TOOTH ERUPTION Discomfort is commonly associated with the eruption of primary or deciduous teeth in infants. Irritability, drooling, and decreased intake are commonly associated findings. An associated low-grade fever (37.9°C) and diarrhea are more controversial findings. No scientific data support an association of teething, fever, and diarrhea. It is plausible that mild dehydration from excessive salivary production or a decrease in intake may result in a low-grade fever, and changes in feeding habits may result in diarrhea. One must be careful in attributing either to tooth eruption. Other sources for fever must be carefully sought. 2 Other common causes of orofacial pain are listed in Table... .23.4-?.
TABLE 234-2 The Differential Diagnosis of Orofacial Pain
As with the primary dentition, eruption of permanent teeth, especially third molars, or wisdom teeth, may result in significant pain. Gingival irritation and inflammation associated with tooth eruption are common and must be distinguished from pericoronitis. Pericoronitis, although usually associated with the eruption of third molars, can be associated with any tooth. Gingival tissue overlying the occlusal surface of an erupting tooth, or operculum, progressively becomes inflamed secondary to impaction of food and debris beneath the operculum. Direct trauma from opposing teeth during mastication compounds the inflammatory process. Normal gingival irritation associated with tooth eruption is replaced by a progressive inflammatory process resulting in frank infection. Because of the close proximity of the masseteric space to third molars, associated trismus is common and portends the potential for extension into the communicating parapharyngeal spaces. Treatment consist of appropriate antibiotic therapy with penicillin VK 500 mg qid, erythromycin 250 mg qid, or clindamycin 300 mg qid, local irrigation of food and debri from underneath the operculum, saline mouth rinses, and analgesic therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) and narcotic preparations as appropriate. Referral to a general dentist or an oral and maxillofacial surgeon within 24 to 48 h is essential. If pericoronitis is related to trauma from an opposing tooth, as is frequently the case with third molars, concomitant extraction of the opposing tooth and antibiotic therapy will bring marked relief within 24 h. 3 Definitive treatment is extraction of the associated tooth by a general dentist or oral and maxillofacial surgeon.
DENTAL CARIES AND PULPAL PATHOLOGY Dental caries represents the loss of integrity of the tooth enamel secondary to dissolution of hydroxyapatite from prolonged exposure to the acidic metabolic by-products of plaque bacteria. Caries most commonly occurs in areas where plaque accumulates such as pits and fissures of the occlussal surface, interproximally, and along the gingival margins. When a sufficient breach of enamel integrity has occurred, sensitivity to cold or sweet stimulus may result. With dentinal involvement, caries progression occurs more rapidly, spreading along dentinal microtubules. At this stage, direct communication between the oral environment and the vital dental pulp has been established, and inflammatory changes in the pulpal tissue are evident histologically.
