LITMIR.BIZ

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INTRODUCTION

      Any tooth that fails to erupt into the dental arch within the expected time frame and is no longer expected to do so is, by definition, an impacted tooth. Failure of a tooth to erupt into the arch in timely fashion can be due to several factors such as crowding from inadequate arch length (Bolton discrepancy), delayed maturation of the third molar, malpositioned adjacent teeth, associated pathology (odontogenic cysts and tumors), trauma, previous surgery, dense overlying bone (lateral positioning), or soft tissue and systemic conditions (syndromes). The mandibular and maxillary third molars are the most commonly impacted teeth, followed by the maxillary canines and mandibular premolars. It is of no surprise that extraction of third molars, usually impacted, is the procedure performed with the highest frequency on daily basis by oral and maxillofacial surgeons.

      The indications and timing for removal of impacted teeth and specifically third molars are set forth by the American Association of Oral and Maxillofacial Surgeons (AAOMS) Parameters of Care and these will not be discussed here. Complication rates from the removal of impacted third molars range from 4.6% to 30.9% with an average of approximately 10% [1–6]. The incidence of these complications varies with surgeon experience, patient age, and depth of impaction. Several factors are known to increase the risk of complications and these include increased age, female gender, presence of pericoronitis, poor oral hygiene, smoking, depth of impaction, and surgeon inexperience [2, 5, 6]. The aim of this chapter is to provide a comprehensive review of the common, as well as the less common and rare, peri‐ and postoperative complications associated with impacted third molar surgery and their prevention and management.

MANAGEMENT OF COMPLICATIONS IN THIRD MOLAR SURGERY

       Alveolar Osteitis

       Etiology: patient risk factors, preoperative infection and inflammation, smoking, surgical time, surgical trauma, inadequate irrigation during surgery

       Management: prevention, irrigation, debridement, medicated packing

Alveolar osteitis (AO), or “dry socket,” is a clinical diagnosis with an incidence of 1–37% [1,4–7]. This wide range can best be explained by the lack of a uniform clinical definition of AO, with some studies defining AO as pain that requires the patient to return to the surgeon's office, while other definitions are simply based on a clinical diagnosis of AO, which is also variable. In addition, some studies report only those teeth that required surgical, versus nonsurgical, extraction, or use varied surgical protocols [5–8]. The average incidence of AO in a private practice setting based on a survey of AAOMS members was 6.5% [6]. Contributing factors to the development of AO include the use of oral contraceptives, smoking, increasing age, female gender, presence of pericoronitis, length of surgery, surgical trauma, and compromised medical status [6–8].

      AO is often described as the loss, lysis, or breakdown of a fully formed blood clot prior to its maturation into granulation tissue in the extraction socket. Patients may present with a myriad of symptoms and signs approximately three to five days following tooth extraction. The most common complaints are pain, breath malodor, and a foul taste that do not respond well to oral analgesics and often keep a patient awake at night. Clinically, a gray‐brown clot, or the complete absence of an organized clot, may be present in the extraction socket. Food debris may or may not be present, and the surrounding tissues may be erythematous and edematous. The site is exquisitely tender to palpation and often patients will have referred pain to other areas of the head and neck, including the ear, eye, or temporal and frontal regions.

      The incidence of AO can effectively be decreased through a variety of interventions, all of which focus on decreasing the bacterial load at the surgical site. Chlorhexidine gluconate 0.12% presurgical socket irrigation or mouth rinsing either with or without postoperative rinses has shown to be beneficial in decreasing the AO incidence [7–9]. Copious irrigation and lavage of the surgical site with normal saline have also been reported to effectively decrease AO. In one study, normal saline was as effective as pre‐ and postoperative rinses with chlorhexidine, and “Cepacol.” Others have demonstrated no significant difference between pulse lavage and hand syringe irrigation. Intra‐alveolar antibiotics, specifically tetracycline, lincomycin, and clindamycin, may also decrease the incidence of AO [8]. Postoperative antibiotics have not consistently shown an ability to influence the development of AO, and the evidence to support preoperative or intraoperative systemic antibiotics is controversial [3, 7, 8]. Most studies do not demonstrate a significant difference. Overall, proper surgical technique with minimal iatrogenic tissue trauma, copious irrigation, and the use of chlorhexidine rinses or topical antibiotics have shown promise in decreasing the incidence of AO.

The aim in the management of AO is to relieve the patients' pain until adequate maturation of the healing socket may occur. Most treatment paradigms focus on gentle irrigation with or without mechanical debridement, with the placement of obtundent dressings (e.g. iodoform gauze lightly soaked with benzocaine, eugenol, balsam of Peru, and chlorobutanol). Interestingly, there is very little evidence to support the use of a particular dressing or medicament over another. Commonly, iodoform gauze and eugenol are used to “pack” the socket and this packing is changed q.d. or q.o.d. [4, 8]. Eugenol is a member of the phenylpropanoid class of chemical compounds and is beneficial due to its inhibition of neural transmission and neurotoxicity. Iodoform is an organoiodine compound that has antibacterial properties and has been used since the early twentieth century as an antiseptic wound dressing. Most commercially available dry socket pastes or dressings include eugenol in combination with various other medicaments such as guaiacol, chlorobutanol, balsam of Peru, and butamben. The use of gelfoam as a carrier for eugenol materials and as an obtundent dressing has also been reported. Patients should be seen regularly for follow‐up to ensure elimination of symptoms, and if non‐resorbable iodoform packing is used, patients should be seen to change or eventually remove the packing. This is important since if the patient's pain is resolved, they may not return for a follow‐up and a nonresorbable material can lead to infection. It is important to avoid the use of eugenol and other neurotoxic chemicals in the presence of an exposed inferior alveolar nerve (IAN) or lingual nerve (LN). The use of systemic antibiotics has not been shown to be efficacious, and is not recommended for treatment of AO [8]. Typically, patients will have resolution of symptoms within 3–5 days; however, in certain patients it may require 14 days for complete resolution [4, 8]. In summary, AO is one of the more common complications of third molar surgery. Its incidence can be decreased though a combination approach of preoperative rinses, irrigation, and/or local antibiotic application and its treatment is straightforward (Algorithm 2.1).

Algorithm 2.1: Alveolar Osteitis

       Infection

       Etiology: preoperative infection or inflammation, surgical debris, inadequate irrigation, patient risk factors

       Management: incision and drainage, irrigation, antibiotics

      Surgical wound infection rates as a result of third molar extraction range from 0.8% to 4.2% and almost exclusively involve the mandibular third molars [1–6, 10, 11]. According to most general surgery and infectious disease literature, any surgical procedure within the oropharynx is considered a clean‐contaminated wound, a class II wound, and carries a <10% risk of surgical site infection (SSI). If inflammation without purulence is noted, such as that with pericoronitis, the wound is then classified as contaminated, class III, and carries an SSI rate of 20%. The presence of purulence or necrotic tissue at the time of surgery results in a 40% risk of SSI. Class I data are available to support the use of preoperative antibiotic prophylaxis for

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