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Soft tissue lesions of the oral cavity in children

Soft tissue lesions of the oral cavity in children
Literature review current through: Jan 2024.
This topic last updated: Apr 20, 2022.

INTRODUCTION — Soft tissue lesions of the oral cavity in children may be normal/developmental findings or indicative of gingivitis, periodontal disease, local or systemic infection, benign tumors, or life-threatening systemic conditions (table 1).

The clinical features and management of common soft tissue lesions of the oral cavity in children will be reviewed here. Congenital anomalies of the oral cavity, gingivitis, periodontal disease, and the oral manifestations of systemic conditions are discussed separately. (See "Congenital anomalies of the jaw, mouth, oral cavity, and pharynx" and "Gingivitis and periodontitis in children and adolescents" and "Periodontal disease in children: Associated systemic conditions".)

LESIONS OF THE GUMS

Eruption cyst or hematoma — Eruption cysts are dome-shaped soft tissue lesions associated with the eruption of primary or permanent teeth. They are caused by fluid accumulation within the follicular space of the erupting tooth. Eruption cysts are called eruption hematomas when the cyst fluid is mixed with blood (picture 1). No treatment is needed; eruption cysts resolve spontaneously as the tooth erupts through the lesion. If the tooth does not erupt within two weeks, the child should be reexamined to evaluate other causes.

Pigmentation — In dark-skinned children, pigmentation of the attached gingiva, due to melanin, is a normal finding [1].

Retrocuspid papillae — Retrocuspid papillae are small (2 to 3 mm [0.1 inches] in diameter), firm, round, pink to red, fibroepithelial papules on the gums behind the lower canines in most children (picture 2). They are often bilateral. They usually are asymptomatic and decrease in size with age. No treatment is necessary.

Parulis ("gum boil") — A parulis ("gum boil") is a soft, solitary, reddish papule on the gums above or below a primary tooth with necrotic pulp (ie, an abscess) (picture 3). The parulis forms at the exit point of the draining fistulous tract; pus and drainage may be observed. Obstruction of the sinus tract can cause acute pain and swelling.

The parulis typically regresses shortly after treatment of the abscessed tooth (extraction or complete pulpectomy, depending upon prognosis and strategic importance of the tooth). If the tooth is not treated, the parulis may persist for years or mature into a fibroma (picture 4). (See 'Irritation fibromas' below.)

Gingival overgrowth — Gingival overgrowth or hyperplasia in children can be inflammatory, an adverse effect of certain medications, infiltrative, or, rarely, hereditary.

Inflammatory – Localized or generalized chronic inflammatory gingival enlargement can result from longstanding gingivitis in children, particularly when plaque accumulates around braces (picture 5C) or in the upper and lower front teeth secondary to mouth breathing.

Inflammatory gingival hyperplasia involves the gums between the teeth and at the margin of the teeth. The gums become enlarged and erythematous, with a shiny, smooth, friable surface that bleeds easily.

Gingivectomy is sometimes required, but inflammatory gingival enlargement often resolves with adequate plaque control.

Drug-induced – Drug-induced gingival overgrowth is an adverse effect of phenytoin, nifedipine, and cyclosporin A (picture 5A-B), among other medications [2]. Phenytoin is the most common cause in children. The fibrous overgrowth that occurs is painless and firm, with little tendency to bleed. Initial enlargement occurs between the teeth and may appear lobular; it gradually proceeds to involve gums at the margin of the teeth and may progress to cover the crowns, interfering with occlusion. Drug-induced gingival overgrowth can cause delay or failure of tooth eruption if it occurs before tooth eruption is complete.

Susceptibility to drug-induced gingival overgrowth appears to have a genetic component [3]. The severity of gingival overgrowth is related to the concentration of the medication in the gums and the adequacy of oral hygiene [4]. The inflammatory response to dental plaque can exacerbate overgrowth, particularly on the front teeth. Thus, meticulous dental hygiene is recommended for children who must take drugs that can cause gingival overgrowth. The use of electric toothbrushes may help to prevent further overgrowth by improving gum care.

