Orofacial pain represents a significant burden in terms of morbidity and health service utilization. It includes very common disorders such as toothache and temporomandibular disorders, as well as rare orofacial pain syndromes. Many orofacial pain conditions have overlapping presentations, THIS IS AN EXTREMELY IMPORTANT ASPECT OF OROFACIAL PAIN and diagnostic uncertainty is frequently encountered in clinical practice. THIS UNCERTAINTY IS PARTIALLY DUE TO MULTIPLE CONDITIONS IN THE SAME PATIENT, SOME ARE PREDISPOSING FACTORS THAT WERE PRESENT LONG BEFORE ACUTE PROBLEMS BEGAN This review provides a clinically orientated overview of common and uncommon orofacial pain presentations and diagnoses, with an emphasis on conditions that may be unfamiliar to the headache physician. A holistic approach to orofacial pain management is important, and the social, cultural, psychological and cognitive context of each patient (AXIS 2) needs to be considered in the process of diagnostic formulation, as well as in the development of a pain management plan according to the biopsychosocial model. Recognition of psychological comorbidities will assist in diagnosis and management planning.
Orofacial pain may be defined as pain localized to the region above the neck, in front of the ears and below the orbitomeatal line, as well as pain within the oral cavity. THIS DEFINITION CAN BE DETRIMENTAL TO PATIENT CARE AS THE SOURCE OF PAIN FREQUENTLY CAN BE OUTSIDE OF THE AREA WHERE THE PATIENT PERCEIVES THE PAIN. It includes pain of dental origin and temporomandibular disorders (TMDs), and thus is widely prevalent in the community. Up to a quarter of the population reports orofacial pain (excluding dental pain), and up to 11% of this is chronic pain. TYPICALLY WHEN ACUTE PAIN BECOMES CHRONIC IT IS HARDER TO TREAT DUE TO NEUROPLASTICITY Patients with orofacial pain present to a variety of clinicians, including headache physicians, dentists, maxillofacial surgeons, otolaryngologists, neurologists, chronic pain clinics, psychiatrists, and allied health professionals such as physiotherapists and psychologists. Orofacial pain is associated with significant morbidity and high levels of health care utilization. SHIMSHAK SHOWED IN HIS TWO LANDMARK STUDIES PUBLISHED IN CRANIO JOURNAL THAT PATIENTS WHO CARRY A TMD DIAGNOSIS UTILIZE 300% MORE HEALTH CARE DOLLARS THAN PATIENTS WHO HAVE NOT HAD THAT DIAGNOSIS
This review presents a clinically orientated overview of orofacial pain presentations and diagnoses. The scope of orofacial pain includes common disorders such as dental pain and TMDs, as well as a number of rare pain syndromes. Pain in the orofacial region is derived from many unique tissues such as teeth, meninges, and cornea. THE CORNEA IS EXTREMELY IMPORTANT SOURCE OF INPUT TO THE TRIGEMINAL NERVOUS SYSTEM. ACCORDING TO WIKIPEDIA THE INNERVATION OF THE CORNEA:
“The cornea is one of the most sensitive tissues of the body, as it is densely innervated with sensory nerve fibres via the OPTHALMIC DIVISION OF THE TRIGEMINAL NERVE by way of 70–80 long and short ciliary nerves. Research suggests the density of pain receptors in the cornea is 300-600 times greater than skin and 20-40 times greater than DENTAL PULP BUT ARE FREE NERVE ENDINGS SIMILAR TO THE FIBERS IN DENTAL PULP. making any injury to the structure excruciatingly painful.
THESE NERVES ARE CONNECTED TO THE SPHENOPALATINE GANGLION AND PAIN ASSOCIATED WITH THE EYE CAN BE IMPROVED WITH SPG BLOCKS
The ciliary nerves run under the endothelium and exit the eye through holes in the sclera apart from the optic nerve (which transmits only optic signals). The nerves enter the cornea via three levels; scleral, episcleral and conjunctival. Most of the bundles give rise by subdivision to a network in the stroma, from which fibres supply the different regions. The three networks are, midstromal, subepithelial/sub-basal, and epithelial. The receptive fields of each nerve ending are very large, and may overlap.”
