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 Table of Contents  
REVIEW ARTICLE
Year : 2018  |  Volume : 9  |  Issue : 4  |  Page : 174-180

Chemical burns of gingiva and its management


Department of Periodontics and Implantalogy, KVG Dental College and Hospital, Sullia, Karnataka, India

Date of Web Publication18-Dec-2018

Correspondence Address:
Radhika Priyadarshini M Sooranagi
KVG Dental College and Hospital, Sullia, Karnataka
India
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DOI: 10.4103/srmjrds.srmjrds_16_18

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  Abstract 

Chemical burns on the gingiva can be caused by the use of certain pharmaceutical and nonpharmaceutical products by patients or by injudicious use of caustics by the dental clinician. These lesions in the oral cavity, however, are rarely reported. Hence, information about the product and needful instructions is necessary to be given to the patients for prevention of the same. These burns can be caused by the way of self-infliction, allergic tendency toward certain products, or it may be iatrogenic. A detailed history is the key to diagnosing and managing these cases. Chemical burns are usually treated by eliminating the etiology and managed by palliative therapy.

Keywords: Chemical agents, chemical burns, gingiva, nonpharmaceutical products, self-inflicted injury


How to cite this article:
Dayakar M M, Pai PG, Sooranagi RP, Vijayan V, Waheed A. Chemical burns of gingiva and its management. SRM J Res Dent Sci 2018;9:174-80

How to cite this URL:
Dayakar M M, Pai PG, Sooranagi RP, Vijayan V, Waheed A. Chemical burns of gingiva and its management. SRM J Res Dent Sci [serial online] 2018 [cited 2019 Oct 22];9:174-80. Available from: http://www.srmjrds.in/text.asp?2018/9/4/174/247838


  Introduction Top


The chemical agents used in day-to-day dental practice ranging from mouthwash, cavity varnish, or de-vitalizing pastes if used injudiciously can harm the integrity of the soft tissues in the oral cavity.[1] These lesions may clinically mimic the well-known diseases of oral cavity.[2] The most commonly used classification for chemical burns includes accidental, iatrogenic, and factitious traumatic lesions. Traumatic lesions, caused due to thermal, physical, or chemical agents, are often seen in the oral cavity,[3] with chemical burns being the most common.[4] The causes for chemical burn include local application of medications such as aspirin, chlorpromazine, promazine, alendronate, tetracycline hydrochloride; recreational drugs such as cocaine, 3,4-methylenedioxymethamphetamine (MDMA); some common dental materials such as formocresol, sodium hypochlorite (NaOCl), eugenol, hydrogen peroxide (H2O2); and nonpharmaceutical substances such as garlic, clove, or mint.

Clinical presentation of the chemical injuries might differ according to the composition and concentration, pH of the substance, the quantity applied, the manner and duration of tissue contact, and the extent of penetration into tissue. These oral mucosal changes can vary from diffuse erosive lesions ranging from simple mucosal sloughing to complete mucosal detachment with extension into the submucosa.[2]

In a study, Rawal et a. concluded that a detailed and accurate history is necessary for the diagnosis of traumatic injuries.[3] Clinical diagnosis of a chemical burn may be a diagnostic challenge; therefore, a detailed history and review of a patient's medical condition will help to differentiate the possible causes of the presenting lesion.[2] The management of chemical burns in oral cavity primarily requires identification and removal of the agent responsible followed by symptomatic treatment. This review article aims to highlight the clinical features and management of various burns on gingiva due to chemical agents and nonpharmaceutical substances.


  Classification Top


Mucosal damage in the oral cavity can be iatrogenic during dental procedure, misuse or improper application of medicine and nonpharmaceutical substances by the patients.[5] Pharmaceuticals and nonpharmaceutical substances that cause injury to the oral mucosa are represented as a Schematic reprenstation [Figure 1] which shows classification and its uses described in [Table 1] below.
Figure 1: Schematic representation 1: Chemical agents and nonpharmaceutical substances that cause injury to the oral mucosa

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Table 1: Substances that causes injury to oral mucosa and its uses

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Dental materials



Medications



Nonpharmaceutical substances



Drugs



Alendronate

It belongs to the diphosphonate family and has been used in the treatment of glucocorticoid-induced osteoporosis and various other bone diseases. Even though well tolerated, alendronate may show adverse effects, with the most common being on the mucosa of the upper aerodigestive tract with esophagitis. To overcome this adverse effect, patients have to be advised to consume the medication with a glass of water, advised not to chew or suck the tablet, and to maintain an upright posture for around 30 min.[16]

