{"id":9997,"date":"2019-02-04T09:00:53","date_gmt":"2019-02-04T15:00:53","guid":{"rendered":"https:\/\/www.aae.org\/specialty\/?p=9997"},"modified":"2019-02-19T13:33:45","modified_gmt":"2019-02-19T19:33:45","slug":"diagnosing-orafacial-pain-three-key-ingredients","status":"publish","type":"post","link":"https:\/\/www.aae.org\/specialty\/diagnosing-orafacial-pain-three-key-ingredients\/","title":{"rendered":"Diagnosing Orofacial Pain: Three Key Ingredients"},"content":{"rendered":"\n

By Dr. Donald R. Tanenbaum<\/em><\/p>\n\n\n

\"\"<\/p>\n

“All through the summer of 1946, Babe Ruth had a severe pain over his left eye. What was at first thought to be a toothache or sinus infection eventually caused so much discomfort that Ruth was admitted to a New York hospital. The doctors, suspecting that infected teeth were the cause, extracted three and then administered penicillin and other drugs. A month later though, Ruth was still in pain and still in the hospital.”1<\/sup><\/p>\n\n\n

As the months passed, Ruth’s pains were diagnosed as stemming from a nasopharyngeal carcinoma, providing evidence that the site of his early symptoms was not the source of his suffering. In essence, Ruth experienced what we now call heterotopic pain, when pain is felt at a site different from the injured or diseased organ or body part. <\/p>\n\n\n\n

In\nthe orofacial region, heterotopic pain is common. The definition offered by Merskey and Bogduk that \u201cheterotopic pain is pain perceived\nin a region that has a nerve supply different from that of the source of pain,\u201d2<\/sup> has essential meaning when trying to identify the origins\nof often elusive tooth and\/or jaw pain. Without this understanding, the\npractitioner is more apt to treat the teeth and jaw tissues though the reported\nsymptoms, clinical evaluation findings and imaging may not provide sufficient\nclues to support these actions.  <\/p>\n\n\n\n

To\nfully understand the potential sources of heterotopic pain in the orofacial\nregion, practitioners must not only become familiar with the concept of\nconvergence from the caudate nucleus of the trigeminal system, but also must appreciate\nthe underlying mechanisms differentiating nociceptive and non-nociceptive pain.\n<\/p>\n\n\n\n

Nociceptive Pain<\/strong><\/h3>\n\n\n\n

Over the years, pain has been defined in many\ndifferent ways. One familiar definition states that “pain is a more of\nless, localized sensation of discomfort, distress or agony, resulting from the\nstimulation of specialized nerve endings, often associated with recognizable\ntissue injury or pathology.”3<\/sup> This definition defines what is\ncalled nociceptive or somatic pain. “Nociceptive” means causing or\nreacting to pain – the cause of the pain comes from outside the nervous system,\nand a normally functioning nervous system reacts to it.  In this model of pain, tissue injury which is\nalways associated with inflammation and\ncommonly initiated by trauma, disease, or chemical and thermal irritants,\nstimulates normally functioning specialized nerve endings (nociceptors) initiating\nthe pain experience.\nThe phenomenon of allodynia (when touch is pain) and hyperalgesia (when a\nmildly noxious stimuli produces more pain than is expected) are always\nassociated with this type of pain and are the characteristic elements of what is\ncalled peripheral sensitization. 4<\/sup><\/p>\n\n\n\n

Muscle,\njoint and tooth pains are types of somatic\/nociceptive pain. At the outset, the\nlocation where the patient describes the pain, is the source of the pain. This\nallows for predictable identification and successful treatment. If, however,\nthe pain persists (pathology remains elusive due to its location like the\nnasopharynx) or is initiated by extreme trauma, then the initially purposeful\nperipheral sensitization leads to pain intensification and what is called a\nspreading receptive field. The end result is that the somatosensory cortex\nwhere pain perception occurs becomes \u201cconfused”\nand pain is\nperceived elsewhere other than it’s true source. To make matters more\ncomplicated, under the influence of persistent\/intense nociceptive input, the\ncentral nervous system is altered, so that a patient actually becomes more\nsensitive and experiences more pain with less provocation. This is called\ncentral sensitization. 4<\/sup> Most of our successes therefore occur when\ntrue somatic pain problems are identified within a short timeframe, when the\nsource of injury is identified and removed, and the source of injury is not\nexcessively traumatic.<\/p>\n\n\n\n