HEADACHE ARTICLE: This results in several unique physiological mechanisms that have been well reviewed. Because of these unique mechanisms and the requirement for specialist knowledge of the complex anatomy and physiology of the orofacial region, diagnosis may be difficult. Many patients have consulted multiple clinicians for their condition yet remain undiagnosed or with an incorrect diagnosis. FREQUENTLY THERE ARE MULTIPLE CORRECT DIAGNOSIS EACH ADDRESSING ONLY A PART OF THE PROBLEM LEAVING FRUSTRATED PATIENTS MOVING ON TO OTHER TREATMENTS Our aim is to provide the headache physician with a guide to orofacial pain presentations and diagnoses informed by our clinical experience in the fields of medicine as well as dentistry, and to review the literature relevant to these conditions. We provide an overview of the common presentations of orofacial pain including dental causes of pain, non-dental causes of intraoral pain, and extraoral facial pain syndromes, as the signs and symptoms of many of these conditions can overlap significantly, causing diagnostic difficulty.
We also present a discussion of history, diagnosis, and management considerations relating to the biopsychosocial model of diagnostic formulation and management. This approach is particularly relevant and important in the field of orofacial pain given the significant level of psychological distress and social dysfunction that is associated with these disorders. WHILE THE BIOPSYCHOSOCIAL ISSUE (AXIS 2) MAY BE SIGNIFICANT WHEN AXIS 1 IS IGNORED PATIENTS WILL SUFFER! As with other types of chronic pain, there is often a mismatch between the patient’s expectation of a cure for their pain, and the reality that for many types of chronic pain, a cure is seldom possible. I CLEARLY EXPLAIN TO ALL PATIENTS THAT THERE ARE NO MAGIC CURES! THE ONLY TRUE CURE FOR PATIENTS SUFFERING FROM CHRONIC PAIN FOR WEEKS, MONTHS, YEARS OR DECADES WOULD BE A DO-OVER OF ALL THE TIME THEY HAVE SPENT IN PAIN. TO RECOVER ALL OF THE MULTITUDE LOSSES THEY HAVE SUFFERED DUE TO THE PAIN AND DYSFUNCTION. Medicine alone does not have the tools to manage a condition that has a neurophysiological cause but is also experienced emotionally, socially, financially, and spiritually. Recognition of psychological comorbidities is essential for appropriate diagnosis and successful pain management.
Types of Orofacial Pain
There are few causes for dental pain; however, because of significant neural convergence THIS CONVERGENCE IS BECAUSE THE MASTICATORY SYSTEM IS THE OVERWHELMING PORTION OF INPUT TO THE TRIGEMINAL NERVOUS SYSTEM. NOXIOUS INPUT IS ALMOST ALWAS FROM THE DENTIST’S NERVE in the jaws and face, it may be referred, poorly localized, or misdiagnosed. The 4 major causes of dental pain are pulpitis, cracked tooth syndrome, dental abscess, and dentine sensitivity. These are often acute conditions, but because they are common, they may coexist with other chronic pains.
Both the dental pulp and periodontal ligament contain nociceptors. Nociceptive output in these areas is triggered by changes in pressure and the effect of inflammatory mediators. THERE ARE AT LEAS 29 TYPES NERVOUS RECEPTORS IN THE PERIODONTAL LIGAMENTS ALONE
Pulpitis THE ARTICLE DOES AN EXCELLENT REVIEW OF THIS INFORMATION THAT IS ESSENTIAL BUT WELL UNDERSTOOD BY DENTISTS, UNFORTUNATELY THIS IS OFTEN A MYSTERY TO PHYSICIANS
Pulpitis is the term used to describe pain because of inflammation of the dental pulp, and it is usually due to dental caries. Inflammation of the pulp leads to accumulation of extracellular fluid, inflammatory mediator release, and vasodilatation, which causes an elevation of pressure within the pulp chamber, which is a non-compliant space. The pressure increases further as venous stasis and eventually pulp necrosis occur, with release of inflammatory mediators and necrotic cell contents. Elevated pressure and inflammatory chemicals activate nociceptors in the pulp chamber causing pain.
Reversible pulpitis is defined as a transient pain in response to specific stimuli (hot, cold, sweet), which occurs when the pulp is inflamed. These symptoms resolve when the cause of the inflammation is treated. The pain of reversible pulpitis may be described as fleeting, shooting, stabbing, or sensitive.
