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What's Your Diagnosis?

What Is Causing a Boy’s Palatal Swelling?

  • Answer: Palatal abscess/cellulitis secondary to dental caries

    Results of laboratory workup were as follows: white blood cell (WBC) count, elevated at 18,900/µL (reference range, 4000-11,000/µL), with 82.1% neutrophils; urea nitrogen, 7 mg/dL (reference range, 8-25 mg/dL); glucose, 115 mg/dL (reference range, 60-100 mg/dL); creatinine, 0.3 mg/dL (reference range, 0.5 to1.0 mg/dL); sodium, 136 mEq/L (reference range, 130-135 mEq/L); bicarbonate, 21 mg/dL (reference range 17-25 mg/dL); and C-reactive protein, 2.2 mg/dL (reference range, 0-8.0 mg/dL). Results of a rapid streptococcal test were negative, and blood cultures were sent for further evaluation.

    Based on the patient’s clinical history, physical examination findings, and acuity of presentation, we strongly suspected palatal abscess/cellulitis secondary to dental caries as the most likely etiology. We also considered other benign etiologies as important differentials. The boy was admitted to the pediatric floor for intravenous (IV) antibiotics, IV fluids, and close follow-up. He was started on IV clindamycin, and his pain was well controlled with IV ketorolac followed by oral ibuprofen. An otorhinolaryngology consultant agreed with our provisional diagnosis and antibiotic management. The decision was made to continue the antibiotics and to consider incision and drainage of the lesion if he failed to respond.

    The next day, the midline bright pink lesion developed a dark yellow color in the center (Figure 3) with a slight reduction in size to 2 × 2 cm; the tenderness was much improved, and the patient tolerated liquids well. The palatal swelling over the left side of the hard palate had subsided, and he denied any pain in the area. His dental caries pain persisted, however, but improved with oral ibuprofen as needed. He remained afebrile throughout hospital stay. Because the oral pain and swelling had improved, we planned to discharge him on oral clindamycin for 7 more days.

    Fig 3
    Figure 3. Midline swelling with thick pus (black arrow) and a visible caries in the left second maxillary molar (red arrow).

    He was instructed to follow up with an otorhinolaryngologist in 1 week and with a dentist within 10 days for dental caries management. At a subsequent follow-up visit, his midline swelling had completely disappeared without any residual problems.

    DISCUSSION

    A palatal mass can pose a diagnostic dilemma. The main differential diagnoses of swelling in palate are periapical lesions, periodontal abscess, and neoplastic processes/benign lesions (Table). The palate is very typical for an abscess arising from a nonvital lateral incisor or the palatal root of an upper first molar. Most infections of the oral cavity are primary odontogenic infections originating within the dental pulp (most commonly), periodontal tissue, or pericoronal tissue. Palatal abscess often occurs in the premolar-molar region, showing a fluctuant mass or swelling lateral to the midline.1

    Table

    DIFFERENTIAL DIAGNOSIS

    Hyperplastic candidiasis. Hyperplastic candidiasis is the result of chronic colonization and superficial oral mucosa invasion by Candida species, causing chronic inflammatory changes with edema and epithelial proliferation. The result of these reactive responses is a raised, pebbled-appearing lesion. It is most commonly seen under denture sites in denture wearers.2 It appears as a white plaque that is nonscrapeable and often mimics leukoplakia. It also can present either as an isolated, adherent white plaque (homogenous type) or as multiple white nodules on an erythematous background (nodular or speckled type). This lesion is confirmed histopathologically by the presence of Candida hyphae and by the complete resolution of the lesion with antifungal treatment.

    Torus palatinus. A torus is a wide-based, smooth-surfaced bony protrusion in the midline of the hard palate caused by cortical bone growth with a thin, poorly vascularized mucosa lining. These exostoses are considered developmental anomalies, although they usually do not appear until adulthood. A torus located along the midline of the hard palate is called a palatal torus or torus palatinus, and a torus located along the lingual aspect of the mandible is called a mandibular torus or torus mandibularis. Palatal tori are reported in 20% to 35% of the US population,3 whereas mandibular tori are reported in 7% to 10% of the US population.4 Removal is required only if a torus interferes with function or denture fabrication or is subject to recurrent traumatic surface ulcerations.