Although drug-induced gingival overgrowth is not dose related, it can progress rapidly if two or more overgrowth-inducing drugs are used in combination [3,5]. Such combinations should be avoided if possible. Gingival overgrowth may be partially reversible if the precipitating drug is discontinued. However, in a case report, one dose of azithromycin for three days was associated with a reduction of cyclosporin-induced gingival overgrowth in a patient without discontinuation of cyclosporin [6]. The mechanism of action is unknown but may be related to azithromycin's antimicrobial and anti-inflammatory properties or its ability to persist in low concentrations in the macrophages and fibroblasts of the periodontium. Gingivectomy may be necessary in severe cases. Recurrence is likely if the precipitating medication is not discontinued.

Additional indications for gingivectomy include:

Gingival appearance is unacceptable to the patient

Interference with normal function

Production of a periodontal pocket that cannot be maintained in a healthy state

Post-gingivectomy discomfort is considerable and should be carefully weighed against the potential benefits. This is particularly important for patients with intellectual disability (in whom the most severe cases of gingival hypertrophy are seen), who may not be able to give fully informed consent.

Infiltrative – Leukemia, particularly myelogenous leukemia, can cause gingival enlargement due to infiltration of the gingival tissues [7]. Gingival enlargement due to leukemia is typically edematous and/or hemorrhagic (picture 5D). Patients with leukemic gingival hypertrophy may have difficulty maintaining adequate oral hygiene because of gingival bleeding. The resulting inflammation acts as a stimulus for further connective tissue hyperplasia [8]. Extraoral findings may include systemic symptoms, anorexia, fatigue, bleeding, and fevers. (See "Overview of the clinical presentation and diagnosis of acute lymphoblastic leukemia/lymphoma in children".)

Hereditary – Hereditary gingival fibromatosis (also called idiopathic hyperplasia) is a rare condition with onset in early childhood [9,10]. Some cases are associated with syndromes (eg, Zimmermann-Laband syndrome type 1 or type 2, Rutherfurd syndrome, Ramon syndrome, Jones syndrome) [11].

Hereditary gingival fibromatosis is characterized by progressive nonhemorrhagic fibrous enlargement of the buccal and lingual gingival surfaces of the upper and lower teeth. Hereditary gingival fibromatosis is frequently complicated by failure or delay of eruption of primary and permanent teeth. The treatment of choice is gingivectomy. Meticulous oral hygiene is recommended to reduce the risk of recurrence.

Vascular – Localized juvenile spongiotic gingival hyperplasia presents as a localized area of erythema on the attached gingiva in the front of the mouth, predominately the maxillary gingiva (picture 5E) [12-14]. It is most commonly seen in adolescent females. We treat with topical corticosteroids instead of surgical excision to avoid creating a gingival margin defect.

Gingival recession — The teeth erupt through a band of keratinized gingiva, also known as the attached gingiva. The width of the keratinized band remains relatively constant during growth and development. However, alterations in the normal path of tooth eruption (eg, due to crowding or over-retention of primary teeth) may be associated with narrowing of the band of attached gingiva [15].

Narrowing of the attached gingiva is particularly common when the lower incisors erupt toward the outer edge of the alveolar ridge ("labial eruption") (picture 6). Progressive loss of attachment can lead to "mucogingival defects" (picture 6), which predispose to rapid gingival recession.

In children without mucogingival defects, orthodontic repositioning of malpositioned teeth may reverse or prevent further gingival recession. Mucogingival defects are treated with gingival grafting with palatal tissue. Gingival grafting repairs and stabilizes the attached gingiva.

HIV gingivitis — Human immunodeficiency virus (HIV) gingivitis, also called linear gingival erythema, presents as a brightly inflamed band of marginal gingiva (picture 7). The gums are painful and bleed easily; there may be rapid tissue destruction.

HIV gingivitis is associated with growth of gram-negative anaerobes, enteric bacteria (eg, Escherichia coli, Klebsiella spp), and yeast (Candida albicans), organisms that are not found in routine cases of gingivitis. (See "Gingivitis and periodontitis in children and adolescents", section on 'Gingivitis'.)