Irreversible pulpitis is characterized by spontaneous pain, which may be worsened by or persist following the removal of a stimulus such as heat or cold. It is an indicator of incipient pulpal necrosis. The pain of irreversible pulpitis is often described as persistent, throbbing, dull, or aching. It may be worsened by physical activity and head movement.
Pulpal pain is often poorly localized as the inflammation is restricted to the pulp chamber and is thus not affecting proprioceptive nerve fibers, which are located in the periodontal ligament. It is common for patients to be unable to localize the exact source of the pain. Pulpal pain may respond to simple or opioid-based analgesics, but the pain of irreversible pulpitis will not resolve until pulpal necrosis has occurred or the pulpal tissue has been mechanically removed (by endodontic treatment).
If pulpal inflammation and infection reaches the base of the pulp chamber, an area known as the apex or root tip, it may extrude through the apical foramen into the periodontal space. This will cause pain due to stimulation of nociceptors in the periodontal ligament space, and the pain will be well localized due to involvement of periodontal ligament proprioceptive fibers. Extrusion of inflammatory fluid and necrotic cell products into the periodontal space causes pain because of pressure effects, and the tooth will become exquisitely tender to touch or biting. This leads to the pain becoming very well localized, and the source of pain may be readily identified by gentle tapping on the tooth. When inflammation and infection has progressed through the apical foramen, it is described as a periapical abscess.
Dental infection may progress into the bone, under the oral mucosa or into soft tissue spaces, and form an abscess or spreading infection, with resultant ongoing pain.
Cracked Tooth Syndrome
Cracked tooth syndrome occurs when a crack has occurred in the dental hard tissues and reaches the pulp chamber. The crack is usually not visible to the naked eye. Pain because of cracked tooth syndrome is classically intermittent, provoked on biting or releasing biting on a hard object, and is notoriously difficult to diagnose. It may be described as sharp or sensitive, and is usually related to mastication. The tooth may also become sensitive to hot and cold stimuli. It is thought that the pain is due to fluid shifts within the dentine tubules, which are generated due to pressure differences as the crack opens and closes during mastication. It can be extremely difficult to diagnose.
Pain because of dentine sensitivity is classically stimulated by exposure to cold, heat, sweet foods/drinks, and mechanical trauma such as toothbrushing. The sensation is due to the movement of fluid in dentinal tubules in response to osmotic or temperature-related effects. Dentinal tubules contain the processes of cells residing in the dental pulp (odontoblasts), and fluid movement appears to trigger nociceptive output by mechanisms that are as yet unclear. Gingival recession can lead to exposure of the endings of dentine tubules, as can loss of enamel on the crown of the tooth. Dentinal sensitivity is described as very rapid, fleeting, shooting pain, or sensitivity, and is always in response to an identifiable stimulus. THE INFORMATION IN THE PRECEDING SECTION IS BASIC DENTAL KNOWLEDGE.
Non-dental Intraoral Pain:
THIS TYPE OF PAIN IS OFTEN FAR MORE CONFOUNDING TO GENERAL DENTISTS WITHOUT ADVANCED TRAINING IN PAIN.
Intraoral pain may also arise from non-dental structures. Oral mucosal malignancies such as squamous cell carcinoma or salivary gland carcinoma may be painful because of ulceration or perineural invasion.
Inflammatory oral mucosal diseases such as oral lichen planus, recurrent aphthous stomatitis, vesiculobullous diseases, and oral mucosal infections such as candidiasis or herpes viruses (herpes simplex, varicella zoster) may all cause significant oral pain. Patients with hematinic deficiencies, diabetes, hematological malignancies, HIV/AIDS, and Behçet’s disease may have significant oral mucosal pain and/or ulceration. Examination will usually reveal the associated oral mucosal abnormalities.
Pain may be experienced in the oral cavity, face, and neck because of salivary gland pathology. Blockage of a major salivary gland duct may be due to infection, mechanical obstruction by tumors, docholithiasis, or ductal strictures. Obstruction of the duct will lead to pain as the gland fills with saliva, which cannot be released. Pain due to chronic ductal obstruction typically worsens preprandially or during meal times. Infection of the salivary glands will result in gland swelling, pain, and erythema/warmth of the overlying skin.
