with IAC diversion, and one in four patients with darkening of the root, or interruption of the white line of the IAC, exhibited impairment of sensation. These signs are highly sensitive, but not highly specific, for risk of nerve injury, and the absence of all radiographic risk factor signs has a strong negative predictive value [30]. Therefore, patients without any significant indicators of nerve injury are unlikely to have injury, patients with an injury are likely to have at least one of the predictors, and patients without injury commonly have predictors of injury radiographically. Other reported radiographic indicators such as deflection of the roots, narrowing of the roots, dark bifid root apices, and narrowing of the IAC were statistically unrelated to nerve injury [30].
LN injury is associated with increased age, female gender, distoangular tooth inclination, lingual tooth orientation, perforation of the lingual cortex, and presurgical pericoronitis (this tends to “scar” the LN closer to the surface mucosa increasing vulnerability to injury) [32, 33]. Often, flap reflection, tooth sectioning with extension through the tooth into the lingual plate, or lingual plate fracture may be causal factors in the injury [32, 33]. Due to the nerve's variable position, care must be taken when incisions are made and flaps reflected. Miloro et al. reported 10% of LNs positioned superior to the lingual crest, and 25% in direct contact with the bone of the lingual plate [28, 29, 34]. The mean vertical distance of the LN from the lingual crest is 2.75 mm, and the mean horizontal distance of the LN from the lingual plate is 2.53 mm [29]. Perforation of, or a defect in, the lingual plate may represent normal patient anatomy (50% of preoperative CBCTs may have an anatomic lingual plate defect [personal communication, Roger A. Meyer, Shahrokh C. Bagheri]), or may represent iatrogenic injury from a rotary instrument.
Injury to the LN or IAN due to local anesthetic injection occurs in approximately 1 in 785 000 cases, with 79% affecting the LN and 21% the IAN. The highest incidence is associated with 4% prilocaine (Citanest) or 4% articaine (Septocaine) solutions. The majority of cases, 85%, resolve within eight weeks and of the remaining 15%, one‐third will eventually resolve [31]. Unfortunately, patients with persistent paresthesia are not candidates for microneurosurgical repair since access in the pterygomandibular space is limited, and also, the nerve may not show a readily identifiable area of injury or neuroma formation to resect and repair due to the nature of the injury, which may be mechanical (from the needle itself or a barb on the needle tip) or chemical (from a concentration effect of the local anesthetic solution).
All patients who report paresthesia should be followed closely for resolution and appropriate objective neurosensory testing performed. The clinical neurosensory test should be performed to determine the degree of impairment, and to assess whether microneurosurgical intervention is indicated. There are three levels of testing according to Zuniga et al. [35]. Mechanoreceptive testing begins with level A testing. It is comprised of brush stroke directional discrimination and two‐point discrimination. It is important to test both normal (to establish a baseline) and abnormal areas, map out the area of impaired sensation by marking directly on the patient's skin, and consider photographs of the markings for future reference and comparison. Two‐point discrimination can be tested using a Boley gauge or the two non‐cotton ends of a cotton tip applicator. Testing should proceed in 2 mm increments of widening between the points until the patient can no longer discern two separate points. Normally, the IAN has a discriminatory threshold of 3–5 mm and the LN of approximately 2–4 mm [27]. Level B testing involves contact detection using von Frey hairs or Semmes–Weinstein monofilaments that deflect with a certain amount of pressure application, and normative values exist for these as well. Finally, level C testing of nociception includes pain (pinprick) and thermal discrimination, and typically these are recorded as all‐or‐none responses. Taste is not usually tested in LN injuries. The indications for microneurosurgical repair include the following: complete anesthesia beyond one to two months, profound nonresolving hypoesthesia (below a level of functional sensory recovery) after three months, early dysesthesia (may indicate neuroma formation), and a clinically observed Sunderland V nerve transection at the time of surgery [27, 36]. Referral to a surgeon proficient in microneurosurgery should be made if any of the above criteria are met, or if the surgeon is unfamiliar with nerve testing and possible treatment protocols [27]. In general, dysesthesia is managed with pharmacological therapy (e.g., gabapentin, pregabalin, amitriptyline), while hypoesthesia/anesthesia is managed with microneurosurgery. The details of microneurosurgical repair are beyond the scope of this chapter (Algorithm 2.5).
Algorithm 2.5: Neurosensory Deficit
Bony sequestra and lingual plate exposure are potential complications of low significance, but require thorough and prompt attention. Small bony sequestra will likely spontaneously extrude through the soft tissues and usually cause only temporary discomfort. Reassuring the patient or parent that there is no remaining tooth in the area, the usual concern at presentation, and removing the loose bone is all that is required. The injury to the soft tissues is resolved within few days and the patient is instructed to avoid trauma from chewing in the area until this occurs. Exposure of the lingual plate or a portion of the mylohyoid ridge is common since the overlying mucosa in this area is exceedingly thin. The common complaints will be pain upon swallowing and sharp bone detected in the area. Application of topical anesthetic to allow for a bone file or fine rongeurs to gently smooth or remove any sharp bone is all that is required. The patient is instructed to avoid further injury to the area with certain foods such as popcorn or potato chips and is reassured that the area will spontaneously heal. Oral hygiene and rinses with chlorhexidine will facilitate coverage of the area.
Osteomyelitis
Etiology: patient risk factors, poor surgical technique, infection
Management: antibiotics, surgical debridement, decortication, sequestrectomy, or resection
The incidence of osteomyelitis as a result of third molar extraction is not reported frequently in the literature; however, it is a known complication of postoperative infection, fracture, and/or extractions performed in medically compromised patients. Osteomyelitis is an inflammation of the bone marrow and is most common in the mandible due to its dependence on blood supply from the inferior alveolar artery and periosteum and poorly vascularized thick cortical bone. Since the maxilla has a rich vascular supply from multiple vessels, it is less likely to develop osteomyelitis. The presence of bacteria within the marrow space leads to inflammation and edema with subsequent compression of blood vessels and a decrease in blood supply. This decrease in blood flow results in ischemia, bone necrosis, and proliferation of bacteria. Purulence and bacteria can spread within the marrow via Haversian systems and Volkmann's canals and extend into cortical bone. Once the cortical bone and periosteum are involved, the blood supply is further compromised and perforation of soft tissues can occur resulting in fistula formation. Predisposing factors in the development of osteomyelitis involve suppression of host defenses in some form. Diabetes, alcoholism, malnutrition syndrome, autoimmune disease, radiation therapy, chemotherapy, steroid use, osteopetrosis, and myeloproliferative diseases can contribute to the development of osteomyelitis.
Table 2.1. Types of osteomyelitis
Source: Adapted from Alpert et al. [37].
| AcuteContiguous focusProgressiveHematogenous ChronicRecurrent multifocalGarré's proliferative periostitisSuppurative or nonsuppurativeSclerosing |
The classification of osteomyelitis offered by Hudson is commonly cited in the literature and includes acute and chronic forms, based upon disease presence for either less than (acute) or greater than (chronic) one month (30 days) [37] (Table 2.1).
Patients