HIV gingivitis is unresponsive to improved oral hygiene [16]. Treatment consists of debridement plus antibiotic administration. Antibacterial rinses (chlorhexidine, fluoride) and antifungal rinses/troches (nystatin, fluconazole, etc) may be helpful.

Other lesions — Hemangiomas, irritation fibromas (picture 4), peripheral ossifying fibromas (picture 8), pyogenic granulomas (picture 23B), peripheral giant cell granulomas, traumatic ulcers (picture 9A), aphthous ulcers, and herpetic gingivostomatitis (picture 10A) may occur on the gums and other soft tissues of the oral cavity. (See 'Lesions that occur at multiple sites' below.)

LESIONS OF THE TONGUE

Ankyloglossia ("tongue-tie") — Ankyloglossia (restrictive lingual frenum or "tongue-tie") is the term used to describe restriction of tongue movement caused by a prominent or short frenum between the tongue and the floor of the mouth (picture 11). The clinical features and management of ankyloglossia are discussed separately. (See "Ankyloglossia (tongue-tie) in infants and children".)

Congenital lingual melanotic macules — Congenital lingual melanotic macules are single or multiple asymptomatic pigmented macules that are present from birth [17-19]. The diameter ranges from 3 mm to 3 cm (0.1 to 1.2 inches) and increases proportionally as the child grows. The pigmentation may be homogeneous or heterogeneous.

Presence at birth distinguishes congenital lingual melanotic macules from other conditions associated with hyperpigmentation of the tongue (eg, hairy black tongue, Laugier-Hunziker syndrome, Peutz-Jeghers syndrome [PJS], and pigmented fungiform papilla (picture 12)).

Congenital lingual melanotic macules can be monitored in infants who have no symptoms, no lymphadenopathy, and no family history of systemic conditions associated with mucosal pigmentation (eg, PJS) [17,18]. Tongue biopsy may be warranted if the diagnosis is uncertain. Characteristic histologic findings include increased deposits of melanin in the basal cell layer with variable degrees of overlying hyperkeratosis [17,19].

Geographic tongue — Geographic tongue (benign migratory glossitis) is a chronic, recurring disorder characterized by pink to red, slightly depressed lesions with irregular, elevated, curvilinear white or yellow borders (picture 13). The lesions are areas of dekeratinization and desquamation of filiform papilla. The pattern of dekeratinization and desquamation changes continuously, creating the migratory appearance. The lesions occur predominantly on the top and sides of the anterior tongue. Geographic tongue typically is asymptomatic but may be painful when inflamed [20]. Reassurance is usually the only necessary treatment. We suggest avoidance of acidic and spicy foods and beverages when the lesions are inflamed.

Fissured tongue — Fissured tongue (lingua plicata) is a developmental anomaly characterized by a prominent central, anterior-posterior fissure from which smaller fissures radiate laterally. The fissures may be shallow or deep; deep fissures can trap food debris, which may cause inflammation (picture 14) or secondary fungal infections. Patients with tongue fissures should be advised to brush the surface of the tongue to remove trapped food particles [21].

Tongue fissuring with normal-appearing filiform papillae occurs in approximately 5 percent of the general population and is considered to be a normal variant [22]. Fissured tongue occurs more frequently in adults than children but is a common finding in children with Down syndrome. It is seen in the Melkersson-Rosenthal syndrome, a rare disorder consisting of recurrent facial and/or lip edema and relapsing facial nerve paralysis [23]. (See "Down syndrome: Clinical features and diagnosis" and "Facial nerve palsy in children", section on 'Etiology and epidemiology'.)

Mucoceles — Mucoceles are painless swellings that may occur on the ventral surface of the tongue associated with the glands of Blandin-Nuhn [24]. However, the most common location is the inside of the lower lip (picture 15) [25]. (See 'Mucoceles and ranulas' below.)

Other lesions — Hemangiomas; lymphatic malformations (picture 16); irritation fibromas; traumatic ulcers; aphthous ulcers; thrush (picture 17); herpetic gingivostomatitis (picture 10B); and hand, foot, and mouth disease may occur on the tongue and other soft tissues of the oral cavity. (See 'Lesions that occur at multiple sites' below.)

