A Chemical Erythematous Macule of the Buccal Mucosa Bukkal

OLGU RAPORU (Case Report)
Hacettepe Dişhekimliği Fakültesi Dergisi
Cilt: 30, Sayı: 1, Sayfa: 63-66, 2006
A Chemical Erythematous Macule of the
Buccal Mucosa
Bukkal Mukozada Kimyasal Eritematöz Makül
*Dilek Aynur UĞAR DDS, PhD, *Süleyman BOZKAYA DDS, PhD, *Bülent GÜNER DDS, PhD,
*İnci KARACA DDS, PhD
*Gazi University, Faculty of Dentistry, Department of Oral and Maxillofacial Surgery
ABSTRACT
ÖZET
Electricity, heat, cold, radiation, and chemical or mec-
Elektrik, sıcak, soğuk, radyasyon ve kimyasal veya mekanik stimulus oral mukozada hasara neden olabilir.
Eritematöz bir makül şeklinde ortaya çıkan kimyasal
veya termal yanığın nedeni, genellikle kostik (yakıcı) ilaç
veya sıcak yiyecek veya içeceklerdir. Vakaların çoğunda
kimyasal yanıkların klinik görünümleri doku hasarının şiddetine bağlıdır. Bu yanıklar lokalize mukozitis,
keratotik beyaz lezyonlar şeklinde olabileceği gibi doku
yüzeyindeki koagülasyon nedeniyle; irrite, kanamalı,
ağrılı doku yüzeyleri şeklinde de ortaya çıkabilirler. Bu
makalede sodyum bikarbonat nedeniyle sağ bukkal
mukozasında kimyasal yanık oluşmuş olan bir vaka
sunulmakta ve ayırıcı tanıda hasta hikayesinin önemi
vurgulanmaktadır.
hanical stimuli can be cause injury of the oral mucosa.
The cause of a chemical or thermal burn which presents
as an erythematous macule is usually a caustic drug or
hot foods or beverages. The clinical appearance of the
chemical burns in most cases depends on the severity of
the tissue damage. These burns may produce localized
mucositis, keratotic white lesions or as well as raw, bleeding, painful tissue surface due to the coagulation of
the tissue. In this report, a case of an unusual chemical
burn localized in the right buccal mucosa, produced by
sodium bicarbonate, is reported and the importance of
the history in differential diagnosis is emphasized.
KEYWORDS
Chemical burn, Nodium bicarbonate, Erythematous
macule.
ANAHTAR KELİMELER
Kimyasal yanık, Nodyum bikarbonat, Eritematöz makül.
64
INTRODUCTION
Injury of the oral mucosa can be caused by
electricity, heat, cold, radiation, and chemical or
mechanical stimuli1,2. The cause of a chemical or
thermal burn which presents as an erythematous
macule is usually a caustic drug or hot foods or
beverages3. The severity of the lesion depends on
the type of chemical agent utilized and the concentration and duration of contact of the noxious
agent with the tissues4. Phenol, eugenol, trichloroacetic acid, aspirin, iodine, alcohol, acrylic resin,
sodium perborate, silver nitrate, sodium hypochlorite, paraformaldehyde, chlorine compounds and
agriculture chemical agents are but a few examples.
The signs and symptoms of burns of the oral mucosa vary considerably, depending on the nature of
the causative agent. When the burn is reasonably
severe, the coagulated mucosa can usually, though
painfully, be seperated from the underlying tissues3.
In this paper an exceptional case of a chemical
burn produced by misuse of sodium bicarbonate for
oral hygiene practice which is believed to be caused
for the first time to such a lesion reported in the
dental literature is presented and the importance of
the history in differential diagnosis is emphasized.