MANY OF THE ABOVE PROBLEMS ARE ASSOCIATED WITH WHOLE BODY SYMPTOMS OF AUTO-IMMUNE DISEASE.
Post-Traumatic Trigeminal Neuropathic Pain/Atypical Odontalgia
THESE ARE THE TYPE OF PAIN THAT OFTEN CREATE STRESSFUL SITUATIONS BETWEEN PATIENTS AND DENTISTS AS NO EASY DENTAL ISSUES ARE FOUND.
This definition encompasses intraoral pain that is localized to a non-diseased dentoalveolar structure, such as a tooth or an area of alveolar ridge from which a tooth has previously been extracted. The pain is often described as “burning,” “shooting,” or “shock-like,” and there may be significant hyperalgesia and allodynia of the affected region, often with an associated area of hypoesthesia or dysesthesia. The pain is usually continuous, with some patients experiencing evoked severe episodes. The area is usually clearly defined with little radiation. Patients have described it as “nails being hit the whole time” or “kicked in the face and left bruised and burning.”
IT IS IMPORTANT TO REMEMBER THAT THERE ARE OFTEN MULTIPLE ONLAID PROBLEMS SIMULTANEOUSLY AFFECTING THE PATIENT. ANY NOXIOUS INPUT TO THE TRIGEMINAL NERVOUS SYSTEM FORM ANY SOURCE COMPLICATES BOTH DIAGNOS AND TREATMENT
Controversy remains about nomenclature and criteria for these conditions, and in this article, we differentiate them by the presence or absence of a precipitating event. THE PROBLEM MAY OR MAY NOT BE RELATED TO PERCIPTITATING EVENT WHICH OFTEN IS ASSOCIATED NOT WITH NEW SYMPTOMS BUT EXACERBAATION OF OLD SYMPTOMS. It has been proposed that formal neurophysiological testing would help distinguish those with neuropathic pain compared with inflammatory causes. Patients with trigeminal neuropathic pain OFTEN BUT NOT ALWAYS have an identifiable traumatic episode preceding the onset of the pain. The precipitating event may include physical trauma such as facial fractures, iatrogenic trauma such as restorative, endodontic, or oral surgical procedures (apicectomy, extraction, implant placement), prolonged severe infection of dentoalveolar structures, or dental procedures carried out with ineffective anesthesia. Trigeminal neuropathic pain is persistent and severe, and associated with a high level of psychological distress and a risk of further iatrogenic harm because of patients seeking ongoing dental or surgical interventions for relief of pain. TRIGEMINAL NEUROPATHIC PAIN MAY RESPONT TO SPHENOPALATINE GANGLION BLOCKS
Atypical odontalgia or persistent dentoalveolar pain refers to a similar clinical presentation without a clear precipitating event. “Persistent dentoalveolar pain” is an ontological definition describing the symptoms and signs without attributing a causation or mechanism. Such definitions are developed using analysis of patient interviews. These conditions are usually managed along the same pathways as for other neuropathic pain. Until there are internationally agreed diagnostic criteria based on case–control studies and more well-conducted trials have been carried out, treatment of these conditions can vary substantially between clinicians, leaving patients confused and continually consulting in hope that a “cure” will be found. MANY TIMES THESE PROBLEMS ARE SECONDARY TO LONG TERM NOXIOUS TRIGEMINAL INPUT, PEPETITIVE STRAIN INJURIES AND OTHER AXIS 1 & 2 PROBLEMS.
