DOI: 10.1051/odfen/2018056 J Dentofacial Anom Orthod 2018;21:207 © The authors

Orthodontics and oral mucosal lesions in children and teenagers

L. Sicard1, L. Benmoussa2, N. Moreau3, B. Salmon3, A.-L. Ejeil3 1 DESCO 2 AHU 3 MCU-PH Department of Bretonneau Hospital, Paris Our gratitude to the Orthodontic Department for providing the iconography for this article

SUMMARY Children and teenagers with orthodontics may be affected by infectious, hereditary, traumatic, malig- nant, or idiopathic lesions. Orthodontists have to be able to detect, identify, and treat effec- tively or to address the patient to a specialist. Here we discuss this difference to make their diagnosis and management easier for the practitioner.

KEY WORDS Oral mucosa, orthodontics, oral appliances, oral lesions

INTRODUCTION

The estimated prevalence of oral mucosal a greater risk of traumatic or reactive le- ­lesions is 8%–60% in the general popu- sions18. These are either treatment-induced lation1,8,17,2. In children and adolescents, it or of allergic origin. ­increases with age. The causes can be infec- The diagnosis of oral mucosal pathologies tious, ­hereditary, malignant, idiopathic, or iatro- is based on a rigorous approach including a genic in nature. The four main lesions found are thorough anamnesis, clinical examination canker sores, traumatic lesions, herpes, and lin- with the search for elementary lesions, gual lesions5,20,13,9. In addition, certain systemic and additional examinations. Through reg- pathologies (inflammatory diseases of the co- ular check-up appointments during ortho- lon and intestines, IBD, hemopathies, and dia- dontic treatment, the practitioner is able to betes) may also have oral manifestations5. detect the appearance of lesions, to mon- The presence of intraoral material during itor their evolution, and to manage them if orthodontic treatment is associated with necessary.

Address for correspondence: Ludovic Sicard - Bretonneau Hospital, Department of Oral Medicine – 23 rue Joseph de Maistre – 75018 Paris Article received: 16-10-2017. E-mail: [email protected] Accepted for publication: 25-12-2017.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 1

Article available at https://www.jdao-journal.org or https://doi.org/10.1051/odfen/2018056 L. SICARD, L. BENMOUSSA, N. MOREAU, B. SALMON, A.-L. EJEIL

ELEMENTARY LESIONS AND DIAGNOSTIC APPROACH

The elementary lesion (Table I) is ­appearance of the lesion. The condition used to guide the diagnosis by com- may be accompanied by symptoms or paring it with a nosological group. Its early signs. Its discovery may be fortui- description must include its borders, tous or be mentioned by the patient due texture, color (erythematous, keratotic, to discomfort or pain. The lesion’s and pigmented), suppleness or indura- ­development can be continuous or via tion, and number of lesions (whether intermittent flare-ups, or even consti- single or multiple). tute a recurrence. Family history, ethnic The diagnostic approach is based origins, lifestyle habits, and medications on the patient’s medical history and (antiseptics in mouthwash, ointments, clinical examination. It leads to one or and antibiotics) can help guide the di- more diagnostic hypotheses or even a agnosis. A particular area, such as cur- positive diagnosis. rent conditions or a systemic disease, Obtaining the diagnosis may require can be the cause of oral lesions (IBD or additional tests, such as biopsy and/or hemopathies in particular). excision, biological assessment, serol- The clinical examination must meet a ogy, and imaging15. strict methodology and must system- atically provide information on various The medical history is of particular 16 interest to children and their parents. points . It examines the history of the condi- The extraoral examination begins tion, its date of onset, and the type and with examining the appearance of

Table I: Primary elementary lesions7

Elementary lesion Size Description

Macule <5 mm Not indurated, circumscribed, consisting of a color change of the mucosa without relief or hollow (spot). Erythematous (example: acute myeloid leukemia) or pigmented (example: Range >5 mm idiopathic macular melanoma).

