Toothache and mouth pain
Tooth is a limb that can cause pain even in healthy people. Many patients define mouth, jaw and face pain as toothache. It is often difficult to tell whether a pain is caused by a tooth or by other structures in the face. For this reason, the properties of teeth and facial pain should be well known. The nerves that provide the innervation of the mouth and teeth are maxillary and mandibular nerve. Maxillary Nerve: V. Cranial Nerve is the second branch of Trigeminal Nerve. It originates from the anterior border of the Gasser ganglion.
Sensory fibers. Inervation:
Tooth is a limb that can cause pain even in healthy people. There can be many causes of pain and many patients define mouth, jaw and face pain as toothache. It is often difficult to tell whether a pain is caused by a tooth or by other structures in the face. For this reason, the properties of teeth and facial pain should be well known. The nerves that provide innervation of the teeth and teeth are maxillary and mandibular nerve.
Cranial Nerve is the second branch of Trigeminal Nerve. It originates from the anterior border of the Gasser ganglion. Totally sensory fibers. Inervation:
• The middle part of the face
• Lower eyelids
• Nasal edge
• Nasopharynx, maxillary sinus, soft palate, tonsil and part of mouth mucosa
• Upper gums and teeth
Anterior (Major) palatine nerve:
The maxillary originates from the zygomatic nerve. It provides the inervation of the hard gum until the cutter. It also causes the pain of the mucous membrane of the area with the gums.
Posterior superior alveolar nerve:
The maxillary nerve divides into two branches, as one usually rarely. Maksillanin posterior face, gums and cheek branches. Maksillanin posterior alveolar channels by entering the Middle superior alveolar nerve. Giving the three branches descend, and molar teeth.
Middle and anterior superior alveolar branches:
The fibers from the superior superior alveolar (dental) nerve combine with the fibers from the anterior and posterior branches to form the Superior dental plexus. Anterior superior alveolar branches branch into cutter and canine teeth.
The terminal cutaneous margin of the maxillary sinus. The superior labial dent is the skin covering the upper teeth, the mouth mucosa and the labial glands.
The third branch of the trigeminal nerve. It contains sensory and motor fibers. Regions in which sensory fibers stain:
• External meatus
• Lower lip
• Lower part of the face
• Cheek, tongue and mastoid cavity mucosa
• Lower teeth and gums
• Mandibular and temporomandibular joint
• Duramater and part of its skull
A small sensory branch that emerges from the anterior branch of the mandibular nerve. The buccinator bones the skin and mucous membranes inside the mouth.
Articular branches from the branches of this nerve carry the sense of the temporomandibular joint.
Inferior alveolar nerve:
Is accompanied by the inferior alveolar artery. There are two terminals. From these, the incisor provides the nervous breaker and the innervation of the canine teeth. The mental nerve branches into molar and premolar teeth
The fibers in the dorsal nerves are commonly found in axons containing A-beta, A-delta and C-fibers, and in lesser amounts of sympathetic efferents. Sensitivity to infection is caused by the rapid fluid movement in dental tubules and the stimulation of the tips of the A-fibers within the pulp-dentin border or within 0.1-0.2 mm of the dentinal tubules. The resulting sharp pain is very severe and very different from the pain that occurs in other tissues. This is due to the large amount of nociceptive fibers in normal dentition and some structural features of the dentin layer.
Pulpal inflammation leads to dental specific problems because this layer is rigid and can not counter the increase in pulpal fluid pressure. C-fibers are present in the pulp and are particularly stimulated by inflammatory mediators
Evaluation of Dental and Intraoral Pain
For a correct diagnosis of the pain in the teeth and surrounding tissues, a good anatomy knowledge as well as a systematic approach to physical examination, laboratory and radiological examinations must be done together. The character identification of the pain with the patient's story is the first and most important component of patient evaluation. A detailed story about the location and spread of the pain should be taken. The nature of the pain, intensity, frequency, periodicity and duration should be learned. If the pain is not continuous, the times when the pain has aggravated and relieved during the day should be investigated. The factors that provoke and calm the pain should also be questioned carefully. General oral examinations should be performed and the response to dental percussion, hot and cold application should be evaluated. It is very important to compare to the symmetrical opposite side.