Aspirin

Aspirin, also known as acetylsalicylic acid, is a commonly used medicine in the management of pain, fever, and inflammation. Most cases of chemical burns are encountered by aspirin, also known as acid burn, and its derivatives when sucked, applied as a gel, mouthwash, powder, or as a tablet next to an aching tooth in an attempt to relive pain.[5] Aspirin, if left on the mucosa for an extended period, has a caustic effect. The acidic nature (pH 3.5–5.0) of acetylsalicylic acid can cause aphthous-like ulceration of the oral mucosal layer induced by a cell-mediated response.[18] The binding of organic and inorganic parts of aspirin to the epithelium of oral cavity causes denaturation and coagulative necrosis.[19]

Calcium hydroxide

Calcium hydroxide (Ca (OH)2) has been most widely used in the field of endodontics as lining of cavities, indirect and direct pulp capping, dressing after pulpotomy, dressing of the root canal between appointments, prevention of root resorption, repair of iatrogenic perforations, treatment of horizontal root fractures, and as a constituent of root canal sealers. Its extensive use is because of its properties such as initiation and stimulation of mineralization, the antibacterial characteristics, and the dissolution of necrotic material. Its side effects include necrosis of bone, cytotoxicity on cell cultures, damaged epithelium, and cellular damage.[8]

Cocaine (benzoylmethylecgonine) (C17H21 NO4)

It is an alkaloid derived from the leaves of Erythroxylum coca. Approximately 910,000 people are using cocaine in Europe, making it the second highest cocaine prevalence rate. Cocaine diffuses across the lipid membranes of neurons in its nonionized form. It returns to the active cationic form in axoplasm and binds to the sodium channels, thus, prevents the generation of an action potential, resulting in a reversible anesthetic effect.[42]

Denture cleansers

Patients use a variety of household and commercial cleansers to clean their dentures. Immersion-type denture cleansers marketed as tablets or powders contain potassium monopersulfate, sodium perborate, sodium carbonate, surfactant, sodium bicarbonate, citric acid, and a flavoring agent. When the tablet or powder is dissolved in water, the perborate decomposes to form an alkaline peroxide solution and then decomposes to liberate oxygen. This reaction mechanically loosens debris. The nascent oxygen that is produced may react with products necessary for cell metabolism and may react with cell structures or speed up metabolism to the detriment of cell growth.[24]

Eugenol

Eugenol was first isolated in 1929. The United States of America started its first commercial production in 1940, since then, it has been used widely in the field of dentistry. It is a pale-yellow fluid with a strong smell of carnation and a burning taste. It has been incorporated into several materials such as impression pastes, periodontal dressings, cements, endodontic sealers, and as dressings for dry socket. Eugenol in its unrefined form is mixed with zinc oxide to form zinc oxide-eugenol, which exhibits a combination of physical and therapeutic properties, making it useful as a provisional restorative material, base material, and root canal-filling material. The tissue reaction due to the end products of eugenol can vary from low-grade local reactions to the rare, but serious, anaphylactic reaction. These reactions can be categorized into three types: direct tissue damage due to the nature of the medication; contact dermatitis, stomatitis, and true allergic reaction.[14],[15]

Formocresol

Formocresol has been widely used in pediatric dentistry since its introduction to the field of dentistry by Buckley in 1904. The property of formocresol to fix the tissue when exposed to pulp is used in pulpotomy as medicament. A lot of concern has been expressed and discussed in the field about the safety of formocresol use. Improper use of formocresol has reportedly caused widespread necrosis of soft tissues in the oral cavity.[1]

