics, pathophysiology, diagnostic criteria, differential diagnosis, and treatment are made. The aim of this article is to help the clinician with the diagnosis and management of AO. The prognosis for AO is most often only fair, and the administration of tricyclic antidepressants often resolves symptoms. Invasive and irreversible treatment attempts are not recommended.     

Atypical odontalgia--a form of neuropathic pain that emulates dental pain

In order for the neuropathic pain associated with AO to occur in the oral or facial area, a deafferentation process must be initiated as previously explained. Deafferentation happens when there is a trauma to tissues including, but not limited to, endodontic therapy, a surgical extraction or even a simple one, a deep scaling, an injurious dental injection, and even the placement of a crown. Thankfully, most patients heal uneventfully. Apparently a small percentage of patients have a genetic predisposition to deafferentation pain. In reviewing articles on this subject, there is often material about the inadvertent dental treatment of patients with AO. Many patients often have undergone numerous invasive procedures in an effort to ameliorate pain. It is not possible to read a research paper about AO without reading about the recurrent theme of either overtreatment or unnecessary treatment. Caution should be exercised when performing endodontic therapy solely for the relief of pain without objective need for such therapy. It is common for the AO patient to undergo many other irreversible dental treatments with no resolution of pain symptoms. When the dentist encounters a patient in pain for which there is no dental connection, he or she should strongly consider referring the patient to a facility or practitioner who has expertise in dealing with the non-dental source of dental pain.     

Atypical odontalgia: a systematic review following the evidence-based principles of dentistry

Atypical odontalgia (AO) is a severe and persistent pain involving controversial pathophysiological mechanisms and clinical management. Presented here is a systematic review of the literature on AO, using the SORT criteria (Strength of Recommendation Taxonomy) to assess the level of evidence and the quality of randomized clinical trials (RCT). A total of 54 articles were obtained of which 34 belonged to level 3 evidence, 17 to level 2, and 3 to level 1. Of these, only 8 RCT had an average quality of four points. The main finding of this systematic review is that only a few studies have systematically evaluated AO. It also determines a strength recommendation of level B to the theory of neuropathic origin of pain in AO and strength of recommendation level C for the pharmacological management of this condition. The aim of this study was to carry out a systematic review of the published literature on AO in order to determine the physiopathology and treatment based on the level of scientific evidence and following the evidence-based principles of dentistry.     

An update on pathophysiological mechanisms related to idiopathic oro‐facial pain conditions with implications for management

Chronic oro‐facial pain conditions such as persistent idiopathic facial pain (PIFP), atypical odontalgia (AO) and burning mouth syndrome (BMS), usually grouped together under the concept of idiopathic oro‐facial pain, remain a diagnostic and therapeutic challenge. Lack of understanding of the underlying pathophysiological mechanisms of these pain conditions is one of the important reasons behind the problems in diagnostic and management. During the last two decades, neurophysiological, psychophysical, brain imaging and neuropathological methods have been systematically applied to study the trigeminal system in idiopathic oro‐facial pain. The findings in these studies have provided evidence for neuropathic involvement in the pathophysiology of PIFP, AO and BMS. The present qualitative review is a joint effort of a group of oro‐facial pain specialists and researchers to appraise the literature on idiopathic oro‐facial pain with special focus on the currently available studies on their pathophysiological mechanisms. The implications of the findings of these studies for the clinical diagnosis and treatment of idiopathic oro‐facial pain conditions are discussed.     