LESIONS OF THE LIPS

Herpes labialis — Herpes labialis is a reactivation of the herpes virus that occurs as a vesicular eruption on the skin adjacent to the lip (picture 18). The vesicles rupture to form ulcers and crusts and heal without scarring in one to two weeks. Herpes labialis may be induced by exposure to sunlight, cold, trauma, stress, or immunosuppression. Prodromal symptoms include tingling, burning, or pain.

The clinical features and treatment of herpes labialis are discussed separately. (See "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection" and "Treatment and prevention of herpes simplex virus type 1 in immunocompetent adolescents and adults", section on 'Oral infection'.)

Angular cheilitis — Angular cheilitis (perlèche) is characterized by painful fissuring at the corners of the mouth (picture 19A-B). It is usually caused by C. albicans. Angular cheilitis may occur in immunocompromised children and children who habitually lick the corners of the mouth, creating an environment in which Candida can establish an infection. (See "Cheilitis", section on 'Angular cheilitis'.)

Freckling — Freckling of the lips may be a normal finding in children and adolescents (picture 20B). Multiple perioral and oral freckles may be associated with genetic disorders (eg, Peutz-Jeghers syndrome (picture 20A), Laugier-Hunziker syndrome). (See "Peutz-Jeghers syndrome: Clinical manifestations, diagnosis, and management" and "Acquired hyperpigmentation disorders", section on 'Laugier-Hunziker syndrome'.)

Abnormalities of the labial frena — The labial frenum is the mucous membrane that extends from the center of the upper or lower lip to the gums between the two central incisors. Abnormalities of the upper labial frenum may be associated with dental malalignment and gingival recession; abnormalities of the lower labial frenum are rarely problematic.

In young infants, the upper labial frenum extends over the gums to form a raphe that reaches the palatal papilla (also called the incisive papilla). This raphe usually regresses before dental eruption. Failure to regress may result in widely spaced front teeth (diastema). Orthodontic treatment for diastema is typically delayed until the permanent incisors and cuspids have erupted to allow natural space closure. Frenotomy (also known as frenectomy or frenulectomy) is indicated if the appearance is unacceptable after natural and orthodontic closure of the diastema.

Extension of the labial frenum to the central incisors may cause traction on the gums. Frenotomy may be necessary to prevent gingival recession and bone loss. (See 'Gingival recession' above.)

Absence or hypoplasia of the lower labial frenum has been associated with Ehlers-Danlos syndrome [26,27] and infantile hypertrophic pyloric stenosis [28]. (See "Clinical manifestations and diagnosis of Ehlers-Danlos syndromes" and "Infantile hypertrophic pyloric stenosis".)

Multiple labial frenums at birth have been associated with chondroectodermal dysplasia (Ellis-van Creveld syndrome) and oral-facial-digital syndrome [29]. (See "Skeletal dysplasias: Specific disorders", section on 'Chondroectodermal dysplasia (Ellis-van Creveld syndrome)' and "Kidney cystic diseases in children".)

Mucoceles and ranulas — Mucoceles are painless swellings that typically occur on the inside of the lower lip, but may also occur on the tongue (picture 15) or on the floor of the mouth (ranula (picture 21)) [25]. They are usually less than 1 cm (0.4 inches) in diameter, smooth-walled, and bluish or translucent.

Mucoceles and ranulas are caused by extravasation of mucous from minor salivary glands. They are formed when salivary gland secretions dissect into the soft tissues surrounding the gland, usually as a result of trauma that causes pooling of mucous in the soft tissue [25,30-32].

Mucoceles may spontaneously resolve; if they persist, the surface may become keratinized. Mucoceles that interfere with feeding, swallowing, or speech or that cause discomfort are excised with the associated minor salivary glands. Ranulas also are usually treated surgically. The procedure varies from incision and drainage to marsupialization to complete excision of the sublingual gland, depending upon the extent of the ranula. (See "Congenital anomalies of the jaw, mouth, oral cavity, and pharynx".)