Garlic burn

Garlic (Allium sativum) is considered as a valuable herbal medicine and has been used worldwide for centuries to treat various ailments. The medical use of garlic dates back to thousands of years ago when Egyptian pyramid builders consumed large amounts of garlic to protect themselves from disease. Grave diggers used crushed garlic as prevention against plague. In World War II, garlic was used by Soviet Army as a substitute for antibiotics and was so called “Russian Penicillin.” Garlic has also shown to have lipid-lowering, antihypertensive, and fibrinolytic effects. It is known to have antifungal, antibacterial, and antiviral properties. The most common side effects caused by garlic range from gastrointestinal upset, nausea, to heartburn to diarrhea. It has also been reported to show platelet dysfunctions leading to postoperative bleeding and spontaneous epidural hematoma. Garlic allergy can also present as rhinitis, asthma, anaphylaxis, contact dermatitis, or pemphigus. The first case of garlic burn was reported by Parish et al. in 1987. Few cases of gingival burn on oral mucosa have been reported. The specific components of garlic responsible for skin lesions remain unknown. Garlic contact dermatitis, type IV allergic reactions limited to epidermis, has been attributed principally to diallyl disulfide, allyl propyl disulfide, and allicin. It is hypothesized that these are the agents causing chemical burn.[26]

Hydrogen peroxide

H2O2 was first used in dentistry in 1913. It is used to decrease plaque formation and to control pyorrhea (gum inflammation). The mechanism of antimicrobial action is due to the release of nascent oxygen which is detrimental to anaerobes. It acts on both Gram positive and Gram negative organism. The other mechanism of antimicrobial property is the effect of H2O2 on debridement of bacterial cell walls.[28] It is widely used professional and self-administered dental product. The most common applications of H2O2 include Mouthrinse (1%–3%) and bleaching agent (3%–5%). Oral ingestion of 3% H2O2 solutions usually do not result in severe toxicity, but may cause vomiting; mild irritation to mucosa; and burns in the mouth, throat, oesophagus, and stomach. Ingestion of higher concentrations (>10%) can result in more dangerous sequelae, such as burns to mucus membranes and gut mucosa.[29] It shows a dose-dependent reaction where at high concentration eugenol causes adverse effect on fibroblast- and osteoblasts-like cells. This leads to localized necrosis and compromised healing. In lower concentration, it causes localized hypersensitivity reactions to oral mucosa called “contact stomatitis” and on dermis causes “contact dermatitis,” possibly because it can react directly with proteins to form conjugates and reactive haptens.[14],[15]

Sodium hypochlorite

NaOCl, a reducing agent which is commonly known as liquid bleach, is a clear, straw-colored solution containing about 5% available chlorine. On ionization, it produces chloramines. These amines are responsible for the antimicrobial ability. The disadvantage of NaOCl is that it can cause soft-tissue inflammation and necrosis if it is expressed outside the confines of root canal.[12] It reacts with proteins and fats of oral mucosa which might lead to secondary infections.[13] The effective concentration of NaOCl to use as an irrigant in the root canal is 0.5%–5.2%. Extension of NaOCl into periradicular tissue during root canal therapy has reportedly lead to localized or extensive tissue necrosis in few cases. A severe acute inflammatory reaction leads to rapid tissue swelling both intraorally within the surrounding mucosa and extraoral with in the skin and subcutaneous tissues. If extruded into maxillary sinus, it leads to acute sinusitis.[35]

Tetracycline hydrochloride

It was introduced in 1948 as a broad-spectrum antibiotic that may be used in the treatment of many common infections.[21] It acts by inhibiting the protein synthesis by binding to 30S ribosome in susceptible microorganism. It is the commonly prescribed treatment of choice for aggressive periodontitis.[22] Incidents of chemical burns due to tetracycline have been reported due to the direct placement of tablet over the infectious places [Figure 2]. Clinically, it presents as loosely adherent yellowish white slough on gingiva. Lesion can be erythematous and painful.[3]
Figure 2: Tetracycline hydrochloride burn seen on the labial mucosa

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  Clinical Features Top


The clinical appearance of chemical burns depends on the severity of the tissue damage, the destructive properties, and mode of application of the causative agent.[26] Clinically, the lesions might differ from mild to severe depending on the composition, pH value, concentration of the chemical agents, the quantity applied, the manner and duration of tissue contact, the extent of penetration into tissue, and the mechanism of action. On the mucosa, chemical burns present as diffuse erosive lesions ranging from simple desquamation to complete mucosal detachment with extension into the submucosa.[3] The tissues exposed to chemicals show changes in their color, texture, consistency, and vascularity. The typical chemical burn is manifested as superficial white to yellow, wrinkled lesion. Desquamation of the underlying tissue due to necrosis depends on the duration of exposure to chemicals. As the duration of exposure increases, the necrosis of the tissue increases. On removal of necrotic epithelium, the red bleeding connective tissue can be observed subsequently covered by yellowish fibrinopurulent membrane. Clinical features of each in have been described in detail drug [Table 2].
Table 2: Clinical features of toxic substances in oral cavity