Chronic intraoral pain--assessment of diagnostic methods and prognosis

The overall goal of this thesis was to broaden our knowledge of chronic intraoral pain. The research questions were: What methods can be used to differentiate inflammatory, odontogenic tooth pain from pain that presents as toothache but is non-odontogenic in origin? What is the prognosis of chronic tooth pain of non-odontogenic origin, and which factors affect the prognosis? Atypical odontalgia (AO) is a relatively rare but severe and chronic pain condition affecting the dentoalveolar region. Recent research indicates that the origin is peripheral nerve damage: neuropathic pain. The condition presents as tooth pain and is challenging to dentists because it is difficult to distinguish from ordinary toothache due to inflammation or infection. AO is of interest to the pain community because it shares many characteristics with other chronic pain conditions, and pain perpetuation mechanisms are likely to be similar. An AO diagnosis is made after a comprehensive examination and assessment of patients' self-reported characteristics: the pain history. Traditional dental diagnostic methods do not appear to suffice, since many patients report repeated care-seeking and numerous treatment efforts with little or no pain relief. Developing methods that are useful in the clinical setting is a prerequisite for a correct diagnosis and adequate treatment decisions. Quantitative sensory testing (QST) is used to assess sensory function on skin when nerve damage or disease is suspected. A variety of stimuli has been used to examine the perception of, for example, touch, temperature (painful and non-painful), vibration, pinprick pain, and pressure pain. To detect sensory abnormalities and nerve damage in the oral cavity, the same methods may be possible to use. Study I examined properties of thermal thresholds in and around the mouth in 30 pain-free subjects: the influence of measurement location and stimulation area size on threshold levels, and time variability of thresholds. Thresholds for cold, warmth and painful heat were measured in four intraoral and two extraoral sites. Measurements were repeated 3 times over 6 weeks, using four sizes of stimulation area (0.125-0.81 cm2). The threshold levels were highly dependent on location but less dependent on measuring probe size and time variability was small, and this knowledge is important for the interpretation of QST results. Study II applied a recently developed standardized QST examination protocol (intended for use on skin) inside the oral cavity. Two trained examiners evaluated 21 pain-free subjects on three occasions over 1-3 weeks, at four sites-three intraoral and one extraoral. Most tests had acceptable reliability and the original test instruments and techniques could be applied intraorally with only minor adjustments. Study III examined the value of cone-beam computed tomography (CBCT) in pain investigations. Twenty patients with AO and 5 with symptomatic apical periodontitis (inflammatory tooth pain) participated. The results indicate that when AO is suspected, addition of CBCT can improve the diagnostic certainty compared to sole use of periapical and panoramic radiographs, especially because of the superior ability of CBCT to exclude inflammation as the pain cause. Study IV assessed the long-term prognosis of AO, and analyzed potential outcome predictors. A comprehensive questionnaire including validated and reliable instruments was used to gather data on patient and pain characteristics and pain consequences from 37 patients in 2002 and 2009. Thirty-five percent of the patients reported substantial overall improvement at follow-up, but almost all still had pain of some degree after many years. The initial high level of emotional distress was unchanged. Low baseline pain intensity predicted improvement over time.     

Neuropathic orofacial pain part 1--prevalence and pathophysiology

Neuropathic pain is defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system". Neuropathic orofacial pain has previously been known as "atypical odontalgia" (AO) and "phantom tooth pain". The patient afflicted with neuropathic oral/orofacial pain may present to the dentist with a persistent, severe pain, yet there are no clearly identifiable clinical or radiographic abnormalities. Accordingly, multiple endodontic procedures may be instigated to remove the likely anatomical source of the pain, yet the pain persists. There have been few studies and limited patient numbers investigating the condition. Two retrospective studies revealed the incidence of persistent pain following endodontic treatment to be 3-6% and 5% of patients; one author with wide experience in assessing the condition estimated its prevalence at 125,000 individuals in the USA alone. In one study, 50% of neuropathic orofacial pain patients reported persistent pain specifically following endodontic treatment. Patients predisposed to the condition may include those suffering from recurrent cluster or migraine headaches. Neuropathic pain states include postherpetic neuralgia (shingles) and phantom limb/stump pain. The aberrant developmental neurobiology leading to this pain state is complex. Neuropathic pain serves no protective function, in contrast to physiological pain that warns of noxious stimuli likely to result in tissue damage. The relevant clinical features of neuropathic pain include: (i) precipitating factors such as trauma or disease (infection), and often a delay in onset after initial injury (days-months), (ii) typical complaints such as dysaesthesias (abnormal unpleasant sensations), pain that may include burning, and paroxysmal, lancinating or sharp qualities, and pain in an area of sensory deficit, (iii) on physical examination there may be hyperalgesia, allodynia and sympathetic hyperfunction, and (iv) the pathophysiology includes deafferentation, nerve sprouting, neuroma formation and sympathetic efferent activity.     