    Foreign bodies. Impaction of foreign bodies on the hard palate of infants and children is not a common finding. However, it should be considered in the differential diagnosis of palatal lesions in infants or children who are unable to provide a history and on whom physical examination is difficult to perform. The true nature of these foreign bodies might also be obscured by mucosal molding to their edges, which might result in misdiagnosis and unnecessary biopsy attempts under general anesthesia. Plastic caps, coins, pistachio shells, plastic screw covers, buttons, and billiards cue tips have been reported as embedded foreign bodies at the midline over the palate.5 Careful examination should be made before deciding on additional investigations such as biopsy and advanced imaging studies.

    Mucocele of hard palate. Obstruction of the minor salivary gland ducts can lead to retention of mucus with a cystic lesion lined by salivary duct epithelium, termed as mucus retention cyst. It can develop in the lips, buccal mucosa, tongue, palate, or floor of the mouth. Mucoceles may result from either rupture of a salivary gland duct and extravasation of mucus into the surrounding soft tissues or obstruction of the duct with retention of mucus.6 Most mucoceles are of the extravasation type, in which a pooling of mucus occurs in the connective tissue, presumably arising from trauma to the ducts of the minor salivary glands, mostly at lower lip area. They usually present as small painless nodules with a bluish or pinkish smooth surface. Complete surgical removal of the lesions with their cystic wall is a good treatment option that carries no recurrence risk.

    Oral focal mucinosis. Oral focal mucinosis is a rare lesion of unknown etiology that usually presents as an innocuous soft tissue swelling in the oral cavity that may be pedunculated or sessile.7 The lesions may be a result of an overproduction of hyaluronic acid by fibroblasts at the expense of collagen production. Histopathology results show a nonencapsulated area of loose, myxomatous connective tissue surrounded by denser, collagenous connective tissue. Due to the uncommonness of occurrence and a lack of distinctive clinical features, histological features are used as the basis for diagnosis. Current recommend management of oral focal mucinosis is surgical excision.7 If the lesions occupy a large portion of the palate, a failure to diagnose and manage them promptly may lead to dysphagia and/or speech impairment.

    Squamous papilloma. Oral squamous papillomas are mostly benign and asymptomatic proliferating lesions induced by human papillomavirus. They account for 8% of all oral tumors in children.8 Common site predilection for the lesions is the tongue and soft palate and rarely the uvula and vermilion border of the lip. Papillomas generally measure approximately 1 cm and appear as pink to white exophytic granular or cauliflower-like growths. Histologically, these lesions mainly present as long, thin, fingerlike projections extending above the mucosal surface. They are lined by stratified squamous epithelium and connective tissue centrally. The upper epithelial layers show pyknotic nuclei, often surrounded by an edematous or optically clear zone, the so-called koilocytic cell.9 Removal of the lesion is the treatment of choice for oral squamous papillomas, either by surgical excision, electrocautery, cryosurgery, intralesional injections of interferon, or laser ablation. The recurrence rate is very low for the solitary type compared with multiple lesions.8

    Mucoepidermoid carcinoma (MEC). Minor salivary gland tumor accounts for about 15% of all salivary gland neoplasms, of which MEC accounts for 35.9% of total cases.10 Pleomorphic adenoma is the most common benign neoplasm, and MEC is the most common malignant tumor. MEC occurs most commonly between the third and sixth decades of life and affects women to men in a 3 to 2 ratio. It is frequently seen in the parotid gland, followed by the minor salivary glands. The palate is the most frequent site for MEC (28%), followed by the retromolar region (23%), the floor of the mouth (14%), the buccal mucosa (11%), and the lower lip (9%).11 MEC presents as several histopathologic variants such as clear cell, melanocytic, sclerosing, unicystic, sebaceous, psammomatous, spindle, goblet, and oncocytic variant cells.12 MEC of the hard palate presents as a slow-growing, persistent swelling that is usually painless and soft in consistency. Advanced disease and late diagnosis are associated with extensive spread with the possibility of perforation of the hard palate and invasion into the maxillary antrum or nasal cavity.