Other lesions — Hemangiomas (picture 22A); lymphatic malformations (lymphangiomas); irritation fibromas; pyogenic granulomas (picture 23A); traumatic ulcers (picture 9B); aphthous ulcers (picture 26B); thrush (picture 17); herpetic gingivostomatitis (picture 10B); and hand, foot, and mouth disease (picture 24) may occur on lips and other soft tissues of the oral cavity. (See 'Lesions that occur at multiple sites' below.)

LESIONS OF THE PALATE

Herpangina — Herpangina is a benign clinical syndrome characterized by fever and painful oral lesions located on the posterior soft palate/tonsillar pillar. Herpangina lesions progress from yellow/grayish-white papules to vesicles surrounded by erythema to shallow ulcerations with a rim of intense erythema (picture 25). Herpangina is predominantly caused by group A coxsackieviruses and typically affects children age 3 to 10 years during summer outbreaks. It is discussed separately. (See "Hand, foot, and mouth disease and herpangina".)

Other lesions — Irritation fibromas; traumatic ulcers; aphthous ulcers; thrush; herpetic gingivostomatitis; and hand, foot, and mouth disease may occur on the hard or soft palate and other soft tissues of the oral cavity. (See 'Lesions that occur at multiple sites' below.)

LESIONS OF THE BUCCAL MUCOSA — Hemangiomas; lymphatic malformations (lymphangioma); mucoceles; irritation fibromas; traumatic ulcers; aphthous ulcers (picture 26A); thrush (picture 17); herpetic gingivostomatitis; and hand, foot, and mouth disease may occur on the buccal mucosa and other soft tissues of the oral cavity. (See 'Lesions that occur at multiple sites' below.)

LESIONS THAT OCCUR AT MULTIPLE SITES — The soft tissue lesions described below occur at multiple sites within the oral cavity.

Benign tumors

Hemangiomas — Hemangiomas are benign vascular tumors that typically are red or bluish-red, slightly raised, and moderately firm to palpation. They can occur in any soft tissue location and are common on the lip (picture 22A), dorsum of the tongue, gingiva, and buccal mucosa (picture 22B).

Hemangiomas appear early in life and typically enlarge rapidly during infancy and regress slowly during childhood [33]. They are usually painless but can ulcerate or bleed if traumatized.

Treatment is indicated if the hemangioma interferes with breathing, eating, or speech or is grossly deforming. The treatment of infantile hemangiomas is discussed separately. (See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications" and "Infantile hemangiomas: Management".)

Lymphangiomas — Lymphangiomas are benign tumors of the lymphatic vessels. Superficial lymphangiomas are pink to reddish-blue, soft, and compressible (picture 16); deeper lymphangiomas may not be apparent at the surface. The tongue, lips, and buccal mucosa are the most common sites of occurrence. Large lymphangiomas that involve the floor of the mouth and the neck are called cystic hygromas. Lymphangiomas can be present at birth or develop early in life.

Surgical resection is the most common treatment, despite a high frequency of recurrences and complications. Image-guided percutaneous chemoablation may be an alternative to surgical resection at some institutions [34,35].

Traumatic overgrowth

Irritation fibromas — Irritation fibromas are formed when chronic irritation results in reactive connective tissue hyperplasia. They are typically pale pink, smooth, firm, less than 1 cm (0.4 inches) in diameter, and have a sessile or pedunculated base (picture 4). They commonly occur on the tongue, lip, palate, or buccal mucosa but may occur on any oral mucosal surface. They can be surgically removed; recurrence is rare if the source of irritation is removed.

Peripheral ossifying fibromas — Peripheral ossifying fibromas also are induced by irritation. They predominantly occur on the gingiva and contain mineralized tissues (eg, bone, cementum-like tissue, or calcifications) (picture 8). Treatment involves surgical excision down to the bone. Recurrence is approximately 16 percent [36].

Pyogenic granulomas — Pyogenic granulomas are benign vascular tumors of the skin or mucous membranes. Mucosal pyogenic granulomas usually occur in the oral cavity, typically the lip (picture 23A) and gingival mucosa (picture 23B). They are characterized by rapid growth, friable surface, and easy bleeding. They are more common in females, particularly during pregnancy. Although the cause is unknown, trauma has been suggested as a trigger.

