The orofacial pain–endo interface
Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain has a strong motivational input to behaviour, yet the link between tissue damage, pain and behaviour is not always proportionate or direct. Pain from an accidental burn, such as a hot iron, elicits sharp, transient pain causing a withdrawal reflex; this is acute pain, which is protective in its behavioural drive. A stimulus that is potentially damaging to tissues is considered noxious. The endodontic equivalent of acute pain is that of dentinal, pulpal or periapical origin. Pain that lasts for a few days or a few weeks can follow musculoskeletal or sports injuries; this is prolonged pain, which can also be protective in its behavioural drive. In a proportion of cases, the prolonged pain becomes persistent or chronic, lasting beyond the period of injury and its healing; this no longer has a protective value but it may continue to affect behaviour. The endodontic equivalent is neurogenic pain or pain from other structures that appears to arise from teeth and its associated structures. Although there are relatively few conditions to diagnose for the endodontist, their overlapping presentation and innate subtleties complicate straightforward identification (see Chapter 4). The problem is similar and even more complicated when considering the overlapping presentation of pain from other orofacial structures.
Orofacial pain may arise from or be associated with teeth, periodontium, oral mucosa, temporomandibular joints (TMJ) and associated musculature, cervical spine and associated musculature, maxillary sinuses, nose, eyes, throat, salivary glands, nerve supply, vascular supply, and confounding with headaches. Pain from these different structures and sources may have distinctive characteristics, which aids their identification through knowledge, practice and experience.
It is difficult to determine accurately the true prevalence and incidence of pain, both in general and in the orofacial region. Nevertheless, it is estimated that a quarter of the adult population have suffered from orofacial pain (MacFarlane et al., 2001). In children, toothache is the most common orofacial pain, 12% experiencing an episode before the age of 5 and 32% by the age of 12. Meanwhile, two recent UK studies of adults showed 12–19% of the population reported orofacial pain within the previous month (Drangsholt & LeResche, 2009).
The prevalence of chronic pain is reputed to be 35.5% in the general population (Raferty et al., 2011). In another large scale survey of 15 European countries, 19% of adults reported suffering from chronic pain, which seriously affected the quality of their lives (Breivik et al., 2006). Furthermore, the overall incidence of chronic orofacial pain has been given as 38.7 per 100 000 per year (Koopman et al., 2009). In referred endodontic patients, about 12% may have some form of chronic pain, either as a result of endodontic treatment or because of initial misdiagnosis (Polycarpou et al., 2005).
The sensory transmission of orofacial pain is conveyed predominantly by Aδ and C fibres of the trigeminal nerve, which project to the nucleus caudalis in the medulla. The latter is sometimes referred to as the medullary dorsal horn as it is the functional equivalent of the spinal dorsal horn. Pain input is modulated at this site in the brain stem before fibres then project via the spinothalamic tract to the thalamus and thence to the cerebral cortex. The sensory-discriminative component of pain and activation of the endogenous analgesic system are believed to originate within the cortex. A schematic diagram illustrating the trigeminal pain pathway is presented in Figure 16.1.
Convergence, inflammation and development of central sensitization may collectively serve to intensify and confuse the pain experienced. Convergence to the nucleus caudalis accounts for poor localization, spread and referral of pain as seen in deep pain conditions involving the dental pulp, the TMJ and associated musculature. Deep tissues have fewer nociceptive nerve endings than cutaneous or mucosal tissues, which are more clearly recognized as the source.
Sensitization and neuroplasticity may develop, first peripherally then centrally, when persistent nociceptive facilitation exceeds inhibition. It involves enlargement of the receptive field, decreased activation threshold, wind-up with increased transmission of stimuli perceived as pain, altered gene expression leading to prolonged functional change and, finally, persistent pain and central sensitization. Allodynia and/or hyperalgesia are common clinical presentations. Allodynia represents pain elicited by a normally innocuous stimulus, while hyperalgesia represents pain of an increased or prolonged nature, due to a noxious stimulus. Allodynia may be observed when carefully examining a patient using a wisp of cotton wool on the gingivae and discovering this initiates severe pain. Similarly for hypersensitivity, gentle application of pressure to the apical area can be perceived as intense pain.
Blocking peripheral inflammatory mechanisms by anti-inflammatory drugs or blocking the conduction of nerve impulses with local anaesthetics can reduce nociceptive input and potentially prevent the development of central sensitization.
Chronic OFP can be defined as pain in the face, mouth or jaws that has been present intermittently or continuously for 3 months or longer. In addition, chronic orofacial pain has also been defined by a persistence of pain combined with signs of “chronification”, such as a strong association with psychosocial problems, frequent changes of physicians, and multiple further areas of pain.
Numerous classification systems based on the structures, symptoms or treatment (Table 16.1) have been proposed for the orofacial region, the more detailed assigning individuals to multiple categories, which ideally incorporate both the physical component and the psychological impact of pain. The number of classifications reflects the fact that the discipline is still developing and there is still uncertainty about aetiopathogenesis, in turn reflected in a rich field of research.
Some of the classification systems available for orofacial pain
RDC/TMD (Research Diagnostic Criteria for Temporomandibular Disorders) 1992
IASP (International Association for the Study of Pain) 1994
AAOP (American Academy of Orofacial Pain) 2008
ICHD (International Classification of Headache Disorders) 2nd edn 2004
A careful history is obtained to determine the characteristics of the orofacial pain, as well as any history of other generalized chronic pain conditions. Information on co-morbid anxiety, depression, sleep problems, social and family history should all be recorded. Pre-consultation questionnaires may be useful when managing chronic pain to assess the behavioural impact of pain and in establishing the patient’s goals and expectations. Clinical examination, together with special tests if required, is used to confirm diagnosis. The differential diagnoses of orofacial pain constitute a vast list but a broad assessment is essential to exclude rare presentations of intra- or extracranial malignant neoplasia, severe infective inflammatory conditions before considering the more commonly encountered presentations of pain. The main causes of chronic orofacial pain are then often classified into inflammatory, vascular, musculoskeletal, neuropathic and idiopathic (Fig. 16.2).