What supply the gingival buccal tissue of premolars m canines, and incisor.. Inferior alveolar nerve

What supply the gingival buccal tissue of premolars m canines, and incisor?
A- Long buccal
B- Inferior alveolar nerve***
C- Superior alveolar nerve.
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Oral paraesthesia is described as a tingling sensation in the lower lip, which may be continuous or intermittent. Various terms are used by patients to describe this sensation: heat, cold, burning, pricking, tingling, tingling, numbness, itching. Paresthesia may be associated with mechanical trauma, compression, neurotoxic effect, or thermal burn.
The following case study describes the imaging results and surgical treatment of a patient with paresthesia due to compression.

Case study:
A 23-year-old woman presented to a private practice in September 2009 for left and right side mouth pain that was due to irreversible pulpitis of teeth 26 and 36. The woman had never smoked or consumed d alcohol and she did not have a relevant personal or family history. Intraoral clinical examination revealed a fracture of the closure of tooth 37, as well as several dental caries and significant gingivitis.
A retro-alveolar radiograph showed the presence of a broken endodontic instrument in the mesial root of tooth 37. The radiograph also showed chronic apical periodontitis of the distal root, as well as a radiolucency that was very close to the inferior alveolar nerve and who seemed in direct contact with the nerve. The patient was asked about her previous endodontic treatment. She recalled that the treatment was done in 2003 and she has since experienced numbness in the left lip and a small part of the chin. She also mentioned tingling in the vestibular gingiva and indicated that these symptoms were more pronounced in the morning and when she was stressed. As these numbness worried the patient, she had consulted a neurologist about it. We did not evaluate the sensitivity of the patient's soft tissues during our consultation because the symptoms of paresthesia were not apparent.
Due to the proximity of the foreign body to the lower alveolar nerve, a CT scan was performed to determine the location and dimensions of the object and its relationship to the anatomical structures. Computed tomography showed that the broken endodontic instrument was in direct contact with the mandibular canal. The instrument protruded approximately 3 mm from the apex of the tooth and periapical radiolucency.
It was proposed to the patient to extract tooth 37 and remove the broken instrument. The patient was informed of complications that could occur during and after surgery. The tooth was sectioned and the distal and mesial roots were removed separately. The area was thoroughly cleaned with a curette until the small fragment of the broken instrument could be removed. The periapical radiological lesion associated with the distal root was also cleaned with the curette.
To prevent edema and pain after surgery, we prescribed an antibiotic (amoxicillin 1 g, 1 tablet 2 times daily for 8 days), a corticosteroid (methylprednisolone 16 mg, decreasing dose of 4 tablets on the first day at 1 tablet on day 4), analgesic (paracetamol 1 g, 1 tablet 2 times daily for 3 days) and vitamin B complex [Neurobion (Merck KGaA, Darmstadt, Germany), 1 tablet, once daily for 2 days month]. We also recommended that he rinse his mouth with chlorhexidine gluconate 0.2% 3 times daily for 15 days. Eight days after the surgery, the patient reported that the numbness had stopped.

Discussion:

There are 4 main causes of oral paresthesia. The first - mechanical trauma - results mainly from overinstrumentation beyond the apex that causes lesions of the lower alveolar nerve normally associated with second molars6. The second cause (compression phenomenon) can occur when filling materials or endodontic instruments are present in the lower alveolar canal. The third (neurotoxic effects) is related to solutions that are used to clean the root canal or sealants6. Finally, the fourth cause is thermal burn. Hyperextension and overinstrumentation are the most common etiological factors associated with paresthesia following orthodontic (conventional) endodontic treatment.

Dental paresthesia may occur in association with a root canal, although it is not limited to this context. For example, as indicated by Cohenca and Rotstein, tests to detect the presence of necrotic pulp in adjacent teeth should be done in some patients with symptoms of paresthesia.

Investigations should also be made to find other localized factors such as mandibular fracture, expansive or compressive lesions (including malignant tumors), included teeth, iatrogenic lesions resulting from tooth extraction. administration of anesthetic injection, implants or sequelae of orthodontic surgery. Iatrogenic lesions are the most common cause of sensory disturbances of the lower alveolar nerve.

There seems to be a correlation between the duration, origin and extent of the trauma and the prognosis of paresthesia. Thus, the longer the mechanical or chemical irritation lasts, the greater the degeneration of the nerve fiber and the greater the risk that paresthesia becomes permanent.