Neuropathic orofacial pain. Part 2-Diagnostic procedures, treatment guidelines and case reports

Neuropathic orofacial pain can be difficult to diagnose because of the lack of clinical and radiographic abnormalities. Further difficulties arise if the patient exhibits significant distress and is a poor historian regarding previous diagnostic tests and treatments, such as somatosensory local anaesthetic blockade. Valuable information can be obtained by utilising the McGill Pain Questionnaire that allows the patient to choose words that describe the qualities of his/her pain in a number of important dimensions (sensory and effective). Basal pain intensity should be measured with the visual analogue scale, a simple instrument that can evaluate the efficacy of subsequent treatments. The dentist or endodontist can employ sequential analgesic blockade with topical anaesthetics and perineural administration of plain local anaesthetic to ascertain sites of neuropathology in the PNS. These can be performed in the dental chair and in a patient blinded manner. Other, more specific, tests necessitate referral to a specialist anaesthetist at a multidisciplinary pain clinic. These tests include placebo controlled lignocaine infusions for assessing neuropathic pain, and placebo controlled phentolamine infusions for sympathetically maintained pain. The treatment/management of neuropathic pain is multidisciplinary. Medication rationalisation utilises first-line antineuropathic drugs including tricyclic antidepressants such as amitriptyline and nortriptyline, and possibly an anticonvulsant such as carbamazepine, sodium valproate, or gabapentin if there are sharp, shooting qualities to the pain. Mexiletine, an antiarrhythmic agent and lignocaine analogue, may be considered following a positive patient response to a lignocaine infusion. All drugs need to be titrated to achieve maximum therapeutic effect and minimum side effects. Topical applications of capsaicin to the gingivae and oral mucosa are a simple and effective treatment in two out of three patients suffering from neuropathic orofacial pain. Temporomandibular disorder is present in two thirds of patients and should be assessed and treated with physiotherapy and where appropriate, occlusal splint therapy. Attention to the patient's psychological status is crucial and requires the skill of a clinical psychologist and/or psychiatrist with pain clinic experience. Psychological variables include distress, depression, expectations of treatment, motivation to improve, and background environmental factors. Unnecessary dental treatment to "remove the pain" with dental extractions is contraindicated and aggravates neuropathic orofacial pain.     

Blink reflexes in patients with atypical odontalgia

AIMS: To use the human blink reflex (BR) to explore possible neuropathic pain mechanisms in patients with atypical odontalgia (AO). METHODS: In 13 AO patients, the BR was elicited using a concentric electrode and recorded bilaterally with surface electromyographic (EMG) electrodes on both orbicularis oculi muscles. Electrical stimuli were applied to the skin above branches of the V1, V2, and V3 nerves and to the V branch contralateral to the painful branch. Sensory and pain thresholds were determined. The BR examination of the painful V branch was repeated during a capsaicin pain-provocation test. The data were analyzed with nonparametric statistics. RESULTS: The BR responses (R2 and R3) evoked by stimulation of V3 were significantly smaller than the BR responses evoked by stimulation of V1 and V2 (P < .004). There were no differences in BR (R2 or R3) between the painful and nonpainful sides (P > .569), and the BR (R2 and R3) was not significantly modulated by experimental pain (P > .080). The sensory thresholds were significantly lower on the painful side compared to the nonpainful side (P = .014). The pain thresholds were not different between sides (P > .910). CONCLUSION: No major differences between the V nociceptive pathways on the right and left sides were found in a relatively small group of AO patients. Future studies that compare BRs in AO patients and healthy volunteers are needed to provide further knowledge on the pain mechanisms in AO.     