The pulpal inflammatory process is initially reversible, but with continued stimuli, the pulp's ability to respond and repair is jeopardized. Irreversible pulpitis can be distinguished from reversible pulpitis by the duration of symptoms. Both require a stimulus to initiate a painful response; however, in reversible pulpitis, the duration of pain is short, lasting seconds, as compared with irreversible pulpitis, in which the pain may last for minutes to hours. The most common stimulus is thermal, although sweet or sour stimulus also can elicit a painful response. Spontaneous odontogenic pain most frequently represents pulpal death or necrosis. Pain elicited with heat stimulus is most commonly associated with pulpal necrosis, but some painful response to heat with irreversible or irreversible pulpitis may occur. Distinguishing where a particular tooth falls on the continuum is impractical for the emergency physician. Treatment focuses on providing adequate analgesia and referral to a general dentist. The definitive treatment for irreversible pulpitis and pulpal necrosis is root canal therapy or dental extraction. 45
PERIRADICULAR PATHOLOGY The most common cause of severe odontogenic pain is periapical pathology. Periapical granuloma, more appropriately termed periradicularperiodontitis, is the most common periapical lesion. This lesion is not a true granuloma but rather slowly expanding granulation tissue associated with the root apex. Most commonly, periradicular periodontitis is a result of pulpal inflammation or necrosis, but it can be associated with trauma. Periapical or radicular cyst and periradicular abscess are clinically and radiographically identical lesions to periradicular periodontitis. A periapical cyst has an epithelial lining originating embryologically from the rest of Malassez, and a periradicular abscess represents the accumulation of associated inflammatory cell. All three lesions are only associated with the apical region of teeth with severely inflammed or necrotic pulps and may cause significant pain. Radiographically, these periapical lesions appear as a slight widening of the periodontal ligament space, thinning of the lamina dura, or a frank radiolucent area associated with the apex on a periapical dental radiograph (Fig 234-4). Radiographic evaluation with a panorex is rarely useful for identification of all but the most extensive periradicular lesions but can be important in identifying more significant painful osseous pathology. Erosion of a periradicular abscess through the cortical bone results in subperosteal extension with intraoral or facial swelling and fluctuance. A small swelling of the gingiva with a draining fistula adjacent to the affected tooth is known as a parulisA5
FIG. 234-4. A. The radiographic appearance of a healthy tooth with a normal periodontal ligament space and distinct lamina dura compared with the radiographic appearance of a periapical abscess, periradicular periodontis, and periradicular cyst. B. A frank periapical radiolucency. C. Subtle radiographic loss of the periapical lamina dura and widening of the periodontal ligament space. ( Courtesy of Gary M. Beaudreau, D.M.D.)
Pain of dental origin may be diffuse in nature, presenting as a headache, sinus pain, eye pain, or jaw or neck pain or may be localized to a single tooth. One must remember to consider myocardial infarction as an etiology of jaw pain. Identification of the offending tooth is best accomplished by eliciting pain with percussion of the suspected teeth with a dental mirror handle or similar metallic object. Definitive treatment of periradicular periodontitis, periapical cysts, and abscesses is root canal therapy or extraction of the affected tooth. This, however, is not prudent in the ED. Subperiosteal extension and the resulting fluctuant abscess should be incised and drained orally. The emergency physician should treat dental abscesses or other periapical lesions with oral antibiotics such as penicillin VK 500 mg qid, clindamycin 300 mg qid, or erythromycin 500 mg qid and provide adequate analgesia with an NSAID. Narcotic analgesia may be indicated in the first 24 to 48 h. Prompt referral to a dentist for definitive treatment such as root canal therapy or extraction is indicated. 45
FACIAL CELLULITIS Spread of odontogenic infections into the various facial tissue spaces is relatively common. Buccal extension of a periapical infection of the mandibular teeth will involve the buccinator space. Maxillary labial extension of infection primarily will involve the infraorbital space. Perforation through the lingual cortical bone of mandibular molars, particularly the second and third molars, usually occurs below the mylohyoid ridge, affecting the submandibular space. Lingual spread of periapical infections associated with mandibular anterior teeth will affect the lingual space. The submandibular space and lingual space communicate with each other at the posterior border of the mylohyoid muscle.
Cellulitis of bilateral submandibular spaces and the lingual space is called Ludwig's angina and is potentially life threatening. Clinically, Ludwig's angina is a rapidly spreading cellulitis that results in brawny induration of the suprahyoid region and elevation of the tongue. Involvement of the floor of the mouth pushes the tongue posteriorly. Epiglottic involvement is not uncommon. As a result, airway compromise is the immediate primary concern. The primary focus of initial management is maintenance of a patent airway. Timely administration of high-dose penicillin and metronidazole or cefoxitin is essential. An aminoglycoside may be added to extend coverage, and in the penicillin-sensitive person, clindamycin may be substituted. Immediate oral and maxillofacial surgical consultation and hospitalization for incision and drainage and intubation as indicated are necessary.6
Infection of the infraorbital space may have a potentially devastating outcome if retrograde spread via the ophthalmic veins occurs, and the cavernous sinus becomes involved. Cavernous sinus thrombosis presents as an infraorbital or periorbital cellulitis with rapidly developing meningeal signs, sepsis, and coma. Early recognition and treatment with high-dose intravenous antibiotic as above are essential in decreasing morbidity and mortality.