Papula <5 mm In relief, firm, non-liquid, protruding, circumscribed, palpable. Increased epithelio-conjunctival volume. Red, white, or pigmented. The plaque may result from the confluence of several Plaque >5 mm papules. Firm, non-protruding, round or oval, deep (of the chorion), sometimes painful, linked to Nodule inflammatory or tumoral (benign or malignant) involvement. Generally large. Keratotic, erythematous, or pigmented. Vegetation Hypertrophic or hyperplastic circumscribed epithelio-conjunctival proliferation consisting of growths (cauliflower appearance). Of variable morphology (filiform or lobulated appearanc- es). Pediculated or sessile. Usually refers to papillomas, , and condylomas. Vesicule <5 mm Elevated circumscribed intraepithelial elevation with serous or hemorrhagic fluid content. The thin roof is quickly eliminated in the , giving way to erosion (secondary lesion). Bubble >5 mm Clear, yellowish, or hemorrhagic fluid collection. Fragile roof that breaks easily (formation of a secondary erosive lesion or post-bullous ulcerative lesion). May be intra- or subepithelial. Pustule <5 mm Vesicle that contains pus. A vesicle can turn into a pustule due to bacterial contamination. Erosion Loss of superficial substance (epithelial involvement without involvement of the chorion). Heals without leaving a scar. Most often secondary to a vesicle or an intraepithelial bubble after the rupture of its roof. Surface most often erythematous. Ulceration Loss of epithelial and conjunctive tissue. Leaves a fibrinous layer by exudation after removal of the basal membrane. More painful than erosion. Usually heals in about 10 days, some- times with cicatricial sequelae. Most common causes are canker sores, trauma, subepitheli- al bubbles, and carcinomas.

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Table 2: Types of additional examinations

Additional examinations Examples of indication Complete blood count Recurrent ulcerations, testing for anemia, or hemopathy Fasting blood glucose, HbA1c Diabetes control Vitamin assessment (B9, B12 ...) Canker sores with macrocytic anemia Ultrasound tumor Magnetic resonance imaging Assessment of bone/soft tissue tumor Serology HSV1 or HSV2 testing for atypical primary herpes infection Biopsy Histological confirmation of the diagnostic hypothesis Mycological examination Mycosis resistant to first-line treatment

­integuments (skin and skin- associated any possible induration. For red le- structures, such as nails, hair, and dan- sions, the vitropressure test makes it der) and mucocutaneous diseases that possible to establish if the lesion is of can be associated with oral manifesta- capillary origin or not. If the lesion turns tions. This is followed by palpation for white, it indicates a vascular origin. lymphadenopathy and salivary glands The initial lesion can frequently and and the search for any swelling or facial rapidly undergo changes due to cer- asymmetry. tain elements of the oral environment The extraoral examination is thor- ­(humidity, variable pH, dental micro- ough. The practitioner spreads the trauma, food, hygiene, and occurrence cheeks, explores the vestibular and lin- of superinfections). gual floor, while holding the tongue in These observations are recorded on place with a compress. They look care- a diagram of the oral mucosa as well as fully at the lesion, describe the clinical images of the lesion. These documents aspect (color, texture, induration, and are attached to the medical file to mon- boundaries) and topography (location itor the evolution of the condition. and size). The lesion may be homoge- Additional tests are ordered when neous (one type of primary lesion) or there is still doubt about the diagno- heterogeneous (multiple primary le- sis. They are guided by the diagnostic sions at the same site). The palpation hypotheses and are not systematic evaluates the consistency and reveals (Table II).

MUCOSAL PATHOLOGIES RELATED TO ORTHODONTIC TREATMENTS

Mucosal pathologies related to ortho- with the presence of erosion or kera- dontic treatment have three major caus- tosis caused by friction on the corre- es: traumatic, infectious, or reactive. sponding mucous membranes. Arches Traumatic pathologies take different are often associated with wound ulcers forms depending on severity. They by piercing the mucosa facing them18. vary according to the type of orthodon- Mini-screws are frequently associated tic appliance. Brackets are associated with and erosions19. After

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­removal, they create cicatricial seque- lae in >40% of cases21. The definitive diagnosis of a traumat- ic injury is only made when the lesion disappears after elimination of the sus- pected cause. with regular and light friction. It is clinically translated by a homogeneous white plate. Traumatic ulceration (Fig. 2) is painful; Figure 1 it results from the aggression and iatro- Reactive jugal opposite the end genicity of a piece of orthodontic equip- of a Ni-Ti arch. ment or the head of a mini-screw (the placement of composite on the head of It settles in reaction heals in 10–15 days the mini-screw can minimize this risk).12 after elimination of the cause. Located next to the causal element, it Sometimes, the healing process is Keratosis (Fig. 1) is a defensive reaction­ painful and botryomycoma can be ob- of the mucosa in the face of ­aggression. served (Fig. 3).