Clinical management of alveolar osteitis. A systematic review

Background Alveolar Osteitis (AO) is one of the most common complications of tooth extraction. Several therapeutic interventions have been described for the treatment of AO, however, there are no treatment standardized protocols. The aim of this study was to conduct a systematic review on the efficacy in pain control of the different treatments for AO. The feasibility of the application of these interventions is also discussed.Material and Methods A structured electronic and hand search strategy was applied to PubMed, Scopus, Cochrane Library, OpenGrey, and Google Scholar between January 2010 and July 2020 to identify studies according to PRISMA guidelines. The inclusion criteria were original English and Spanish clinical trials that analyzed pain-control parameters according to visual analog scale (VAS, 0-10 scale), or pain relief patients’ percentages. Those treatments that reach VAS ≤ 4 on day 2 or before; or ≥ 85% of patients with absence of pain symptoms at day 7 or before were considered accepTable for their recommendation.Results The final review included 17 clinical trials. Among them, there were analyzed a total of 39 different AO treatments. 53,8% of the treatments fulfill the proposed parameters for pain control.Conclusions Treatment alternatives are multiple, heterogeneous, and difficult to compare. The management of AO is summarized in basic (intra-alveolar irrigation) and specific procedures (Alveogyl®, Neocones®, SaliCept Patch®, Low-Level Laser, Platelet-Rich Fibrin) that reach pain control success. They could be selected according to their availability and advantages or disadvantages. Key words:Dry socket, alveolar osteitis, treatment, management, pain control, pain relief.     

Management issues of neuropathic trigeminal pain from a dental perspective

Neuropathic trigeminal pain conditions are more common than is generally appreciated. Sites inside the mouth as well as involvement of extraoral tissues are common manifestations of these disorders. There is a general lack of recognition of the complex characteristics of neuropathic trigeminal pain that frequently lead to mischaracterization of the nature of the complaint. Dentists are in an excellent position to detect the presence of neuropathic trigeminal pain and help to provide a rational diagnosis. The high prevalence of orofacial pain of dental origin and the dramatic similarities between neuropathic orofacial pain and odontogenic and other pathologic pains in the region frequently lead to incorrect diagnoses and, more importantly, inappropriate treatments that are frequently invasive and irreversible. The records of patients presenting with neuropathic pain at our university pain clinic were reviewed to gain insight into dental factors as they related to the etiology, presentation, diagnosis, and management of neuropathic pain of the trigeminal system. Relative to etiology, the records review revealed that most onsets were associated with a specific dental treatment or odontogenic symptom that resulted in a dental diagnosis or treatment. Initial treatment modalities that either caused the pain or were used to address painful symptoms commonly included replacement of restorations, endodontic therapy, apicectomy, extraction, splint therapy, and occlusal equilibration. Correct diagnosis, and particularly early definitive diagnosis, of neuropathic trigeminal pain is crucial to avoid invasive and potentially more damaging forms of treatment.     