The clinical features and management of pyogenic granulomas are discussed separately. (See "Pyogenic granuloma (lobular capillary hemangioma)".)

Peripheral giant cell granulomas — Peripheral giant cell granulomas are overgrowths of tissue due to trauma. They typically occur on the gingiva and are slightly more common on the lower than the upper gums [37]. They may be up to 2 cm (0.75 inches) in diameter. Although the clinical appearance is similar to that of pyogenic granuloma, peripheral cell granulomas are usually bluish-purple, whereas pyogenic granulomas are red. Peripheral giant cell granulomas are more common in children with mixed dentition and individuals between 30 and 40 years of age [37]. There is a female predominance. Treatment for peripheral giant cell granulomas is surgical excision.

Ulcerations

Traumatic ulcers — Traumatic ulcers are the most common oral ulcers in children. They may occur on the gums, tongue, lips, palate, or buccal mucosa. The clinical features vary with the type and intensity of the trauma; examples include:

Thermal burns of the anterior palate from eating foods or drinking liquids that are too hot

Mechanical trauma to the soft palate from sucking on a thumb, finger, or pacifier

Lip-biting related to self-injurious behavior (eg, in children with the Lesch-Nyhan syndrome (picture 9B))

Factitious injury (eg, fingernail scratching of the gingiva) (picture 9A)

Iatrogenic injury secondary to caustic materials inadvertently applied to the oral soft tissues during dental procedures (eg, formocresol, sodium hypochlorite)

Traumatic ulcers typically heal within two weeks of removal of the source of trauma. Children who have self-injurious behaviors may need a comprehensive treatment plan, including sedation, bite guards, lip bumpers, or extraction.

Aphthous ulcers — Aphthous ulcers, also called canker sores, are painful oral lesions that appear as localized, shallow, round to oval ulcers with a grayish base (picture 26A-B). Aphthous ulcers may occur on the gums, tongue, lips, palate, and buccal mucosa. Susceptibility appears to be familial.

The clinical features and management of aphthous ulcers are discussed separately. (See "Oral lesions", section on 'Erosive, ulcerative, and bullous lesions'.)

Infections — Infections that frequently are associated with lesions of the oral mucosa in children are discussed in detail separately:

Thrush (pseudomembranous candidiasis, oropharyngeal candidiasis) (picture 17) (see "Candida infections in children", section on 'Oropharyngeal candidiasis')

Herpetic gingivostomatitis (picture 10A-B) (see "Herpetic gingivostomatitis in young children" and "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection")

Hand, foot, and mouth disease (picture 24) (see "Hand, foot, and mouth disease and herpangina")

SUMMARY

Significance of soft tissue lesions of the oral cavity – Soft tissue lesions of the oral cavity in children may be normal/developmental findings or indicative of gingivitis, periodontal disease, local or systemic infection, or life-threatening systemic conditions (table 1). (See 'Introduction' above.)

Lesions of the gums – Soft tissue lesions of the gums include eruption cysts or hematomas (picture 1); gingival pigmentation; retrocuspid papillae (picture 2); "gum boils" (picture 3); gingival overgrowth (picture 5A-E); gingival recession (picture 6); HIV gingivitis (picture 7); hemangiomas; irritation fibromas (picture 4); peripheral ossifying fibromas (picture 8); pyogenic granulomas (picture 23B); peripheral giant cell granulomas; traumatic ulcers (picture 9A); aphthous ulcers; and herpetic gingivostomatitis (picture 10A). (See 'Lesions of the gums' above.)

Lesions of the tongue – Soft tissue lesions of the tongue include ankyloglossia (picture 11); congenital melanotic macules; geographic tongue (picture 13); fissured tongue (picture 14); mucoceles (picture 15); hemangiomas; lymphatic malformations (picture 16); irritation fibromas; traumatic ulcers; aphthous ulcers; thrush (picture 17); herpetic gingivostomatitis (picture 10B); and hand, foot, and mouth disease. (See 'Lesions of the tongue' above.)

