Orofacial Pain

Learning Objectives

Discuss the trigeminal pain pathway.
Explain the components involved in nociceptive pain.
Discuss odontogenic nociceptive pain and give examples.
Discuss mucosal nociceptive pain and give examples.
Discuss pain associated with TMD.
What is referred pain and how does it relate to orofacial pain?
What is neuropathic pain and how does it differ from nociceptive pain?
Give examples of neuropathic pain that is of neurovascular origin.
What are the causes of orofacial neuralgia and describe that condition associated with cranial nerve (CN) V and CN IX.
What is burning mouth syndrome and why is it considered atypical orofacial pain?
How do head and neck cancers produce pain?

Overview of Orofacial Pain Pathways

Pain information for the head and oral cavity is largely carried on the trigeminal nerve (CN V). The first-order cell bodies for the trigeminal system are located in the trigeminal ganglion. Nociceptive information is transmitted from the periphery into the central nervous system (CNS) via sensory receptors that communicate with the first-order neurons. The peripheral process of the first-order neuron travels in the three divisions of CN V: ophthalmic (V1), maxillary (V2), and mandibular (V3). The central processes of the first-order neurons project to the trigeminal nuclear complex, specifically the spinal trigeminal nucleus (STN), where the second-order neurons reside. In general, pain information from the face will synapse in the pars caudalis nucleus. Nociceptive input from the oral cavity (teeth, periodontal ligament [PDL], and oral mucosa) will terminate in the pars oralis nucleus. Although it is less well characterized, it is generally accepted that some oral pain information will also travel to the pars interpolaris nucleus. Secondary afferents from the STN decussate to form the ventral trigeminothalamic tract, which then ascends and synapses in the contralateral ventral posteromedial (VPM) nucleus of the thalamus (third-order neurons). Fibers from the third-order neurons of the thalamus project toward the sensory strip of the cortex (postcentral gyrus) where they synapse in their respective somatotropic-specific area (; see Chapter 13).

Fig. 26.1 Pain information from the face and oral cavity is carried on the trigeminal nerve and ascends to the somatosensory cortex via the trigeminothalamic tract. (Reproduced with permission from Schuenke M, Schulte E, Schumacher U. THIEME Atlas of Anatomy Second Edition, Vol 3. ©Thieme 2016. Illustrations by Markus Voll and Karl Wesker.)

Nociceptive Orofacial Pain

Nociceptive pain is evoked as a result of the stimulation of pain receptors. This is the most common type of pain and results from trauma/injury or local inflammation. The sensation of pain is initiated by the stimulation of nociceptors. Dental pain originating from hot and cold stimuli is perceived quite differently, with heat producing dull, long-lasting pain and cold producing short, sharp pain. It has been proposed that pain from hot and cold temperatures is the result of dentinal fluid movement within microtubules present in the dentin of sensory neurons expressing nociceptors (hydrodynamic theory). Another theory on pain resulting from thermal stimuli is the neural theory, which suggests that temperature changes at the surface of the tooth are conducted through the enamel and dentin to the nociceptors located at the dentin–enamel junction (DEJ). The nerve fibers that transmit noxious stimuli are lightly myelinated alpha d or unmyelinated C fibers. The major categories of nociceptive orofacial pain include odontogenic, mucosal, musculoskeletal, and referred.

Odontogenic Pain

Odontogenic pain refers to pain that initiates from teeth or the periodontium, the maxilla or the mandible. A “toothache” is caused by inflammation of the dental pulp, often due to dental caries (tooth decay). Periodontal disease is a common cause of infection that can produce odontogenic pain (). The source of odontogenic pain is the pulpo-dentin complex and periapical tissue. In healthy pulp, thermal stimuli produce short, sharp pain that lasts approximately 1 to 2 seconds (). This indicates that the nerve fibers are functioning. A response to cold indicates vital pulp, whereas an increased response to heat suggests a pulpal or periapical pathology that may require endodontic treatment.

Differential diagnoses of endodontic conditions

Differential diagnoses of endodontic conditions
Reversible pulpitis	Short duration of pain Reacts to cold and heat stimuli No reaction to percussion Not evident on radiograph
Irreversible pulpitis	Lingering pain in response to heat and cold Typically does not react to percussion Pain initially sharp, then dull, throbbing Pain poorly localized
Pulp necrosis	May or may not be painful Lingering pain to heat, sometimes relieved by cold
Acute apical periodontitis	Tenderness to percussion Pain with chewing May have pulp symptoms
Chronic apical periodontitis	None to minimal symptoms Periapical radiolucency
Acute abscess	Pus in periapical tissues Tenderness to percussion and palpation Pain when chewing Intraoral swelling may be present
Cellulitis	Facial swelling, red, diffuse Often not painful Fever may be present
Source: Adapted from Linn et al., 2007.