A unified concept of idiopathic orofacial pain: pathophysiologic features

Atypical facial pain, stomatodynia, atypical odontalgia, and some forms of masticatory muscle and temporomandibular joint disorders all seem to belong to the same group of idiopathic orofacial pain illnesses. The many common clinical features they display have been discussed in a preceding paper. Some of their common pathophysiologic mechanisms are reviewed in this article. The role of female hormones is suggested as a risk factor by the strong female prevalence and by the effects of physiologic and therapeutic modification of estrogen levels in patients with these pain conditions. Osteoporosis, which appears with menopause, and neuralgia-inducing cavitational osteonecrosis have been linked to atypical facial pain. Similar clinical features have also prompted a comparison between atypical facial pain and complex regional pain syndrome of the limbs. The presence of psychosocial factors is also a common feature, but it is not known whether these are causal or whether the pain induces the psychosocial problem. Local inflammatory, infectious, or mechanical irritation as well as minor nerve trauma are frequently reported in these conditions and can also be considered as risk factors. However, none of the above factors can currently be considered as the sole etiologic factor, and instead the following hypothesis is proposed: the idiopathic pain entities depend on one or several neuropathic mechanisms, the development of which is triggered or favored by one or several events or risk factors. Different neuropathic mechanisms may be at work: nociceptor sensitization, phenotypic changes and ectopic activity from the nociceptors, central sensitization possibly maintained by ongoing activity from initially damaged peripheral tissues, sympathetic abnormal activity, alteration of segmental inhibitory control, and hyper- or hypoactivity of descending controls. Research directions that are suggested include epidemiologic approaches to improve the clinical definition of these conditions, studies to test for the factors and mechanisms proposed, and definition of mechanism-based diagnostic and treatment strategies.     

Management issues of neuropathic trigeminal pain from a medical perspective

The purpose of this article is to review the pharmacological treatment of neuropathic trigeminal pain by means of a systematic review. A number of randomized controlled trials and important historical and uncontrolled studies in trigeminal neuralgia and postherpetic neuralgia were identified. Trigeminal neuralgia is a unique neuropathic pain disorder with a specific therapy. It does not respond to the usual drugs used for other neuropathic pains. The drug therapy of trigeminal postherpetic neuralgia is similar to that of other neuropathic trigeminal pain conditions.     

Inhibition of alveolar osteitis in mandibular tooth extraction sites using platelet-rich plasma

Alveolar osteitis (AO), also known as dry socket, continues to be a complication of tooth removal. Platelet-rich plasma (PRP) can be used to accelerate both soft and hard tissue healing. This paper is a retrospective review of the benefits of PRP in AO prevention. PRP was obtained from patients for use in the postremoval alveolar sockets of mandibular molar extraction sites. Statistical analysis of 904 extraction sites with and without PRP use was examined. PRP significantly reduced the incidence of AO by 62.1%, from 9.57% in patients not receiving PRP to 3.63% in patients who received PRP (P = .00043). PRP use had benefits in all subpopulations. The odds of AO occurring in patients not receiving PRP treatment following tooth extraction was 2.81 times greater than in patients receiving PRP treatment immediately following tooth extraction. Four statistically significant risk factors for AO were identified: complete impaction, oral contraceptive use, bruxism, and failure to administer PRP. The application of PRP can significantly reduce the incidence of AO even in patients with risk factors for AO, such as removal of impacted teeth, bruxism, and oral contraceptive use. PRP may be of benefit because it helps initiate clot formation, provides growth factors to facilitate the healing process, and contains concentrated white blood cells to inhibit infection. The use of PRP following tooth extraction is a simple, cost-effective technique that can be used to decrease the incidence of AO and therefore decrease postoperative pain.     

Diagnosis and treatment of atypical odontalgia: a review of the literature and two case reports

AIM: This report presents two cases diagnosed with atypical odontalgia (AO) and successfully treated with amitriptyline as well as providing a review of the current literature on the subject. RESULTS: The literature indicates the most important issue is an accurate differential diagnosis to distinguish between AO, pulpal pain, myofascial pain, and trigeminal neuralgia. CONCLUSION: Once the correct diagnosis is made the prognosis of AO is usually fair and the administration of tricyclic antidepressants often resolves symptoms. An effort should be made to avoid any unnecessary dental treatment that would only aggravate the problem.     

