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/100.2°F) and diarrhea are more controversial findings. No scientific data support an association of teething, fever, and diarrhea. One must be careful in attributing either to tooth eruption. Other sources for fever must be carefully sought.² Table 242-2 lists common causes of orofacial pain.

Table 242-2 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 is inflammation of the operculum, or the gingival tissue overlying the occlusal surface of an erupting tooth. Impaction of food and debris beneath the operculum results in a severe inflammatory response. Without intervention this progressive inflammatory process will result in frank infection. Because of the close proximity of the masticator space (comprised of the masseteric space, pterygomandibular space, and the superficial and deep temporalis space) to third molars, associated trismus is common and portends the potential for extension into the communicating parapharyngeal spaces. Treatment consists of appropriate antibiotic therapy with penicillin VK 500 mg PO qid, erythromycin 250 mg PO qid, or clindamycin 300 mg PO qid, local irrigation of food and debris from underneath the operculum, saline mouth rinses, and analgesic therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) and opiate 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 during mastication, as is frequently the case with third molars, concomitant extraction of the opposing tooth and antibiotic therapy will bring marked relief within 24 h. 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 occlusal 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, carious 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 stimuli 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. Determining a particular tooth’s position in this continuum of disease 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.

Periradicular Pathology

The most common cause of severe odontogenic pain is periapical pathology. Periapical granuloma, more appropriately termed periradicular periodontitis, 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 indistinguishable from periradicular periodontitis, yet histologically separate entities. A periapical cyst has an epithelial lining originating embryologically from the rest of Malassez, and a periradicular abscess merely represents the accumulation of associated inflammatory cell. All three lesions are only associated with teeth with severely inflamed or necrotic pulps and may cause significant pain. Radiographically, these periapical lesions appear as a slight widening of the periodontal ligament space, a thinning of the lamina dura, or a frank radiolucent area associated with the root apex on a periapical dental radiograph (Figure 242-4). Radiographic evaluation with a Panorex panoramic x-ray machine is rarely useful for identification of all but the most extensive periradicular lesions, but can be important in identifying other more significant painful osseous pathology.

View Large Fig. 242-4. Add to ‘My Saved Images’ 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 periodontitis, and periradicular cyst. B. A periapical radiolucency. C. Subtle radiographic loss of the periapical lamina dura and widening of the periodontal ligament space. (Courtesy of Gary M. Beaudreau, DMD.)

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. A small swelling of the gingiva with a draining fistula adjacent to the affected tooth is known as a parulis, and can help identify the involved tooth. Erosion of a periradicular abscess through the cortical bone and subperiosteal extension results in intraoral or facial swelling and fluctuance that, if possible should be incised and drained intraorally. The emergency physician should treat dental abscesses or other periapical lesions with oral antibiotics such as penicillin VK 500 mg PO qid, clindamycin 300 mg PO qid, or erythromycin 500 mg PO qid, and should provide adequate analgesia with an NSAID. Opioid 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.

Facial Cellulitis

Spread of odontogenic infections into the various facial 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 and involves 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 angina (see Chap. 243) and is potentially life-threatening. Clinically, Ludwig 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. As these spaces and the masticator spaces ultimately communicate with the parapharyngeal space, involvement of the epiglottis 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 intravenous 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.

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 a high-dose IV 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. Displacement 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. Risk factors for developing postextraction alveolar osteitis include smoking, preexisting pericoronitis or periodontal disease, a traumatic extraction, a prior history of alveolar osteitis, and hormone replacement therapy.³

The incidence of postextraction alveolar osteitis is 2 to 5 percent of all extractions but is considerably higher (20 to 35 percent) among impacted third molar extractions. 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.^3,4

Managing postoperative dentoalveolar sequelae is in the realm of emergency medicine. Postoperative pain requiring analgesics, is a common presentation. Pain immediately postoperative is most commonly related to the trauma of surgery. Postoperative edema such as with extraction of third molars peaks within the first 24 to 48 h and is best managed with ice packs and elevation of the head of the bed to 30 degrees. Trismus, also common postoperatively, 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 persisting for greater than 1 week will usually require stretching exercises prescribed by the oral and maxillofacial surgeon.^3,4

Postrestorative Pain

Pain may occur after a dental restorative procedure. Normal 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. After endodontic therapy, patients may experience exquisite pain secondary to instrumentation or a buildup of gaseous pressure in the pulp chamber. Providing analgesia and referral to the patient’s general dentist are the treatment of choice.

Periodontal Pathology

Periodontal Disease

Gingival inflammation and bleeding, or gingivitis, results from the accumulation of plaque along the gingival margins. Hormonal variations of puberty, adolescence, and pregnancy, as well as many medications such as phenytoin, may exacerbate gingival inflammation. As the inflammatory process progresses, destruction of the periodontal attachment apparatus occurs, and the gingival sulcus deepens, resulting in periodontal pockets and periodontitis. Periodontal pockets create a favorable environment for plaque accumulation, maturation, and mineralization into calculus. Further destruction of the periodontal attachment results. Eventually, sufficient bone loss causes tooth mobility and tooth loss.^1,5

The pathogenesis of periodontal disease is uncertain, but there is a very strong association between adult periodontitis and Bacteroides gingivalis. Many other specific bacteria have been shown to have a role in periodontitis. Destruction of tissue collagens, proteoglycans, and the connective tissue matrix is a major feature of gingivitis and periodontitis. Three theories for the etiology of this destruction have been proposed. Tissue destruction may occur as a result of the direct effects of bacterial plaque and their metabolic products, an accelerated host immune response, or immune deficiencies involving neutrophil function or the autologous mixed lymphocyte response.^1,5