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Histopathological examination reveals the features of coagulative necrosis.[26] Salivary gland duct involvement might end up with transient obstructive sialadenitis, the resulting scarring of ductal opening can end up with permanent obstruction. Chronic sialadenitis may require surgical excision of duct/gland.[1] Chemical burns are often localized and are rarely confined solely to the anatomic distribution of the masticatory mucosa.[43]

  • Alendronate: Clinically, it may present as ulcers located on the palate, tongue, and lower lip. The ulcers cause intense pain[16]
  • Aspirin: It causes a localized white scurf with a reddened and thickened border,[5],[18] while chromic acid produces a characteristic yellow lesion with a flat border[43]
  • Calcium hydroxide: Patients present with a swollen lip and mucosa, no history of pain and an extensive necrotic zone on gingiva with perforation[8]
  • Cocaine: Lesions develop at the site of application. A white slough, which could easily be removed, showing underlying ulceration and erythema seen on the gingiva. Patients may report painful, retracted gingiva[42]
  • Denture cleansers on chewing and swishing it around the mouth show burning sensation, swelling of the floor of the mouth and the salivary glands, inflammation of the soft palate and tongue. The orifices of the submandibular glands can also present with red and ulcerated with sloughing of the mucosa. There have been several reports of upper digestive tract injury associated with the accidental ingestion of denture cleansers. Furthermore, it can depict as diffuse erosive lesions ranging from simple desquamation to complete obliteration of the oral mucosa with extension past the basement membrane into the submucosa. On ingestion, it also presented with perioral, glossal, and laryngeal edema and respiratory stridor leading to death. On autopsy, it showed extensive hemorrhagic bronchopneumonia and widespread gastrointestinal ulceration[24]
  • Eugenol burns usually presents with burning sensation and pain over the exposed area. Patient also complains of itching sensation. Intraoral examination may reveal allergic reaction “contact stomatitis” over the gingiva and adjacent mucosa[14]
  • Formocresol burns usually presents with pain and swelling on the exposed area. Extensive ulcerative lesion extending along exposed surface will appear like coagulative necrosis covered by slough. Patient also presents with symptoms of restricted mouth opening and reduced food intake[1]
  • Garlic burns are clinically manifested as an area of slough and mucosal ulceration extending along the area of placement. The lesion may be painful on palpation[26]
  • H2O2 burns present as extensive areas of ulceration and erythema involving the alveolar mucosa and the marginal and attached gingival regions. Focal areas of ulceration and sloughing with necrosis of the surface layers of the epithelium may be seen[29]
  • NaOCl burns manifest clinically as soft-tissue inflammation and necrosis if it is expressed outside the confines of root canal. The swelling may be edematous, hemorrhagic, or both and may extend beyond the region that might be expected with an acute infection of the affected tooth. The sudden onset of pain is a hallmark of tissue damage and may occur immediately or be delayed for several minutes or hours. Associated bruising and ecchymosis of adjacent tissues may occur due to bleeding into interstitial spaces.[35]
  • Tetracycline hydrochloride burns are manifested as loosely adherent yellowish white slough on gingiva. It may show erythematous margins, and patients complain of severe pain.[3]



  Treatment Top


The diagnosis of a chemical burn depends on the proper clinical history by eliciting the relevant information from the patient as he/she may be unaware of the significance of these potentially injurious agents.[1] Schematic representation [Figure 3] general treatment protocol followed after chemical burns.
Figure 3: Schematic representation 2: Treatment plan for chemical burns

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The early detection by the patient and the immediate institution of therapeutic measures will ensure a rapid cure and possibly prevent further mucosal damage.[43] Some of the therapeutic measures are mentioned below:

  1. Permanent removal of the agent will be sufficient for the removal of the cause
  2. Copious irrigation with normal saline or betadine
  3. Analgesia if required
  4. Topical application of the corticosteroids and benzocaine
  5. Nutritional supplements in the form of multivitamins that would improve the healing
  6. If required, antibiotics to prevent secondary infections
  7. Advise the patient to be on soft and cold diet without spice for a week
  8. Recall after 1 week.



  Conclusion Top


The oral injuries caused due to chemical burns occur mainly due to injudicious use of pharmaceutical or nonpharmaceutical substances. Management depends on the proper identification of the etiology and removal of the same.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2]


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