Lesions of the lips – Soft tissue lesions of the lips include herpes labialis (picture 18); angular cheilitis (picture 19A-B); freckling (picture 20A-B); abnormalities of the labial frena; mucoceles (picture 15); hemangiomas (picture 22A); lymphatic malformations; irritation fibromas; pyogenic granulomas (picture 23A); traumatic ulcers (picture 9B); aphthous ulcers (picture 26B); thrush (picture 17); herpetic gingivostomatitis (picture 10B); and hand, foot, and mouth disease (picture 24). (See 'Lesions of the lips' above.)

Lesions of the palate – Soft tissue lesions of the palate include herpangina (picture 25); irritation fibromas; traumatic ulcers; aphthous ulcers; thrush; herpetic gingivostomatitis; and hand, foot, and mouth disease. (See 'Lesions of the palate' above.)

Lesions of the buccal mucosa – Soft tissue lesions of the buccal mucosa include hemangiomas; lymphatic malformations; mucoceles; irritation fibromas; traumatic ulcers; aphthous ulcers (picture 26A); thrush (picture 17); herpetic gingivostomatitis; and hand, foot, and mouth disease. (See 'Lesions of the buccal mucosa' above.)

Lesions that occur at multiple sites – Soft tissue lesions that occur at multiple sites within the oral cavity include hemangiomas (picture 22A-B); lymphangiomas (picture 16); mucoceles (picture 15) and ranulas (picture 21); irritation fibromas (picture 4); peripheral ossifying fibromas (picture 8); pyogenic granulomas (picture 23A-B); peripheral giant cell granulomas; traumatic ulcers (picture 9A-B); aphthous ulcers (picture 26A-B); thrush (picture 17); herpetic gingivostomatitis (picture 10A-B); and hand, foot, and mouth disease (picture 24). (See 'Lesions that occur at multiple sites' above.)