Four distinctive types of periodontal disease have been identified. These include adult, rapidly progressing, juvenile, and prepubertal periodontitis.⁵ Etiology, age and gender predilection, and clinical course of disease vary by type. A definite association between juvenile periodontitis and Actinobacillus actinomycetemcomitans exists. More severe and rapidly progressing periodontitis, especially those types affecting a younger population such as the prepubertal and juvenile periodontitis, appears to be associated with decreased neutrophil chemotaxis or phagocytosis. Systemic illnesses such as human immunodeficiency virus (HIV) infection, diabetes, lazy leukocyte syndrome, Down syndrome, and cyclic neutropenia are associated with severe periodontal disease.¹

Periodontal disease usually progresses painlessly but may present as gingival bleeding or tender, swollen gingival tissue. Treatment is directed at slowing or arresting the progression of disease primarily by the removal of plaque and its by-products.¹ Antibiotics may play a role in treatment. Referral to a dentist for definitive treatment is indicated because the treatment involves extensive dental cleaning, instruction and improvement in oral hygiene, and in some cases, periodontal surgery.

Periodontal Abscess

When plaque and debris are entrapped in the periodontal pocket, a periodontal abscess may form, resulting in severe pain. Small periodontal abscesses respond to local therapy with warm saline rinses and antibiotics such as penicillin VK 500 mg PO qid or erythromycin 250 mg PO qid. Larger periodontal abscesses require incision and drainage. Saline mouth rinses four times a day are useful. Analgesics are essential.

Acute Necrotizing Ulcerative Gingivitis

Acute necrotizing ulcerative gingivitis (ANUG) is an aggressively destructive process (Figure 242-5). Also known as Vincent disease or trench mouth, it is part of a spectrum of disease ranging from localized ulceration of the gingiva to often fatal noma, in which localized ulceration and necrosis spread to the adjacent tissues of the cheeks, lips, and underlying facial bones.^6,7 The diagnostic triad includes pain, ulcerated or “punched out” interdental papillae, and gingival bleeding. Secondary signs include fetid breath, pseudomembrane formation, “wooden teeth” feeling, foul metallic taste, tooth mobility, lymphadenopathy, fever, and malaise.^7,8

View Large Fig. 242-5. Add to ‘My Saved Images’ Acute necrotizing ulcerative gingivitis. (Courtesy of Philip J. Hanes, DDS.)

The differential diagnosis for ANUG is quite extensive, but herpes gingivostomatitis is most difficult to differentiate. Herpes gingivostomatitis usually has smaller vesicular eruptions, less bleeding, more systemic signs, and lack of interdental papilla involvement.^7,8

The etiology of ANUG is still poorly understood. It appears to be an opportunistic infection in a host with lowered resistance. It is believed that suppression of the humoral and cell-mediated immune response in HIV infection, severe malnourishment, and perhaps stress may be responsible for a lowered host resistance. Anaerobic bacteria such as Treponema, Selenomonas, Fusobacterium, and Prevotella are uniformly identified. These bacteria appear to invade otherwise healthy tissue, resulting in an aggressively destructive disease process.^7,8

The most important predisposing factor is HIV infection. Previous necrotizing gingivitis infection is the second most important predisposing factor. Other contributing factors include poor oral hygiene, unusual emotional stress, poor diet, inadequate sleep, white heritage, age less than 21 years, poor socioeconomic status, recent illness, alcohol use, tobacco use, acatalasia, and various infections such as malaria, measles, and intestinal parasites.^7,8

Treatment consists primarily of bacterial control. Chlorhexidine oral rinses bid, professional debridement and scaling, and adjunctive antibiotic therapy with metronidazole 250 mg PO tid are the mainstay of treatment. Reduction in pain can be expected within 24 h of institution of this regimen. Identification and resolution of the predisposing factors, and supportive therapy with a soft diet rich in protein, vitamins, and fluids are important in establishing and maintaining a disease-free state.⁷

Cranial Neuralgias

Trigeminal neuralgia is the most common of the cranial neuralgias. Others include postherpetic neuralgia, glossopharyngeal and vagal neuralgia, and superior laryngeal neuralgia. Trigeminal neuralgia is undoubtedly one of the most painful entities involving the face. Most commonly affecting adults 30 to 60 years of age, females constitute 60 percent of the patients. Trigeminal neuralgia is almost always unilateral, following the anatomic distribution of the involved cranial nerve. The maxillary branch of the fifth cranial nerve is most commonly affected. Recurrent episodes of excruciating, electric shock like paroxysmal pain of short duration, separated by pain-free periods are characteristic. Associated contraction of the facial and masticatory muscles is typical, resulting in the term tic douloureux. Physical stimulation of a trigger point is the usual inciting event.⁹

The pathogenesis of trigeminal neuralgia is still uncertain. Diagnosis is clinical, requiring the exclusion of organic pathology such as acoustic neuroma or a nasopharyngeal carcinoma. Thus referral to a neurologist is important.⁹

Trigeminal neuralgia may respond well to the administration of carbamazepine (100 mg PO bid initially and gradually increasing as needed to a maximum dose of 1200 mg daily). Surgery is reserved for patients who do not respond to medications.⁹

Nonparoxysmal pain of neuropathic origin may develop 1) in patients who have had long-standing neuralgias, 2) secondary to surgical trauma along the distribution of the affected nerve branch, and 3) in association with viral infections, drugs, or heavy metal intoxication. Other neuropathies such as alcoholic and diabetic sensory neuropathies also may affect the oral cavity.

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