CASE REPORT
A 51-year- old female was referred to the Oral
and Maxillofacial Surgery Department with a complaint of a red and painful lesion on her right buccal mucosa by her general dental practitioner. Her
history revealed that her gingiva was red, swollen
and she observed bleeding both during the brushing and sometimes spontaneously. She had decided
on her own to get antibiotic orally and use sodium
bicarbonate as an adjunct to brushing for improving her oral hygiene. For this purpose she used
sodium bicarbonate/water mouthwash with each
tooth-cleaning episode. Because she didn’t satisfied from the outcome, she decided to use sodium
bicarbonate powder on her gingiva directly. She
continued both to get antibiotic and use sodium
bicarbonate approximately for three weeks. When
she saw a red, painful area in her right buccal mucosal region, she admitted to a dental practitioner.
She was called that the cause of this erythematous
lesion may be an atrophic candidiasis due to long
lasting antibiotic use and antifungal treatment was
recommended. Although such a treatment, there
was no improvement.
The patient’s past medical history was non-contributory and there were no extraoral findings. The
intraoral examination showed a red, 2 x 1,5 cm,
tender, superficial lesion extending from the corner
of the mouth to the posterior buccal mucosa in the
right side (Fig 1). Visual examination of the remaining intraoral soft tissues disclosed unhealthy periodontal condition.
An incisional biopsy was performed with local
anesthesia. Histologic examination showed marked
intracellular and extracellular edema in the surface
of the epithelium. The superficial part of the lamina
propria contained dense inflammatory cell infiltrate (Fig 2). PAS-staine sections demonstrated the
absence of fungal organisms in the epithelium.
Treatment consisted of triamcinolone in Orabase as a protective coating, an analgesic and a
bland diet. The burn healed in 2 weeks (Fig 3).
DISCUSSION
The clinical appearance of the chemical burns
in most cases depends on the severity of the tissue
damage. These burns may produce localized mucositis, keratotic white lesions or as well as raw, bleeding, painful tissue surface due to the coagulation of
the tissue3,5. In the case presented the clinical appearance of the lesion was red and painful.
Chemical burns most often result from the patient applying analgesics such as aspirin or acetaminophen near to the mucosa adjacent to an aching tooth1,6. It is also reported that caustic ingestion, accidental ingestion of hot foods or beverages,
excessive consumption of fresh fruit and fresh fruit
juice, and wrong oral hygiene practice may cause
burns of the oral tissues7. In the present case, the
gingiva was hyperemic and swollen due to the poor
oral hygiene.
65
FIGURE 1
Patient shown on day of admission
FIGURE 2
Surface of the epithelium showing marked intracellular and
extracellular edema. The lamina propria contained dense
inflammatory cell infiltrate (H&E x 40).
FIGURE 3
The right buccal mucosa after 2 weeks of treatment.
Sodium bicarbonate that the patient used for
improving her oral hygiene is a white, crystalline
powder chiefly used a gastric antacid. In aqueous
solution, it is used locally for washing the nose,
mouth, and vagina, and as a cleansing enema7. Although it is known that in saturated solution sodium bicarbonate is used as a dressing for minor
burns, in this case according to the patient’s history we have thought that the use of sodium bicarbonate, especially the application of its powder
caused an erythematous macule. Some products as
toombak and snuff that are known to contain sodium bicarbonate have strong alkalinity. Idris et al8
detected the clinical and histopathological characteristics of toombak-associated oral mucosal lesions. They reported that this property of toombak
may contribute to the epithelial surface changes
which are similar to those seen in lesions induced
by snuff. It is concluded that chronic exposure of
these products may result in an alkaline burn on
the oral mucosa.
The Keyes technique that is used for the treatment of periodontal disease involves local mechanical therapy, local chemical therapy and systemic
antibiotics. For the local chemical therapy baking
soda and peroxide are used as an adjunct to home
plaque control. However it is emphasized that abuse
of the practices may lead to gingival injury 9. Herrin
et al10,11 investigated whether the oral application of
a baking soda - % 3 hydrogen peroxide dentifrice
and a nearly saturated sodium chloride mouthwash,
as a home care method for treating periodontal disease, creates a sodium burden for human subjects.