In order to determine the exact location of the pain, some physicians also use factors such as the response to electrical stimulation of the pulppan or the effect of local anesthetic infiltration on pain. Radiologic examination is also helpful during diagnosis.
Toothache or odontalia can be caused by periodontal structures (periodontal ligament and bone), exposing dentin layer or root surface, broken external, trauma and iatrogenic causes of the tooth from the pulp layer or the root apex.
Teeth consists of dental, enamel, dentin and cement layers and is attached to the periodontal ligament of the supporting bones. This hard box contains pulp, which is the main source of pain in the mouth. In the pulppan there is a mixed artery network, lymphatic tissue and nerve tissue. The protection of the pulp is based on the external hard tissue. When it comes out, every theme is hypersensitive.
Stimulation of the dental pulp causes a similar response, which is caused by a visceral stimulus. This touch, the excited nerve, is induced only in pain, and is independent of the severity of the severity of the pain.
The injury to the pulp may be due to thermal, mechanical or chemical irritation. The most common cause is tooth decay. The classic findings of inflammation are temperature elevation, swelling and pain, and may result in pulpal necrosis. The swollen dental pulp becomes more painful as the intra-dental pressure increases.
The most prominent feature of hyperreactive pulpalgin is susceptibility to cold. When ice is applied on the suspected tooth, a short, sharp pain occurs which lasts slightly longer than the stimulus. Such a discomfort may be associated with a new dental restoration. Pulpalji is usually reversible. The emergence of pain with hot application suggests a pulpal pathology involving transient pulpal hyperemia, pulpal inflammation or necrosis. Typically, there is a delay of a few seconds between the onset of pain and the application of warmth. The discomfort may take a few seconds after the temperature is restored. Pain is in the sinker and pulsatile style. In the presence of advanced pulpitis, visual and radiological examination shows dentin and sometimes tooth decay extending to the pulpal tissue. Treatment should be performed with pulpotomy, pulpectomy and removal of the tooth as the last solution, while in the case of slow caries progress the decay is cleaned and the tooth repair is sufficient. Acetyl salicylic acid and other non-steroidal anti-inflammatory drugs and effectil in the medical treatment of pain.
Periapical and Periodontal Pain (musculoskeletal pain)
The musculoskeletal component of toothache originates from the periodontal ligament. This structure ties the teeth to the bone. The periodontal ligament forms a sinusoidal joint that is richly preserved. Acute periapical abscess is the most common result of acute pulpitis due to untreated rot. Purified material from necrotic dental pulp is discharged through apical foramen into the nerve-rich cavity. When irritated, there is a blunt, throbbing pain in the presence of inflammation or infection. This pain can be well localized and provoked. It can take hours. The severity of the pain increases in proportion to the severity of the inflammatory event, the cellular damage, the amount of pus that is formed, and the prevalence of the infection. A very specific finding in periapical inflammation is the sensitivity of the tooth to percussion. Depending on the severity of the periapical pathology, localized tissue erythema, local or diffuse cellulitis, trismus, and lymphadenitis may occur together. Periodontal inflammation or increased pressure on an infected tooth also increases pain. The swelling of the periodontal ligament also causes it to rise slightly from the tooth socket. During chewing, the tooth is exposed to an extra functional load, further deepening the problem. Therapeutic antibiotic treatment for abscess, non-steroidal anti-inflammatory drugs for pain, and meperidine codeine are effective for drainage of absenin.
Broken Tooth Syndrome:
This pain is caused by incomplete (broken tooth) or complete tooth break (fallen tooth). A broken tooth is caused by dental pulp sensitization and pulpitis, and deep periodontal pockets also cause a strong pain. This is especially the case in molar and premolar teeth. Vertical canal fractures most commonly occur in endodontically treated posterior teeth of patients aged 45-60 years. An incomplete fracture provokes pain when a posterior tooth contains the dentin layer. Caries, inappropriate dental restorations, atypical root canal anatomy can cause this syndrome. The pain is intermittent, short - lived and sharp - shocked. Side bite and chewing exacerbate the pain. Localization of the dentinal fracture is difficult and requires an accurate history, thermal pulp test and examination of the dentinal walls of the suspected tooth. Intra-alveolar root fractures can only be identified by x-ray.