Seddon described stages of nerve damage based on lesion severity, prognosis, and recovery time: neurapraxia, axonotmesis, and neurotmesis. Neurapraxis is mainly due to nerve compression; the recovery is complete and it occurs after a few hours or a few days. Axonotmesis is defined as a decrease in nerve continuity; recovery takes several months, but it is incomplete. Finally, neurotmesis is the most serious stage of peripheral nerve damage. There can not be complete recovery, but partial recovery is possible if primary repair is performed.

Compression is the main mechanism that causes peripheral nerve damage. The compression of the artery that irrigates a nerve causes an increase in vascular permeability, edema and ischemia and thus reduces the supply of oxygen to the nerve. The classic reaction to neurapraxis is paresthesia, but there may also be axonotmesis if the compression lasts long enough. In such cases, recovery can take up to a year.

According to the anatomical study by Tillota-Yasukawa et al, cancellous bone in the molar region contains many vacuoles, and no cortical bone protects the pedicle. In 8 of the 40 cases examined by these authors, the cancellous bone was slightly denser around the canal, but the perforations remained numerous, thus preventing effective protection of the nerve. These authors also determined that there was less than 1 mm between the inferior alveolar nerve and the apex of the second and third molars. Littner et al. however, there are contrary data that the upper edge of the mandibular canal is usually located 3.5 to 5.4 mm below the apex of the first and second molars and the mandibular canal is never located near the apex of the first and second molars. These latter observations have been corroborated by Knowles et al. who have confirmed that the mandibular canal is cribriform, and not solid. When endodontic treatment is to be performed on the second molar, rigorous radiographic evaluation should be done to estimate this distance.

During endodontic treatment, X-rays should be taken using files of the appropriate working length to avoid punctures and lesions of the inferior alveolar nerve. If an endodontic instrument causes mechanical damage to the lower alveolar nerve, it can be repaired by a healing process that will cause immediate but temporary paresthesia. The extensive preparation required for endodontic treatment results in the disappearance of the apical constriction, which allows the passage of irrigation products and sealing materials and thus causes nerve damage of the chemical or mechanical type.

There may also be overinstrumentation if granuloma is present at the apex. This type of lesion forms an osteolytic zone made of less dense bone in the periapical region, which may allow instruments to pass beyond the apex and thereby damage the lower alveolar nerve.

Whenever possible, treatment should begin with the elimination of the immediate cause. Inflammation, edema, hematoma or infection must be controlled2 to prevent irreversible damage such as reactive fibrosis and neuroma. Various drugs may be administered, including antibiotics, nonsteroidal anti-inflammatory drugs and corticosteroids, proteolytic enzymes (to break down the coagulum) and vitamin C (for its antioxidant action). Gatot and Tovi15 suggested that prednisolone be used to reduce the duration of the problem, prevent fibrosis and reduce the severity of sequelae. However, no consensus could be reached on the type or dose of steroids appropriate or the duration of treatment. Surgical treatment is indicated when the nerve has been severed, a foreign body causes compression, or there is nerve neoplasia or persistent anesthesia or paresthesia. The main benefit of surgery during the early stages of paresthesia is the restoration of the microvascular system of the nerve that allows nerve regeneration. The results of surgical decompression are, however, unpredictable and the surgery involves certain risks, including the severing of the nerve or the formation of another lesion that could cause complete anesthesia. Girard recommends caution during the execution of any procedure that may cause nerve damage.

Several drugs to promote recovery from nerve damage were evaluated, including vitamins B1, B6 and B12 (composition of vitamin B complex that was administered to the patient in the case study). Although these substances improve the regeneration of peripheral nerves in animal models, there is no scientific evidence to support these effects in humans.

In the case presented here, several factors may have contributed to paresthesia, including the broken endodontic instrument, the periapical radiolabial lesion in direct contact with the mandibular canal, and the associated inflammatory responses. The rapid resolution of paresthesia suggests that it was due to compression of the lower alveolar nerve, a phenomenon compatible with neurapraxis.

Because of the close anatomical relationship between the second molars and the inferior alveolar nerve, careful clinical and radiographic examination should always be done before endodontic treatment of these teeth, to prevent iatrogenic lesions of the type described in this article. Dentists should also know the anatomical features of the mandibular canal (ie cribriform rather than solid), as well as the consequences of overinstrumentation.