They concluded that raw, erosive desquamative
gingival lesions were seen in all treated subjects. In
this case, it is thought that because of the high concentration of baking soda that the patient applied
caused a red, tender, superficial lesion just after the
application. This clinical appearance is consistent
with the observation of Herrin et al.
Until a careful history is taken, the patient is
usually unaware of the cause of the lesion6. The
identification of the chemical burn lesion is best
accomplished by determining, through the patient
history6,12.
66
In chemical burns, a white, white-brownish or
red surface can be seen12. In the chemical burn lesions which appear as a red surface, as in this patient, erythema from mechanical trauma, purpiric
macule, cellulitis, allergic manifestations, erythroplakia, atrophic candidiasis, herald spot of disseminated red conditions, and fungal infections should
be taken into account in differential diagnosis6.
This patient had been previously treated under an
incorrect diagnosis of atrophic candidiasis due to
long lasting antibiotic use and inappropriate antifungal treatment was recommended. In our clinic
the chemical burn lesion was differentiated from
the atrophic candidiasis via a detailed patient history and histologic examination confirmed the diagnosis.
The treatment for chemical burns is the application of a protective coating such as Orabase with
or without steroids and initiation of a bland diet1,6.
In most cases, treatment is mainly symptomatic. If
the agent is completely eliminated and there are no
further exposures, prompt recovery is the rule1,3. If
pain is a problem, systemic analgesic may be administered. The analgesic tablets are to be swallowed and not be used topically6. In the current
case besides triamcinolone in Orabase and a bland
diet, a systemic analgesic was recommended.
Treatment. 7th ed. Philadelphia, 1977, J.B.Lippincott
Company.
4. Regezi JA, Sciubba, JJ. Oral Pathology. ClinicalPathologic Correlations. Philadelphia, 1989, W.B. Saunders
Company.
5. Laskaris G. Color Atlas of Oral Diseases. 2nd ed. Stutgart,
1994, Thieme Medical Publishers Inc.
6. Wood NK, Goaz PW. Chemical Burns. In: Differential
Diagnosis of Oral Lesions. 4th ed. St. Louis: Mosby Year
Book; 1991; 68-70, 144-145
7. Dorlan’s Illustrated Medical Dictionary. 26th ed.
Philadelphia, 1981, W.B. Saunders Company.
8. Idris AM, Warnakulasuriya KA, Ibrahim YE, Nielsen R,
Cooper D, Johnson NW. Toombak-associated oral mucosal
lesions in Sudanese show a low prevalence of epithelial
dysplasia. J Oral Pathol Med. 1996; 25(5): 239-44
9. Current understanding of the role of microscopic monitoring,
baking soda, and hydrogen peroxide in the treatment of
periodontal disease. Committee on Research, Science and
Therapy. The American Academy of Periodontology. J
Periodontol. 1998; 69(8): 951-4
10. Herrin JR, Rubright WC, Squier CA, et al. Local and
systemic effects of orally applied sodium salts. J Am Dent
Assoc. 1986;113(4):607-11
11. Herrin JR, Squier CA, Rubright WC. Development of
erosive gingival lesions after use of a home care technique.
J Periodontol 1987; 58(11): 785-8
12. Strassburg M, Knolle G. Diseases of the oral mucosa. A
Color Atlas. 2nd ed. Chicago: Quinteisence Publishing Co
Inc; 1994.
REFERENCES
1. Baruchin AM, Lustra JP, Nahlieli O, Neder A. Burns of the
Oral Mucosa. J Craniomaxilofac Surg. 1991; 19: 94-6
2. Touyz LZG, Hille JJ. A Fruit-mouthwash chemical burn.
Oral Surg. 1984; 58: 290-2
3. Lynch MA. Burket’s Oral Medicine. Diagnosis and
CORRESPONDING ADDRESS
Süleyman BOZKAYA DDS, PhD
Gazi University, Faculty of Dentistry, Department of Oral and Maxillofacial Surgery
Tel: +90 312 212 62 20 extention 350, Fax: +90 312 223 92 26, E-mail: [email protected]