Figure 2 Left palatal ulcer in relation to a quad-helix and a brace on 26. a) Device in place. b) Traumatic ulceration.

Figure 3 a) Botryomycosis of the lower with reactive keratosis. b) Position of the lesion opposite orthodontic brackets.

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Necrosis represents the extreme painless translucent or bluish collection, stage of the traumatic lesion. A case is hemispherical, and ranges in size from using a Nance arch has been reported a few millimeters to a few centimeters in in the literature11. diameter. Treatment is through excision. and mucoid cysts are less On the oral floor, it is called a or a common lesions. “little frog” colloquially (Fig. 6). Epulis (Fig. 4) is a benign inflamma- Infectious diseases are favored by tory tumor of the gingiva and develops dental congestion and the presence of in response to a local chronic irritative exogenous material, which constitute factor (brackets, tartar, and interden- a bacterial retentive factor. The most tal spaces). Clinically, epulis appears common is (Fig. 7). It is ­treated as a localized nodule appearing on the with proper oral hygiene, complicated marginal gingiva or alveolar processes. by the presence of the multi-­attachment Inflammatory epulis is most common device. Parental involvement and child following orthodontic treatment. Its empowerment are fundamental, as size can be significant. Highly vascu- well as the demonstration and use of larized, it bleeds easily. Its treatment adapted hygiene equipment. is based on excision up to the bone Mycotic infections are very rare, with contact, removal of the causal factor if the main causative agent being Can- possible, and oral hygiene reeducation. dida albicans. C. albicans is present in In children, the presence of an inflam- matory epulis requires a CBC to rule out leukemia. The mucoid cyst (Fig. 5) is a pseudo- cyst, often of traumatic origin, resulting­ from the extravasation of saliva after the rupture of the excretory canal. It develops mainly in the accessory salivary glands and particularly on the lower lip and the floor of the mouth. It takes the form of a

Figure 5 Mucoid cyst on the ventral side of the tongue.

Figure 4 Fibrous epulis, pediculated, related to a Figure 6 local irritant factor between 45 and 46. Ranula on the oral floor.

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Without treatment, candidiasis evolves, either toward spontaneous cure if the aggravating factors are eliminated or to- ward chronicity and possibly digestive dissemination. Angular is a particular form of candidiasis. It is characterized by angu- lar cheilitis with bilateral involvement of the labial commissures on the cutane- Figure 7 ous and mucous slopes. It is affected Gingivitis after removal of the orthodontic by salivary flow and maceration in the appliance. commissural folds and maintained via a licking behavioral tic. the oral flora of >30% of the popula- The diagnosis of candidiasis is clinical. tion and its concentration increases in Treatment involves the elimination the presence of removable resin devic- of aggravating factors and a local treat- es6. Its presence in the mouth is not ment with amphotericin B (­Fungizone®) enough for it to become pathogenic as a first-line defense (oral suspension, (candidiasis). The main risk factors in 2 spoonfuls in mouthwash 5 times a children are long-term use of antibi- day for 3 weeks; take the mouthwash otics or a background of immunosup- then swallow to prevent digestive dis- pression/ depression. Clinically, acute semination). mycosis (or thrush) manifests as dif- Mycological testing is reserved for am- fuse erythematous of the biguous or treatment-resistant forms. mucous membranes. Whitish granu- Reactive pathologies include hy- lations converge to form slightly fluffy perplasia, diapneusias, canker sores, white layers, which are more or less non-viral papillomas,4 and allergies. extensive and detach easily on scrap- occur in the context ing to give way to an erythematous of chronic irritation created by mul- (or even bleeding). ti-attachment devices or palatal plates When these layers are very extensive, (Figs. 8, 9 and 10). Localized around they form a pseudo-membrane. the irritative cause, they take the form

Figure 8a and b and sagittal erythema in relation to a palatal plate.

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Figure 9 a) Hyperplasia around the head of a mini-screw. b) Aggravation of hyperplasia after placement of the elastic.