POSTEXTRACTION ALVEOLAR OSTEITIS Pain in the initial 24 to 48 h after dental extraction, termed periosteitis, is common and responds well to analgesics. Depending on the tooth removed, density of the bone, and amount of associated trauma that occurred during extraction, significant discomfort can occur. Postextraction alveolar osteitis, or dry socket, usually occurs on the second or third postoperative day and is associated with exquisite oral pain. Dislodgment of the clot from the socket or fibrinolytic dissolution of the clot results in exposure of the alveolar bone to the oral environment. This initiates an inflammatory response resulting in a localized osteomyelitis of the exposed bone. A higher incidence of dry sockets has been identified in females on hormone replacement therapy probably secondary to increased plasmin fibrinolytic activity as a result of exogenous estrogens. Other risk factors for developing postextraction alveolar osteitis include smoking, preexisting pericoronitis or periodontal disease, traumatic extractions, and a prior history of alveolar osteitis. 78
The incidence of postextraction alveolar osteititis is 2 to 5 percent of all extractions but is considerably higher (20-35 percent) among impacted third molar extractions. Many studies have shown that topical antibiotic placement such as tetracycline or clindamycin at the time of surgery or chlorhexidine mouth rinses after extraction reduce by nearly tenfold the incidence of dry sockets. Dental radiographs should be taken to ensure the absence of a retained root tip or other foreign body. Thorough irrigation of the dental socket with sterile normal saline and packing it with oil of cloves- or eugenol-impregnated gauze results in an almost immediate improvement in level of comfort. Dental anesthesia may be necessary to adequately irrigate and pack a dry socket. Antibiotic therapy is indicated in the most severe cases, and daily packing changes are important. Thus referral to a dentist within 24 h is indicated. 78
Managing postoperative dentoalveolar sequelae is in the realm of emergency medicine. Postoperative pain is a common presentation. Pain immediately postoperative is most commonly related to the trauma of surgery. Providing adequate analgesia is important in these patients. Postoperative edema such as with extraction of third molars is best managed with ice packs and elevation of the head of the bed to 30°. Most oral and maxillofacial surgeons premedicate patients with Decadron in complex cases to minimize swelling. Swelling normally peaks in the first 24 to 48 h. Trismus is common postoperatively and can result from infection, direct injury to the temporomandibular joint, injury to the muscles of mastication during administration of the inferior alveolar nerve block or during the surgery, and most commonly, normal perioperative inflammation. Trismus peaks in the first 24 h and usually decreases thereafter unless an infective process is the etiology. Postoperative trismus should resolve entirely by 1 week. If trismus persists, stretching exercises usually are initiated by the oral and maxillofacial surgeon. 9
DENTINAL SENSITIVITY Improper tooth brushing techniques may result in cervical erosion and abrasion, recession of the gingival tissue, and exposure of the root surface to the oral environment. In this setting, teeth may be very sensitive to cold stimulus. Microscopic or macroscopic fractures of the enamel also will result in pain on cold stimulus or mastication. Avoidance of the inciting stimulus is recommended. There are several therapies available to a dentist such as topical flouride application or restorative repair of areas of significant toothbrush abrasion that may be helpful. 3
POSTRESTORATIVE PAIN Pain may occur after a dental restorative procedure. Trauma from mechanical instrumentation of the tooth or direct exposure of the pulpal tissue during instrumentation may result in pain. Pain associated primarily with mastication may be a result of improper occlusion of the new restoration. Analgesia and referral to the patient's general dentist are the treatment of choice. After endodontic therapy, patients may experience exquisite pain secondary to instrumentation or a buildup of gaseous pressure in the pulp chamber and may require a dentist to reopen the tooth because analgesics may be inaffective.
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