  1. Masilana A, Khammissa RAG, Lemmer J, Feller L. Physiological oral melanin pigmentation in a South African sample: A clinical study. J Investig Clin Dent 2017; 8.
  2. Dongari A, McDonnell HT, Langlais RP. Drug-induced gingival overgrowth. Oral Surg Oral Med Oral Pathol 1993; 76:543.
  3. Thomason JM, Seymour RA, Ellis JS, et al. Determinants of gingival overgrowth severity in organ transplant patients. An examination of the rôle of HLA phenotype. J Clin Periodontol 1996; 23:628.
  4. Majola MP, McFadyen ML, Connolly C, et al. Factors influencing phenytoin-induced gingival enlargement. J Clin Periodontol 2000; 27:506.
  5. Bökenkamp A, Bohnhorst B, Beier C, et al. Nifedipine aggravates cyclosporine A-induced gingival hyperplasia. Pediatr Nephrol 1994; 8:181.
  6. Martín JM, Mateo E, Jordá E. Azithromycin for the Treatment of Ciclosporin-Induced Gingival Hyperplasia. Actas Dermosifiliogr 2016; 107:780.
  7. Delaney JE, Keels MA. Pediatric oral pathology. Soft tissue and periodontal conditions. Pediatr Clin North Am 2000; 47:1125.
  8. Oral Pathology: Clinical-Pathologic Correlations, 2nd, Regezi JA, Sciubba J (Eds), WB Saunders, Philadelphia 1993. p.196.
  9. Singer SL, Goldblatt J, Hallam LA, Winters JC. Hereditary gingival fibromatosis with a recessive mode of inheritance. Case reports. Aust Dent J 1993; 38:427.
  10. Raeste AM, Collan Y, Kilpinen E. Hereditary fibrous hyperplasia of the gingiva with varying penetrance and expressivity. Scand J Dent Res 1978; 86:357.
  11. Poulopoulos A, Kittas D, Sarigelou A. Current concepts on gingival fibromatosis-related syndromes. J Investig Clin Dent 2011; 2:156.
  12. Chang JY, Kessler HP, Wright JM. Localized juvenile spongiotic gingival hyperplasia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008; 106:411.
  13. Solomon LW, Trahan WR, Snow JE. Localized juvenile spongiotic gingival hyperplasia: a report of 3 cases. Pediatr Dent 2013; 35:360.
  14. Vargo RJ, Bilodeau EA. Reappraising localized juvenile spongiotic gingival hyperplasia. J Am Dent Assoc 2019; 150:147.
  15. Andlin-Sobocki A, Bodin L. Dimensional alterations of the gingiva related to changes of facial/lingual tooth position in permanent anterior teeth of children. A 2-year longitudinal study. J Clin Periodontol 1993; 20:219.
  16. Leggott PJ. Oral manifestations of HIV infection in children. Oral Surg Oral Med Oral Pathol 1992; 73:187.
  17. Chaput L, Samimi M, Maruani A. Congenital Melanotic Macules of the Tongue. J Pediatr 2016; 174:270.
  18. Savoia F, Ricci L, Patrizi A, Gaddoni G. Congenital melanotic macules of the tongue. A case report and brief review of the literature. Pediatr Dermatol 2015; 32:109.
  19. Dohil MA, Billman G, Pransky S, Eichenfield LF. The congenital lingual melanotic macule. Arch Dermatol 2003; 139:767.
  20. Sigal MJ, Mock D. Symptomatic benign migratory glossitis: report of two cases and literature review. Pediatr Dent 1992; 14:392.
  21. Mueller DT, Callanan VP. Congenital malformations of the oral cavity. Otolaryngol Clin North Am 2007; 40:141.
  22. Geographic tongue and fissured tongue. In: Online Mendelian Inheritance in Man. http://omim.org/entry/137400 (Accessed on November 07, 2011).
  23. Orlando MR, Atkins JS Jr. Melkersson-Rosenthal syndrome. Arch Otolaryngol Head Neck Surg 1990; 116:728.
  24. Lajolo C, Favia GF, Fantasia J, et al. Blandin-nuhn gland mucocele: presentation of a new case and review of the literature. Ann Stomatol (Roma) 2013; 4:24.
  25. Bodner L, Manor E, Joshua BZ, Shaco-Levy R. Oral Mucoceles in Children--Analysis of 56 New Cases. Pediatr Dermatol 2015; 32:647.
  26. De Felice C, Toti P, Di Maggio G, et al. Absence of the inferior labial and lingual frenula in Ehlers-Danlos syndrome. Lancet 2001; 357:1500.
  27. Machet L, Hüttenberger B, Georgesco G, et al. Absence of inferior labial and lingual frenula in Ehlers-Danlos syndrome: a minor diagnostic criterion in French patients. Am J Clin Dermatol 2010; 11:269.
  28. De Felice C, Di Maggio G, Zagordo L, et al. Hypoplastic or absent mandibular frenulum: a new predictive sign of infantile hypertrophic pyloric stenosis. J Pediatr 2000; 136:408.
  29. Mintz SM, Siegel MA, Seider PJ. An overview of oral frena and their association with multiple syndromic and nonsyndromic conditions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005; 99:321.
  30. Langlais RP, Miller CS. Color Atlas of Common Oral Diseases, Lea & Febiger, Philadelphia 1992. p.32.
  31. Baurmash HD. Mucoceles and ranulas. J Oral Maxillofac Surg 2003; 61:369.
  32. Nico MM, Park JH, Lourenço SV. Mucocele in pediatric patients: analysis of 36 children. Pediatr Dermatol 2008; 25:308.
  33. Fishman SJ, Mulliken JB. Hemangiomas and vascular malformations of infancy and childhood. Pediatr Clin North Am 1993; 40:1177.
  34. Shiels WE 2nd, Kang DR, Murakami JW, et al. Percutaneous treatment of lymphatic malformations. Otolaryngol Head Neck Surg 2009; 141:219.
  35. Cahill AM, Nijs E, Ballah D, et al. Percutaneous sclerotherapy in neonatal and infant head and neck lymphatic malformations: a single center experience. J Pediatr Surg 2011; 46:2083.
  36. Carrera Grañó I, Berini Aytés L, Escoda CG. Peripheral ossifying fibroma. Report of a case and review of the literature. Med Oral 2001; 6:135.
  37. Tandon PN, Gupta SK, Gupta DS, et al. Peripheral giant cell granuloma. Contemp Clin Dent 2012; 3:S118.
Topic 6282 Version 35.0

References

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