Figure 10 Hypertrophic reactive papillae. Figure 11 of an increase in tissue volume, are Diapneusia of the mucosal side of the firm and covered with a healthy, ery- lower right lip following a suction tic. thematous, or keratotic mucosa. Diapneusia (Fig. 11) is indirectly linked corresponds to a delayed cell-­mediated to orthodontic appliances via the spaces hypersensitivity (type IV of the Gell and they create. Frequently, it presents as Coombs classification). an asymptomatic nodule and is general- It occurs in two phases: a sensitiza- ly <1 cm in diameter. It can be located tion and an expression phase. Clinically, on the cheeks, , and tongue and is 2–3 days after the second exposure, it caused by excessive suction (wide inter- manifests as contact dermatitis or ede- dental space). Treatment consists of the ma. Reactions at the mucosal level are removal of the lesion’s root. Relapses rare because the nickel is coated with a may be avoided if the cause is corrected. salivary film, the alloy is of better quality Cases of nickel allergy are reported dur- than that of a piercing, and the mucosa ing orthodontic treatment (use of Ni-Ti­ presents fewer antigen presenting cells arches). This allergy affects approximate- than on the skin. In addition, the oral ly 19% of the general ­population7 and medium may induce nickel tolerance3.

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MUCOSAL PATHOLOGIES NOT RELATED TO ORTHODONTIC TREATMENT

Many of them are more common in may be present. These erosions can children and adolescents. ­converge to create large painful ero- Lesions related to are sive expanses with polycyclic contours. usually found in patients with a pro- nounced overlapping Angle Class II. The lesion is located on the op- posite the free edge of the mandibular incisors (Fig. 12). Primary herpes infection (Fig. 13) corresponds to a patient’s first contact with the virus 1 (HSV1). It usually affects children before the age of 10. Preceded by fever and oro- pharyngeal pain, vesicules appear in Figure 12 the oral mucosa. They lead to erosions Traumatic lesion of the palate in relation that produce acute gingivostomati- to a Class II division 1, with ulceration of tis. Peri-oral cutaneous involvement traumatic origin in relation to the occlusion.

Figure 13 Primary herpes infection. a) Erythematous tongue with cyclic erosion at the right edge. b) Gingivitis and left jugal erosion. c) Extraoral view with herpetic vesicule on the lower lip.

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­Accompanying signs are general state or fleeting) followed by a moderate alteration (GSA), severe , fever with characteristic vesicular and hypersialorrhea, and frequent cervical pruritic rash (dewdrop on healthy skin), lymphadenopathies. Bacterial superin- polyadenopathy, and oral enanthema fection can occur due to the impossi- (generalized erythematous stomatitis bility of brushing due to pain. Healing with vesicle formation giving way to occurs in 2 weeks without sequelae. painful circular or oval superficial ero- During this period, the patient is con- sions). Healing takes 10 days without tagious through direct contact with in- sequelae. fected secretions (saliva). Treatment of chickenpox is symp- The first contact with the HSV usual- tomatic and is based on analgesics ly goes unnoticed. Symptoms are trig- (NSAIDs are contraindicated). gered in only 10% of cases. is the clinical expression of Differential diagnoses include other the resurgence of VZV, with unilateral viral pediatric diseases: ; eruptions following a nerve pathway. It hand, foot, and mouth disease; and mainly affects adults and occasionally chicken pox. Others that should also teenagers. be considered are infectious mononu- Hand, foot, and mouth disease cleosis, bacterial angina, oral aphthosis (Fig. 15), caused by a virus (coxsackie in its miliary form (without GSA orade- virus A16), particularly affects young nopathy), rarely , children aged <5 years, usually as an or drug toxicity. epidemic in spring and summer. Clini- The treatment of a primary herpes cally, it results in an enanthema begin- infection is based on a symptomatic ning with bright red macules 2–8 mm in component (analgesic, antiseptic, and diameter, evolving toward grayish ves- antibiotic) and an etiological compo- icles, surrounded by an erythematous nent (antiviral in the replicative phase, halo in a moderate influenza context. acyclovir type, systemically). Diagnosis is based on the simultane- After healing, the virus remains latent ous presence of cutaneous elements in the body. is the most in the fingers and toes (palmoplantar le- classic clinical form of recurrence, but sions). Healing is spontaneous and oc- this recurrence may occur in the oral curs within 2 weeks without sequelae. mucosa, more frequently in the palate Measles, also caused by the virus compared with the first molars. Morbillivirus, usually affects pre-school Treatment of recurrences is based on children who have not yet been vacci- an antiviral (acyclovir) topically applied nated. The invasion phase is manifest- up to 5 times daily for 4–5 days (should ed by oculo-respiratory catarrh with be started at the prodromal level) and high fever, digestive symptoms, and local antiseptics (chlorhexidine). Köplik sign. Almost pathognomonic Chicken pox and shingles (Fig. 14) are but fleeting, Köplik sign is character- diseases caused by varicella zoster vi- ized by bluish and keratotic papules on rus (VZV) (HHV-3 group). Chicken pox is the inside of the cheeks, often facing the primary infection. the first molar. The condition phase Its diagnosis is clinical. It is charac- corresponds to a morbilliform exanthe- terized by fever and skin rash (transient ma (maculopapular rash) with a healthy