Removal of the fracture of the tooth immediately reduces the pain. Root fractures often require removal of the tooth.
Dentin and Cement Pain:
Sensitivity of normally healthy teeth is believed to be due to hydrodynamic stimulation of the nerve extensions within the open dentinal tubules. External dentin and cementum are not preserved. Mechanical, thermal or chemical (sweet) stimulation follows sharp, intermittent pain. Treatment includes fluoridated dentifrices, application of strontium chloride solution, and fluoroantral anesthesia.
It is thought that bruxism pain is caused by periodontal ligament or prolonged traumatum which is caused by periodontium, which causes pulpal inflammation. There is generalized blunt pain seen in maxillary and mandibular teeth, including one or both sides of the mouth. Psychological approach in treatment and plastic dental protectors used at night are useful.
Orofacial Pain Associated with Lyme Disease:
Lyme Disease, also known as Lyme Borreliosi, is a spirochete infection caused by Borrelia Burgdorferi. Lyme Disease can occur with very different multisystemic symptoms such as joint pain, musculoskeletal aches and headache. The diagnosis of the disease is still very difficult. As the symptoms are very similar to other diseases, specific laboratory tests are limited.
Patients usually refer to the physician with a facial or headache. There are a number of features that make the pain a secondary to the Lyme Disease. This is known as the Jarish-Herxheimer Reaction, which increases the physical symptoms due to a spirochete infection with a therapeutic dose of antibiotic administration.
The severity of pain associated with Lyme Disease may increase or decrease over a period of 1-2 months. In particular, dental pain is severe and may recur on the ipsilateral or contralateral side. Invasive interventions for treatment may be inadequate, but may also increase the severity of pain.
Pain Associated With Dental Prostheses:
Prosthetics can cause myalgia because they can be placed above the muscle entry sites. Over time they may loose and mucosal irritation similar to glossodini or burning mouth syndrome. Partial prostheses may cause periodontal complaints by compressing the teeth. Glossodini may be due to nonhygienic prostheses, aphthous ulcers, prosthesis irritation or psychological reasons.
Trigeminal neuralgia (Tic Douloureux):
Tic Douloreux, V. Cranial Nerve can be defined as recurrent pain, sudden, usually unilateral, severe, short, steeping, felt in the spread of one or more branches. Trigeminal It is thought that trigeminal root pressure is the main etiology of neuralgia. Vascular structures and anomalies, aneurysms and bony structures may cause this compression.
Paroxysmal pain attacks are usually unilateral. Pain typically increases with light touch. A nonspecific factor such as hot, cold, wind may also cause pain. It is 50% less visible in males; It occurs with people in their 40s. Pain is more frequently seen in the spread of Maxillary and Mandibular branches. Pain is always temporary and may last from a few seconds to a few minutes. Classic pain is precipitating pain, resembling electric shock. Among the episodes, in the affected area, the sensation is normal and there is no loss of pain or sensation. A short refractory period follows the attacks of pain.
Trigeminal neuralgia responds to anticonvulsants such as carbamazepine,. While clonazepam and baclofen are also effective, barbiturates are contraindicated. If a sufficient dose of carbamazepine is used to completely pass neuralgic pain and no other neurological abnormalities are found, Trigeminal Neuralgia is diagnosed. Trigger Zone local anesthetic injection also relieves paroxysmal episodes.
More invasive methods can be used in treatment. These include blockage of the Gasser ganglion with alcohol, thermocoagulation, transcutaneous nerve stimulation, retrogasserian glycerol injection, and radiofrequency lesion creation. Surgical treatment should come to mind when pharmacological and other interventions are ineffective
Traked to Trauma Trigeminal Neuralgia
Peripheral neuropathy is more commonly caused by fractures in orthognathic surgery and trigeminal spread. Deafferentiation and partial injury of the peripheral nerves result in degeneration and regeneration. There is flammable pain, hypoesthesia and dysesthesia. Allodynia and hyperalgesia are also frequently observed.
