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Vol. 12. Issue 6.
Pages 357-358 (November - December 2016)
Vol. 12. Issue 6.
Pages 357-358 (November - December 2016)
Letter to the Editor
DOI: 10.1016/j.reumae.2016.02.003
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Response to: Sjögren's Syndrome and Halitosis: A Case Report
Respuesta a: Síndrome de Sjögren y halitosis: descripción de un caso clínico
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Rami Qanneta
Servicio de Reumatología, Hospital Universitari Joan XXIII, Tarragona, Spain
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Dear Editor:

I read very carefully the publication of Ruiz Serrato et al.1 in Reumatología Clínica, where the authors report a case of halitosis secondary to Sjögren's syndrome (SS). I would like to express a few considerations, which I hope will contribute to a better understanding of this association.

Sjögren's syndrome is a systemic, autoimmune disease, with a prevalence that ranges between 0.1% and 0.5%, with a predominance of women (4th and 5th decades of life).2 Histopathological studies show it to be characterized by lymphocytic infiltration at the level of the exocrine glands.2 This syndrome can be primary or secondary (associated with systemic lupus erythematosus, rheumatic arthritis and scleroderma).2 The destruction of the exocrine glands leads to “sicca syndrome” (xerostomia and xerophthalmia).2 However, SS can show extraglandular manifestations, including general, cutaneous, musculoskeletal, respiratory, urogenital, thyroid, gastrointestinal and hepatobiliary.2 The association between halitosis and SS is multifactorial.

First: Parotid gland dysfunction results in xerostomia and a decrease in salivary flow that leads to periodontal diseases due to Treponema denticola, Porphyromonas gingivalis and Bacteroides forsythus, which produce mercaptan and sulfur that are associated with the level of halitosis (oral cause of halitosis).3 Saliva has antimicrobial properties; thus, the amount and quality of saliva are essential to prevent halitosis. Therefore, in patients with SS and xerostomia, the production of saliva is reduced, increasing the possibility of generating volatile sulfur compounds (VSC), the result of the degradation of proteins with sulfur-containing amino acids from the exfoliation of human epithelial cells, leukocytes and the remains of food, and with it, oral malodor.3 Volatile sulfur compounds are associated not only with halitosis, but can enter into a vicious circle of pathogenesis of gingivitis and periodontitis.3

Second: Extraglandular manifestations are factors that trigger halitosis in SS. Patients with SS are more predisposed to develop chronic rhinosinusitis (a perioral cause of halitosis) and bronchiectasis (an extraoral cause of halitosis). Among the gastrointestinal manifestations, they may present esophageal dysfunction, chronic gastritis, Helicobacter pylori infection and bacterial overgrowth, which also cause halitosis (extraoral cause). Primary biliary cirrhosis, as a hepatobiliary manifestation, is an extraoral cause of halitosis.

Third: Diseases associated with secondary SS play their own role. For example, gastroesophageal reflux (an extraoral cause) in SS secondary to scleroderma produces dental erosion and dysphagia that provoke halitosis.4 Moreover, patients with SS have an elevated risk of developing non-Hodgkin's B-cell lymphoma, which can be an extraoral cause of halitosis. On the other hand, the symptomatology of halitosis in SS patients can, subjectively, be worse (not genuine), by psychosomatic halitosis, halitophobia or because the xerogenic medicine they take (antidepressant and nonsteroid anti-inflammation drugs). With respect to the case reported by Ruiz Serrato et al.,1 as the authors, reasonably explain, it is true halitosis due to oral causes (xerostomia), with a favorable response to pilocarpine. However, we recommend follow-up, to screen for possible perioral and/or extraoral causes related to SS, in the case of therapeutic failure or recurrence. I conclude that, halitosis is a prevalent entity (up to 50% of the general population), and has been studied little in SS. Although, it is considered more a problem related to poor dental hygiene or to diseases of the oral cavity (87%), on occasions, it may be a manifestation of the disease at other levels—perioral—or even of a psychiatric or systemic disease—extraoral—(13%).3 Therefore, an initial approximation should include a complete history (diet, drugs, poor habits and dental hygiene), a thorough examination, a complete analysis, as in screening. The therapeutic management requires a multidisciplinary evaluation, with hygienic, dietetic, pharmacological (pilocarpine hydrochloride) and/or etiological—oral, perioral, extraoral or mixed, as in the case of SS.

References
[1]
A. Ruiz Serrato, R. Infantes Ramos, A. Jiménez Ríos, P.P. Luján Godoy.
Sjögren's syndrome and halitosis: a case report [Article in English, Spanish].
pii: S1699-258X(15)00191-6. [Epub ahead of print] http://dx.doi.org/10.1016/j.reuma.2015.11.005
[2]
M. Ramos-Casals, P. Brito-Zerón, A. Sisó-Almirall, X. Bosch.
Primary Sjögren syndrome.
Praxis (Bern 1994), 101 (2012), pp. 1565-1571
[3]
G.S. Madhushankari, A. Yamunadevi, M. Selvamani, K.P. Mohan Kumar, P.S. Basandi.
Halitosis – an overview: Part-I – Classification, etiology, and pathophysiology of halitosis.
J Pharm Bioallied Sci, 7 (2015), pp. S339-S343
[4]
M. Hinchcliff, J. Varga.
Systemic sclerosis/scleroderma: a treatable multisystem disease.
Am Fam Physician, 78 (2008), pp. 961-968

Please cite this article as: Qanneta R. Respuesta a: Síndrome de Sjögren y halitosis: descripción de un caso clínico. Reumatol Clin. 2016;12:357–358.

Copyright © 2015. Elsevier España, S.L.U. and Sociedad Española de Reumatología y Colegio Mexicano de Reumatología
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