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Figure 14 a) and b) Chicken pox in a young adult with a cutaneous vesicle on the left and lingual erosions on the right. c) and d) V3 area shingles, intraoral view on the left and extraoral on the right.

Figure 15 Hand, foot, and mouth disease. a) and b) Enathema on the right foot and the right hand. c) Grayish vesicles and peri-oral erythematous halos.

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skin interval between the elements. Treatment is symptomatic and relies on analgesics and antibiotic therapy in case of superinfection. Vaccination re- mains the best preventive treatment. Due to insufficient immunization cov- erage, measles is resurging in Europe and should not be ignored in adoles- cents and young adults due to the se- vere complications it causes. Figure 16 Herpangina is a vesicular pharyngitis Canker sore on the tip of the tongue with of viral etiology (coxsackievirus A4) and fibrinous border and erythematous halo. particularly affects children. It results in fever accompanied by dysphagia fol- common canker sore (<1 cm), giant lowed by ulcerated lesions located on canker sore (>1 cm), and miliary aph- the veil of the palate and its anterior tosis (1 mm). While most are idiopathic pillars It affects the tonsils and tongue. in origin, some causes should not be Spontaneous evolution is favorable in a overlooked10 such as IBD, Behçet’s few days. disease, neutropenia, anemia, and/or (or Cannon’s vitamin deficiency. The treatment of spongy white nevi) is a hereditary common canker sores is symptomat- dyskeratosis localized preferentially ic. The literature does not indicate a di- to the jugal mucosa, which takes on rect relationship between orthodontic a white-gray, slightly wrinkled appear- treatment and canker sores. ance, similar to an opalescent veil. The Malignant pathologies, which are for- mucosa remains supple. These white tunately very rare in children, are the spots, slightly raised, are detached by second leading cause of death in this scratching in the form of scales, reveal- age group after accidents. With the ing an intact submucosa underneath. exception of leukemia and lympho- The palatal and gingival mucosa, which ma, children with cancer appear to be do not have a submucosa, are almost al- in good health. A peculiarity of these ways unaffected. The lesion occurs less pathologies in children is their rapid frequently in other mucous membranes progression. Any swelling without an of the aerodigestive tract or the geni- infectious portal of entry, especially in tal system. The differential diagnosis is the maxillary or mandibular regions, white lesions of the oral mucosa. should evoke this diagnosis. Oropharyngeal canker sores (Fig. 16) Acute lymphoblastic leukemia (ALL) are painful ulcerations of the mucosa, affects children more than adults. with rounded regular margins, sur- ­Accompanied by an alteration in the rounded by an erythematous inflamma- ­patient’s general health status, it is tory halo. These lesions are common ­visible in the mouth in the form of pur- and affect up to 50% of the popula- pura and gingivorragia. tion. Three types of canker sores are More generally, hemopathies can distinguished according to their size: result in diffuse or localized gingival

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­hypertrophies, often bluish-red in color, panied by fever and lymphadenopathy, which bleed at the slightest trauma. skin paleness (anemia), infections (neu- Hypertrophy results from the infiltra- tropenia), and hemorrhagic syndromes tion of tissues by leukemic cells. The (thrombocytopenia). Neutropenia can clinical picture is that of fatigue accom- result in mouth ulcers.

CONCLUSION

Oral mucosal pathologies encoun- clinically manifest as vesicles. The ad- tered by the orthodontist are often age says that a child who falls ill quickly benign and acute. Treatment-related will get better quickly. The persistence lesions are mostly reactive and require of lesions or deterioration of the child’s correction of causal factors, improve- general condition necessitates their ment of oral hygiene, and/ or mucosal referral to a specialized department for protection. Pathologies not associated further examinations in search of an with treatment are most often viral and underlying general pathology.

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