Burning Mouth Syndrome
BURNING MOUTH SYNDROME IS VERY FRUSTRATING TO BOTH DENTAL PATIENTS AND DENTISTS
Burning mouth syndrome describes a collection of symptoms affecting the oral cavity, including a “burning” or painful sensation, often with an associated alteration in taste sensation and an altered perception of the quality and quantity of saliva. The symptoms are most commonly localized to the tongue. On clinical examination, the oral mucosa appears entirely normal. The area of abnormal sensation does not typically follow anatomic boundaries, is usually bilateral, and is continuously present. Patients may describe their symptoms as “discomfort” rather than pain. One patient described their symptoms as a “Prickly feeling like an injection wearing off,” and when choosing photographic images as representative of their symptom, many choose images of fire. Other causes of oral burning sensations such as hematinic deficiencies, diabetes, other systemic diseases, and oral infections should be ruled out. The condition is most common in perimenopausal or postmenopausal females, and is strongly associated with psychological comorbidities such as anxiety and depression. TRICYCLIC ANTIDEPRESSANTS IN SYSTEM AND/OR TOPICAL APPLICATION ARE OFTEN EFFECTIVE. GELCLAIR IS A PRESCRIPTION PRODUCT USED TO TREAT ORAL MUCOSITIS AND STOMATITIS SECONDARY TO CHEMOTHERAPY AND RADIATION THERAPY. THE ACTIVE INGREDINT IS HYALOURONIC ACID. Patients often report that their symptoms are worsened during periods of psychological stress. The etiology of the condition is unclear, although recent studies have suggested the presence of a small-fiber sensory neuropathy, thus suggesting it is a form of neuropathic pain, but others propose a steroid dysregulation mechanism. THESE ARE BOTH DISORDERS OF THE AUTONOMIC NERVOUS SYSTEM LEADING US TO BELIEVE BURNING MOUTH SYNDROME IS PROBABLY AN AUTONOMIC DYSFUNCTION AND IT FREQUENTLY RESPONDS TO SPHENOPALATINE GANGLION BLOCKS. The condition can be difficult to manage, and a variety of RCTs have been reported, which include drug therapies and cognitive behavior therapy. Research on this condition is difficult to conduct in part due to its rarity and a lack of animal models; however, studies are being undertaken that indicate evidence of central changes on functional magnetic resonance imaging (MRI), thus supporting the hypothesis that there are definite neurophysiological elements to this condition, rather than it being a psychosomatic condition as has been previously suggested.
Facial Pain With/Without Intraoral Pain
TMDs are the most common causes of orofacial pain, affecting 10–15% of the population. THIS NUMBER CAN VARY WIDELY AND IS PROBABLY LOW.. MANY PHYSICANS AND DENTISTS DO NOT UNDERSTAND THAT TMD DOES NOT REQUIRE THE PRESENCE OF JOINT NOISES OR JOINT PAIN A MORE PROPER DIAGNOSIS WOULD BE MASTICATORY SYTEMS DISORDERS BECAUSE THE MYOFASCIAL AND FUNCTIONAL COMPONENT OF TMD ARE OFTEN OVERLOOKED IN THE ABSENCE OF TMJOINT ISSUES. Presenting features include pain localized to the pre- and post-auricular areas, the angle and ramus of the mandible, and the temporal region. There may be associated clicking, sticking, or locking of the temporomandibular joints. The pain may be intermittent or continuous, and is usually described as dull, aching, (MUSCLE) or throbbing, or in the words of patients: “weight on the side of the face getting heavier and heavier,” “pressure feeling,” “elastic band that is too tight,” or “needles digging in.” Some patients experience pain that is sharp or shooting in character, intermixed with dull continuous pain. The pain commonly radiates into the temporal or occipital regions into the neck and across the malar region of the face; it can be unilateral or bilateral, and of varying severity. There may be an associated bruxing or clenching habit. The pain is typically aggravated by opening the mouth wide, yawning, or chewing. There may be limitation of mouth opening.
TMD has historically been classified using the Research Diagnostic Criteria into myofascial pain, disc displacement, and other disorders, as the International Classification of Headache Disorders (ICHD)-II of TMD was not useful in clinical settings. Newer classification criteria refer to myalgia, myofascial pain with referral, and myalgia with disc involvement. THESE NEWER CLASSIFICATIONS ARE FAR MORE ACCURATE AND REFLECT MASTICATORY AND POSTURAL MUSCLE PAIN, THE EFFECT OF THE JAW ON HEAD AND NECK POSTURE OFTEN RESULTS IN CERVICAL, UPPER BACK AND SHOULDER MUSCLES REFERRING PAIN TO THE HEAD AND NECK. THE NHLBI ALSO PUBLISHED A REPORT ON THE CONNECTION OF TMD AND SLEEP APNEA AND OTHER SLEEP DISORDERS
A large prospective cohort study is currently underway in the USA investigating the prognostic factors related to the development of TMD. Participants with and without TMD participate in a battery of psychometric, biometric, and genetic tests. Baseline data on the psychological characteristics of the TMD cases demonstrate that this population shows higher levels of distress, catastrophizing, and increased somatic awareness compared with non-TMD controls. A number of other studies have reported similar findings. THE BIG QUESTION IS THE EFFECT ON THE TMD SYMPTOMS ON THE BIOMETRIC TESTING RESULTS. DO PATIENTS HAVE “higher levels of distress, catastrophizing, and increased somatic awareness” SECONDARY TO THEIR TMD ISSUES?