Acute Herpes Zoster: Trigeminal Distribution
Latent Varicella Zoster virus remains in Trigeminal and Geniculate Ganglia, and when the immunity of the patient decreases, infection includes Trigeminal Nerve and Facial Nerve branches, respectively. Virus affects skin, nerves, veins, bones and other structures. Sensory abnormalities occur in moderate and severe cases. The skin eruptions heal spontaneously within 3 weeks and are associated with residual pigmentary changes in moderate to severe cases. In general, high fever and lymph node enlargement can be seen. Trigeminal nerve involvement is present in 30% of herpes zoster cases. Most commonly, the first branch of the trigeminal nerve is involved, of which 60% have vesical eruptions. One of the most frequent complications in the Herpes Zoster ophthalmia is the deterioration of the corneal opacity-related vision. In some very serious cases, vision loss due to corneal ulceration occurs. Rarely, ophthalmoplegia, meningoencephalitis and hemiplegia are seen. In advanced cases, alveolar bones may be damaged and tooth loss may occur in maxillary and mandibular regions.
Postherpetic neuralgia: Trigeminal spread
Postherpetic neuralgia is characterized by chronic pain associated with residual somatosensory anomalies following recovery of acute Trigeminal Herpes Zoster eruptions. Postherpetic neuralgia is defined as pain that lasts longer than 4 months after the onset of the rash. It is evident that the affected nerve in the pathology is denervated. Anesthesia in the area of the skin that is still advanced. Characteristically, hyperalgesia, allodynia and dysesthesia accompanied by a history of episodes of herpes zoster with inflammatory pain are present. Pain is present for much longer than the clinical appearance of herpes zoster vesicles.
It is characterized by severe, constipated, paroxysmal pain associated with sympathetic nervous system paralysis (Horner's Syndrome) seen in the first part of the trigeminal nerve. The most common clinical manifestation is severe, pulsatile, supraorbital headache associated with pitosis and myosin in a middle-aged male patient. The headache can last from a few weeks to months.
Atypical Facial Neuralgia:
It was first described in 1924. It is a pain that is blunt, irritant and has intermittent burning properties. It comes from deep tissues, felt on the surface and bones. Pain is usually continuous, but may be temporary exacerbations and stresses. It can be limited to a single point for months, even years. Orbita can spread to the ears, shoulders and arm. Autonomic disorders such as vasodilatation, nasal discharge, piloerection and lacrimation may also occur in some patients.
Glossodynia, Atypical Odontalgia and Burning Mouth Syndrome (Atypical Facial Nerve Loggins) are oral types. The diagnosis of the source of pain from the mouth is difficult. The diagnosis of these conditions can only be made by excluding other possible causes. It is more commonly seen in female patients over 40 years of age. Patients with cluster headache or migraine history are more susceptible to this clinic.
Atypical facial neuralgia, when seen as a toothache, are the following findings: 1- Spontaneous multiple tooth pain 2- Local dental cause unsuitable for pain 3- Stimulant, inflammable, non-pulsatile toothache 4- Continuous, non-invasive, unchanging toothache 5- Persistent, Repetitive ovules 6- Pain ache of the tooth with local anesthesia 7-Proper dental treatment toothache does not respond
The patient relaxes when he is rested. Excessive conversation is aggravated after activities such as eating, brushing teeth, washing the face. It is never as violent as Trigeminal Neuralgia, but rather with a more moderate pain. There is no pathological or definitive physical examination or radiological evidence. The treatment is very difficult. In addition to topical anesthetics, antidepressants and psychotherapy are also studied.
Burning Mouth Syndrome:
Glossodini is characterized by inflammation of the mucous membranes of the tongue (most commonly), the mouth, the hard palate and the lips. Pain starts step by step without being an initiating factor and is usually bilateral. Together with a changing sense of taste and mouth is seen. Intraoral physical examination is normal. The origin of the pain is still uncertain. It is suggested that the peripheral nerve damage of the Chorda tympani may cause pain by inhibiting Trigeminal Nerve Inhibition. There is no reliable radiological or laboratory examination for diagnosis. 50% of the patients recover spontaneously. This improvement can take years. Tricyclic antidepressants such as amitriptyline, nortriptyline and desipramine and sertraline, a serotonin reuptake inhibitor, may be effective in treatment. Clonazepam, topically applied into the mouth, is also a treatment option. In most of the patients pharmacological treatment is ineffective and these patients need psychological support.