Diagnostic tests for dental pain

Diagnostic tests for dental pain
Pulp sensitivity test	Ice is applied on the neck of the tooth. Pain indicates pulp is vital. No response indicates pulp necrosis
Percussion test	Tooth is tapped on longitudinal angle with instrument. Pain response indicates potential periapical inflammation (abscess)
Probing	A blunt probe placed into the gingival sulcus around the tooth can provide information regarding the health of the tissue. Bleeding and/or depths greater than 3–4 mm indicates gum disease
Mobility test	Visible movement with manipulation indicates bone loss
Palpation	Palpation of the area in question can demonstrate tenderness and swelling
Mucosal sinuses	Dental abscesses often drain to the buccal surface creating sinuses that extend through the mucosa
Radiology	Radiographs will show apical and periapical structures of the tooth in question and those adjacent as well as caries
Source: Adapted from Renton 2011.

Dental pulpitis (inflammation of the pulp) can be due to caries present near the pulp. It is classified as reversible or irreversible.
- In reversible pulpitis, the pulp can remain viable if treated, which typically requires removal of the caries followed by restoration. It is characterized by short, quick bursts of pain induced by a cold stimulus that ceases immediately upon its removal.
- Irreversible pulpitis occurs when the pulp is damaged beyond repair. It is characterized by intense pain and is one of the most common reasons for emergency dental visits. As the inflammation spreads, the cellular organization of the pulp breaks down. It is typically associated with tooth decay, a cracked tooth, or trauma. Management for irreversible pulpitis is either pulpectomy (root canal treatment) or tooth extraction. Pain symptoms with irreversible pulpitis include:
  - Intense persisting pain with warm stimulus. After removal of the stimulus, the pain becomes dull and pulsating. Early pain information is carried on both A-d and C fibers; however, as the inflammation progresses, C fibers become the predominant carriers for pain transmission.
  - Pain subsides with cold stimulus, likely due to vasoconstriction and a decrease in intrapulpal pressure. This symptom is highly indicative of necrotic pulp.
  - When C fibers become the predominant mode of transmission, the pain becomes more diffuse and is more difficult to localize.
  - Intense and prolonged pain can refer to the ear, temporal area, and the cheek.
  - Once the periapical tissue becomes involved, the tooth becomes sensitive to percussion.
- Necrotic pulp results from continued degeneration of inflamed pulp. There is no reparative potential. In addition to the moderate to severe spontaneous pain, the patient may experience swelling in the jaw and lymphadenopathy. Pain receptors in necrotic pulp often become damaged and may not respond to thermal stimuli. If the pulp is only partially affected, there may be some response present.
Periapical pain can be caused by an infection spreading through the apical foramen of the tooth into the periodontal region. The infection can transform into a dental abscess if left untreated.
Exposed cementum and dentin on teeth can produce pain. Under ordinary circumstances, tooth sensitivity can be present with healthy pulp. If gingival recession is present, the patient underwent recent scaling, or they suffer from gastric reflux, there can be dentin sensitivity. The pain is described as sharp and short in duration. It is thought that the pain is due to movement of fluids in and out of the dentin tubules in response to osmotic or temperature changes.
Incomplete fractures of a tooth may cause pain. Patients often complain of sharp pain when they bite or release from biting. Symptoms may also include sensitivity to cold temperatures. Cracks are often difficult to see in the oral cavity and may not show up on radiographs.
Periodontal disease is a chronic inflammatory disorder initiated by oral microbes that can eventually affect supporting structures of the tooth and the surrounding bone. In general, it is not considered a chronic pain disorder, as initial symptoms are gingival sensitivity and bleeding. However, periodontal abscesses can develop. This type of acute infection does not develop from the pulp but typically arises in a preexisting periodontal pocket. In this situation, the most common symptom is pain. Other symptoms include swelling of the gingiva and oral mucosa surrounding the affected tooth. Lymphadenopathy and fever may be present.
Alveolar osteitis or “dry socket” is one of the most common complications following a tooth extraction. In this condition, the clot that developed post extraction fails, leaving an empty socket and exposed alveolar bone. Bone pain can result from noxious stimulation of the periosteum. Additionally, food and debris can get trapped and become necrotic, further irritating the nerve endings. Pain from a dry socket is typically described as dull and throbbing. Smoking is a major factor in the development of a dry socket, most likely due to the reduction in blood supply. Alveolar osteitis rarely occurs in the maxilla and generally develops 3 to 5 days following a mandibular tooth extraction.