Clinical characteristics and diagnosis of atypical odontalgia: Implications for dentists

BackgroundAtypical odontalgia (AO) is a poorly understood and commonly misdiagnosed condition for which patients often undergo multiple unsuccessful dental or surgical procedures. The authors conducted a study to determine the prevalence and describe the characteristics of patients with AO seen at the University of Southern California Orofacial Pain and Oral Medicine Center (USC OFP-OM Center), Los Angeles.MethodsThe authors conducted a retrospective record review from a database of more than 3,000 patient records from June 2003 to August 2007 to identify patients diagnosed with AO.ResultsThe authors identified 64 patients (44 women and 20 men) between the ages of 26 and 93 years as having a diagnosis of AO. Of those 64 patients, 71 percent initially consulted a dentist regarding their pain, and 79 percent had undergone dental treatment that failed to resolve the pain. The pain of 64 percent of the patients had no known cause.ConclusionsDentists, who often are the first health care providers to see patients with AO, must be aware of this condition and must follow the appropriate steps to determine its diagnosis.Clinical ImplicationsDentists and physicians should understand the implications and importance of early diagnosis of patients with AO and of referral to pain specialists for treatment.     

Persistent orodental pain, atypical odontalgia, and phantom tooth pain: when are they neuropathic disorders?

Patients with unrelenting pain in the teeth, gingival, palatal or alveolar tissues often see multiple dentists and have multiple irreversible procedures performed and still have their pain. Up to one-third of patients attending a chronic facial pain clinic have undergone prior irreversible dental procedures for their pain without success. In these cases, if no local source of infectious, inflammatory, or other pathology can be found, then the differential diagnosis must include a focal neuropathic pain disorder. The common diagnoses given include the terms atypical odontalgia, persistent orodental pain, or if teeth have been extracted, phantom tooth pain. One possibility is that these pain complaints are due to a neuropathic alteration of the trigeminal nerve. There are several diagnostic procedures that need to be performed in any patient suspected of having a trigeminal neuropathic disorder including (1) cold testing of involved teeth for pulpal nonvitality; (2) a periapical radiograph examining the teeth for apical change; (3) a panoramic radiograph examining for other maxillofacial disease; (4) a thorough head and neck examination also looking for abnormality; (5) a cranial nerve examination including anesthetic testing which documents any increased or decreased nerve trigeminal nerve sensitivity and rules out other neurologic changes outside the trigeminal nerve; and (6) MRI imaging in some cases. Finally, when a nonobvious atypical toothache first presents, direct microscopic examination of the tooth for incomplete tooth fracture is also suggested. The majority of these patients are women over the age 30 with pain in the posterior teeth/alveolar arch. Multiple causes exist for sustained neuropathic pain including direct nerve injury (e.g., associated with fracture or surgical treatment), nerve injection injury, nerve compression injury (e.g., implant, osseous growth, neoplastic invasion) and infection-inflammation damage to the nerve itself. Sustained nerve pain is commonly seen in patients with psychiatric impairment. It may be that the unrelenting nature of the pain itself alters the patient's personality. Treatment includes pharmacologic medications which suppress nerve activity. The common medications used for atypical odontalgia and phantom tooth pain include gabapentin, tricyclics, topical anesthetics, and opioids. A list of these medications is provided in table form. Data suggest that once the patient has failed dental treatment and pain persists, the long-term outcome is less than 25 percent will have complete pain relief with treatment. With earlier treatment, better pain control, and improved nerve activity suppression medications, this should also prevent secondary psychiatric disease from developing and lower the number of inappropriate treatments.     

Diagnostic challenges of neuropathic tooth pain

This article presents the clinical characteristics, epidemiology, pathophysiology and treatment of 2 neuropathic conditions: trigeminal neuralgia and atypical odontalgia. A case report highlights the complexities involved in diagnosing neuropathic pain. Neuropathic pain is chronic, diverse in quality, difficult to localize and it occurs in the absence of obvious pathology. To avoid multiple, ineffective dental treatments, general practitioners must be familiar with the signs of nonodontogenic sources of tooth pain.