Non-nociceptive Pain<\/strong><\/h3>\n\n\n\n

Non-nociceptive\npain or what has been called neuropathic pain is defined as pain that arises\nfrom injury, disease or dysfunction of the peripheral or central nervous\nsystem. “Non-nociceptive,\u201d meaning the pain comes from within the nervous\nsystem itself often representing a circuitry malfunction particularly when\noccurring in the absence of a specific definable event or insult to nerve\ntissue.  This is often referred to as\ninside out pain and has no purpose. Essentially our bodies alarm system becomes\ntoo sensitive allowing false alarms to be set off, despite normal stimulation\nof the nervous system. When these pains are focused in the face and jaws, the\ncomplaints may mimic a TM disorder or toothache but will not be responsive to conventional\noutside in treatments. Often times the history provided along with the\ndescriptive symptoms (constant, ongoing, unremitting and distressing pain) and\nexamination findings make the practitioner pause as something does not appear\nto fit. <\/p>\n\n\n\n

Though\nfrom a historical perspective some patients clearly have suffered trigeminal\nnerve injury from dental and surgical interventions and \/or other traumatic\nevents, the majority present with histories that reveal a multitude of risk\nfactors that by themselves are difficult to connect with an orofacial pain\nexperience. This is where the story gets interesting.<\/p>\n\n\n\n

Pain as a Neuro-Immune Phenomenon<\/strong><\/h3>\n\n\n\n

In\nan attempt to understand what is happening to create continuous pathological\npain in the absence of identifiable events, pain research has focused on the\nrole of the immune system and particularly microglial activation. In the eyes\nof researchers, the pain experience is often the end result of the interaction\nof the nervous system with the immune system. 6 <\/sup>In a proposed pain\nmodel, glial cells in both the peripheral and central nervous system are\nthought to monitor the environment around neurons and regulate states of neuronal\nexcitability. They essentially provide surveillance always looking for signs of\ncellular stress. When ‘functioning properly’, microglial cells exhibit\nrestraint and only prompt the release of pro-inflammatory cytokines in the\nbrain (which amongst other things amplify aches and pains) when commonly\nrecognized sources of cellular stress like viruses are identified.7 <\/sup>Microglial\ncells, however, often beat by their own drum, prompting pain emergence and\namplification in the presence of cellular stresses that had been initiated and\nongoing due to seemingly less relatable factors such as insomnia, persistent\nlife stressors, domestic PTSD, primary anxiety disorders, chemotherapy, medications\nused to treat ADD\/ADHD, chronic neck inflammation, migraines, and chronic\ngastrointestinal inflammatory disorders to name a few. 8 <\/sup>Remarkably\nthen, pain can emerge in the face, jaw and teeth and persist though\nrecognizable somatic tissue injury was never there in the first place.<\/p>\n\n\n\n

Summary<\/strong><\/h3>\n\n\n\n

For clinicians evaluating patients with orofacial pain, it is essential therefore to determine if a) the pain has a nociceptive or non-nociceptive origin, b) whether or not heterotopic mechanisms have been triggered and c) enough information has been gathered to “know who the patient is” and identifying risk factors that may be responsible for a persistent pain problem. Once this information is determined, making a diagnosis will be greatly facilitated. <\/p>\n\n\n\n

Donald R. Tanenbaum, D.D.S., MPH, is clinical assistant professor, Hofstra North Shore-LIJ School of Medicine; clinical assistant professor, Dept. of Oral & Maxillofacial Surgery, School of Dental Medicine at Stony Brook University; section head, Facial Pain and Dental Sleep Medicine Section, Dept. of Dental Medicine, Long Island Jewish Medical Center.<\/em><\/p>\n\n\n\n

References<\/strong><\/p>\n\n\n\n

1- JADA,July 2008, Vol. 139:7, pp. 926-93<\/p>\n\n\n\n

2- Merskey\nH and Bogduk N (eds.). Classification of chronic pain. Descriptions of chronic\npain syndromes and definitions of pain terms, 2nd Edition Seattle: IASP Press,\n1994. 240 pp.<\/p>\n\n\n\n

3-\nAnderson DM,2002. Mosby\u2019s Medical Dictionary. Sixth Edition. Mosby: A Harcourt Health\nSciences Company, St. Louis. 1867 pp<\/p>\n\n\n\n

4- Vardeh D.,Naranjo J.F. (2017)\nPeripheral and Central Sensitization. In: Yong R., Nguyen M., Nelson E., Urman\nR., Pain Medicine. Springer, Cham<\/p>\n\n\n\n

5- Current Opin Anaesthesiology,\nMicroglial role in the development of chronic pain. Suter MR, 2016, October:\n584-9<\/p>\n\n\n\n

6-\nPathological and protective roles of glia in chronic pain, Milligan E. and\nWatkins L., Nat Rev Neuroscience, 2009 Jan 23-36<\/p>\n\n\n\n

7- Glial Cells and Chronic Pain, Neuroscientist 2010, October;\n16(5): 519 531,Romain- Dan Gosselin, Marc Suter, Isabelle Decosterd<\/p>\n","protected":false},"excerpt":{"rendered":"

“All through the summer of 1946, Babe Ruth had a severe pain over his left eye. 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