Deafferentation Pain (Phantom Dental Pain):
Phantom Dental Pain is similar to other phantom pain syndromes. There is a sensation of tooth pain that has been withdrawn. Pain is persistent with sharp exacerbations; With local allodynia. Interestingly, the patient's sleep is not affected. The pain is felt less in children when there is no gender difference in feeling. Carbamazepine and phenytoin are generally ineffective and their efficacy in pain suggests the diagnosis of Trigeminal neuralgia. Amitriptyline and other tricyclic antidepressants may also be effective in treatment. Nerve blocks made with local anesthetics and low dose steroids may be effective from time to time, but surgical interventions are ineffective.
Temporomandibular Joint (TME) is a complicated, diarthroidal joint located between the mandible and the glenoid fossa of the temporal bone. A rigid fibrocartilaginous articular disc (meniscus) attached to the joint capsule and its ligaments separates superior and inferior segments of the joint. The disc acts as a shock absorber. Mandibules are held in place with medial and lateral capsular ligaments and posterior meniscotemporomandibular frenum (retrodiscal pad). Stylo and sphenomandibular ligaments are more posterior and medial, while chewing muscles help to hang the mandible. The innervation of the temporomandibular joint is provided by the branches of the Mandibular and Maxillary segments of the Trigeminal Nerve.
Temporomandibular joint disorders can be divided into three categories: Chronic Myofascial Pain (KMA), Internal Disorder and Degenerative Joint Disease (DEH). KMA is the most common form of TME pain and is a psychophysiological disorder that contains the chewing muscles as a primary. Internal Irregularity can be defined as an abnormal relationship with articular discoid mandibular condyle, glenoid fossa and articular eminence. DEH (osteoarthritis) is the organic degeneration of articular surfaces in TME.
TME can be affected by all conditions such as arthritis, trauma, dislocations, ankylosis, developmental abnormalities and neoplasms that affect all other joints.
Craniomandibular Disorders (CMB) includes chewing muscles, TME, or both. These arthropathies and Chronic Myofascial Pain come into this group. It is commonly found in women especialy in their 30’s. This disease is thought to be an important psychosocial component. Increased stress causes bruxism, tooth clenching and even chewing gum too much. In these situations, overuse of the muscles results in fatigue and painful spasms. Most of the collagen tissue diseases such as systemic lupus erythematosis, sjögrens syndrome, rheumatoid arthritis cause musculoskeletal pain in head and neck.
Chronic Myofascial Pain
Chronic Myofascial Pain (KMA) is the most common cause of CMB. It is a disorder caused by trigger points on distinct muscle bands in the regional muscle structure and causing pain to the surface. Avoid stretching the muscles to reduce pain; So that the chewing muscles are held in a short, contracted state and entered into a vicious circle. The myospasm seen causes abnormalities in TME causing arthralgia. Trigger points occur in areas where maximum skeletal tension is present. Pain is blunt, unilateral and preauricular. It is increased by chewing, stretching and stimulation of trigger points. Pain can also be reflected in a distant area, which can be flammable, soggy, throbbing and disturbing. Patients may also present with ear symptoms such as otalgia, tinnitus, ear infections and vertigo.
In the treatment of CAM, fluorimetric spray, cauterization, electrical nerve stimulation with truncus, local anesthetic, or cutaneous counter-stimulation with corticosteroid injections may be beneficial. Non-steroidal anti-inflammatory agents and muscle relaxants are also effective in the short term. A soft diet is required. In the long term, passive and active muscle relaxation exercises, tooth creaking and stopping of boredom, postural rehabilitation and all the psychological factors contributing to this clinical situation should be removed.
Internal Irregularities of Temporomandibular Joint