    Neuroblastoma. Neuroblastoma is the most common neurogenic extracranial solid tumor of infancy and childhood.13 More than 95% of neuroblastomas are diagnosed in children younger than 10 years of age.13 Clinically, neuroblastoma presents with proptosis, periorbital ecchymosis, abdominal distension, bone pain, pancytopenia, fever, anemia, hypertension, paralysis, watery diarrhea, and subcutaneous skin nodules. Oral manifestations of metastasis include soft, fluctuant, bluish swelling on the left and right side of the posterior palate; bleeding ulcer; buccal displacement of the primary teeth; exposure of the tooth bud of the permanent maxillary left first molar; and exfoliation of tooth buds of the permanent maxillary left first molar and the primary maxillary left second molar through ulcer. Oral metastasis can grow rapidly, causing pain, difficulty in chewing, dysphagia, disfigurement, and intermittent bleeding.14 In low-risk patients, surgical resection is the baseline treatment, in conjunction with chemotherapy for high-risk pediatric patients. A combination of aggressive surgical resection, high-dose chemotherapy with stem-cell rescue, radiation therapy, and bioimmunologic therapy has been recommended.15

    Iatrogenic inflammatory fibrosis. Fibrosis is a rare complication after dental extraction and is characterized by formation of excessive fibrous connective tissue, which can be reparative, reactive, benign, or pathological.16 Inflammatory fibrosis manifests as a postextraction complication possibly caused by localized iatrogenic trauma to the soft tissue, deregulating the wound healing process at either the proliferative or remodeling stages. It may also be caused if the irritant persists in the tissues during the healing process. Complications may result from rapid palatal injections of local anesthetic solutions, particularly vasoconstrictors, which cause ischemia, allergic reactions, epithelial desquamation, traumatic injuries, ulcerations, fibrosis, and necrosis.

    ETIOLOGY

    Odontogenic infections arise from bacteria that reside in the oral cavity, and they are often polymicrobial, with mixed aerobic and anaerobic bacteria. Streptococci are isolated most often, in as many as 50% to 65% of infections.17 Anaerobic bacteria involved in odontogenic infections include gram-positive cocci (eg, Peptostreptococcus, Gemella) and gram-negative rods (eg, Bacteroides). Although Staphylococcus species are not a common cause of oral infections, it is interesting to speculate on whether the increase in abscesses especially caused by methicillin-resistant S aureus, is leading to an increase in the incidence of abscess in unusual locations such as the hard palate.

    PATHOGENESIS

    The paired palatine processes of the maxillary bones articulate at the anterior median palatine suture and form the anterior part of the hard palate. The paired palatine bones located posteriorly articulate by the posterior median palatine suture and form the posterior part of the hard palate.18 Suppurative odontogenic infections, particularly pulpal infections, may spread beyond tooth sockets to potential orofacial spaces. Serious complications can occur when they extend to deep fascial spaces or bone. The extension to the palatal side is less common compared with the buccal side, as the infections tend to take the path of least resistance. The thickness between the periapical area and cortical bone is less narrow on the palatal side compared with the buccal side. Moreover, root canal treatment failures occur more commonly with the buccal root, increasing the incidence of buccal abscess.

    Palatal space demarcated superiorly by the cortical plate of the hard palate, inferiorly by the periosteum, and laterally by the alveolar process of the maxilla and teeth is a potential space that does not exist in the healthy condition. Normally, palatal mucosa is tightly adhered to the periosteum. But the spreading dental infection separates the periosteum, and pus accumulates between the periosteum and bone, forming a palatal abscess.19 It is a circumscribed, fluctuant swelling often seen in the maxillary premolar-molar region in a lateral or paramedian location. A palatal abscess usually does not cross the midline because of the tight attachment of mucosa to the periosteum at the midline suture. However, sometimes the surrounding edema gives a false impression of crossing the midline or even contralateral involvement.

    TREATMENT

    Definitive treatment of an odontogenic infection should begin with evacuation of pus. However, it is important to note that toxic patients should be given antibiotics and also should be properly hydrated before surgical intervention. Palatal abscess should be treated by extraction or pulpectomy of the offending tooth, along with incision and drainage of pus.1 Usually IV ampicillin-sulbactam or IV clindamycin are the preferred antibiotics for dental infection and palatal abscess.

    TAKE-HOME POINTS

    Clinicians need to be aware of the differential diagnosis of palatal swelling and be cognizant of the differentials in acute, subacute, and chronic presentations. Early extraction of an offending tooth and incision and drainage tend to shorten the usual course of infection and further complications. Clinically, a palatal swelling may resemble a dental cyst, an abscess, or any benign or malignant neoplasms, which can lead to delays in diagnosis and management. Hence, prompt clinical and histopathologic diagnosis of such lesions is of utmost important for successful management. Clinicians should be aware of the oral manifestations of neuroblastoma, papilloma, submucous fibrosis, and MEC lesions, which help in early diagnosis and prompt referral. Easily detachable small objects should not be accessible to infants and children, since the risks of aspiration, choking, or embedding in the oral cavity are relatively high.

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