TMD has been linked with other psychological and chronic pain conditions, including fibromyalgia, back pain, headaches, chronic widespread pain, and hypermobility. THIS MAY BE DO TO THE PHYSIOLOGICL EFFECTS OF HEAD AND JAW POSITION ON THE REST OF THE BODY. THE CONNECTIONS TO CHRONIC PAIN MAY BE DUE TO POSTURAL CHAIN OF EFFECTS ON TOP OF EFFECTS OF PAIN THRU THE LIMBIC SYSTEM. PAIN IS ACTUALLY AN EMOTIONAL RESPONSE TO A STIMULI Degenerative temporomandibular joint disease is rare but may occur in rheumatoid arthritis. Interest has been raised recently in the possibility of TMD-related headache, which may involve aspects of peripheral and central sensitization. ONE COULD SAY THAT ALL HEADACHES ARE RELATED TO TMD THRU THE TRIGEMINAL NERVOUS SYSTEM. http://www.iccmo.org/all-migraines-come-from-trigeminovascular-system-or-why-physiologic-dentistry-and-spg-blocks-can-cure-or-eliminate-migraines/
Management of TMD is primarily conservative, as in the majority of cases, the disorder is self-limiting. THIS STATEMENT IS PROBABLY LUDICROUS WHEN ONE CONSIDERS THAT 10% GO ON TO DEVELOP DEBILITATING CHRONIC PAIN. Careful explanations are crucial as it has been shown that patients experience a considerable amount of uncertainty both in terms of diagnosis and then management, as dentists also often find it difficult to manage. MANY DENTIST WHO HAVE HAD ADVANCED TRAINING IN TREATING PAIN HAVE CONSIDERABLE EXPERTISE IN TREATING THESE DISORDERS AND CAN PREVENT THE PAIN BECOME WIDESPREAD Approximately 10% of patients develop chronic pain, and this has been linked to fibromyalgia, depression, and chronic widespread pain. Therapies used for TMD include simple analgesia, tricyclic antidepressants, occlusal splints or bite guards, diet modifications, physiotherapy, cognitive behavioral therapy, and surgery. Evidence for the majority of these therapeutic options is poor, THIS IS NOT TRUE, ACTUALLY THERE IS EXCELLENT EVIDENCE BASED ON CLINICAL CASE STUDIES BUT THERE IS LITTLE LONG TERM BLINDED AND RANDOMIZED STUDIES PRIMARILY BECAUSE THESE ARE ALMOST IMPOSSIBLE TO HAVE THESE STUDIES AND ETHICALLY DO YOUR BEST TO RELIEVE PATIENT SUFFERING. DRUG AND PSYCHOSOCIAL STUDIES ARE EASIER TO PREFORM BUT CONTROL OF VARIABLES IS DIFFICULT IF NOT IMPOSSIBLE. and there remains considerable confusion about the best form of management. Surgery is only indicated for TMD with significant functional limitation or in cases with associated degenerative joint disease or disc dysfunction. SURGERY CAN COVER MANY PROCEDURES FROM SIMPLE ARTHROCENTESIS TO OPEN ARTHROTOMIES. MINIMALLY INVASIVE PROCEDURE THAT ARE DONE WHILE STABILIZING THE BITE ARE FAR MORE EFFECTIVE THAN THE SAME PROCEDURES WITHOUT STABILIZATION. Education, psychological support and self-management strategies are recommended as part of a multidisciplinary approach to the management of TMD, and these should be done early to reduce costs. There remains considerable variation in the way TMD is diagnosed and managed partly due to conflicting evidence. It is anticipated that the large US-based Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study will provide more robust evidence, as it is a prospective study that has enrolled asymptomatic participants.