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Diagnosis of systemic sarcoidosis based on oral manifestations: a case report
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY Volume 97, Number 4 either a past biopsy with premalignant/malignant changes or present premalignant biopsy (CDX or surgical). Conclusions. The differential pattern of p53 and Ki67 staining in BB samples indicates that this may prove to be a useful aid for or noninvasive screening and follow-up of premalignant oral lesions.
A COMPARISON OF ORAL GRAFT VS. HOST DISEASE (GVHD) BETWEEN NONMYELOABLATIVE STEM CELL TRANSPLANTATION (NST) AND MYELOABLATIVE HEMATOPOIETIC STEM CELL TRANSPLANTATION (HSCT). S. Elad, R. Or, D. Almog, A. Hirschhorn, M. Y. Shapiram, Hebrew University Hadassah School of Dental Medicine, Jerusalem, Israel, and University of Rochester, Rochester, NY. Objective. In recent years the nonmyeloablative stem cell transplantation (NST) became a common hematopoietic stem cell transplantation (HSCT) conditioning protocol. The NST is based on the concept that graft vs. leukemia (GVL) effect will compensate for the nonablation and the ablation-related toxicities will be avoided. The objective of this study was to evaluate the oral prevalence and manifestations of acute graft versus host disease (aGVHD) in patients undergoing NST compared to patients undergoing myeloablative HSCT. Study design. A prospective longitudinal study including 32 patients undergoing HSCT was undertaken. Patients were classified into 3 groups: NST, ablative HSCT, and autologous HSCT (used as a control group). Oral tissues were examined once every 3 weeks, starting 2 weeks post-HSCT and ending on day 100 post-HSCT. Clinical signs typical to oral GVHD were documented. The examiner was blinded in regard to patient classification. Comparison of systemic GVHD incidence and oral GVHD incidence was done using Pearson’s chi-square test and Fisher’s exact test. Results. The incidence of oral GVHD was 29.4% in the NST group and 75% in the myeloablative HSCT group (P\.08). The mean onset time of oral GVHD was 17 days post-HSCT in the NST group and 21.5 days post-HSCT in the myeloablative HSCT group (P\.76). There were no patients with systemic or oral GVHD in the autologous HSCT control group. Conclusions. There is a trend for a decreased incidence of oral involvement typical for aGVHD in NST compared to myeloablative HSCT. Large-scale studies are warranted to confirm this result.
DIAGNOSIS OF SYSTEMIC SARCOIDOSIS BASED ON ORAL MANIFESTATIONS: A CASE REPORT. M. Fatahzadeh, J. Rinaggio, University of Medicine and Dentistry of New Jersey-New Jersey Dental School, Newark, and New Jersey Dental School. Background. Sarcoidosis is a multifocal systemic disorder of unknown etiology presenting with a constellation of signs and symptoms and characterized histologically by the presence of noncaseating granulomas in the affected organs. Because some symptoms of sarcoidosis are known to manifest within the head and neck, dentists may play an important role in the diagnosis of sarcoidosis. We describe a patient who presented with xerostomia, xerophthalmia, and parotid enlargement but minimal respiratory complaints who subsequently was found to have sarcoidosis, based on the initial histopathological findings of labial minor salivary gland biopsy and further diagnostic evaluations. Case study. A 47-year-old white female presented to the University Oral Medicine Service with complaints of severe dry mouth, burning tongue, and dysgeusia. Her symptoms started several years prior to the appointment, but had exacerbated over the previous months. She also complained of dysphagia, tooth sensitivity on
Abstracts
457
exposure to cold as well as diminished acuity for sweet and salty tastes. She had tried a myriad of products including Biotene gel, Mouth Kote, artificial saliva, and dry mouth lozenges for symptomatic relief. Her past medical history was significant for thyroidectomy, gastroesophageal reflux disease (GERD), asthma, narcolepsy, depression, and chronic sinusitis. Her medications included thyroxine and liothyronine as thyroid hormone replacement, omeprazole for GERD, albuterol for asthma, zaleplon, methylphenidale, and lorazepam for sleep disorder , doxepin and venlafaxine for depression, and montelukast, fexofenidine, and mometasone furoate for seasonal allergy. She was allergic to sulfa drugs. The patient had a distant history of 4 pack-years smoking but quit 15 years prior to presentation. She denied any alcohol or recreational drug abuse. Review of systems was significant for dry skin, mouth, nose and eyes, generalized weakness, occasional shortness of breath and heaviness of chest as well as intolerance to heat. Her eye symptoms had started a few years ago and she had been evaluated by a rheumatologist for Sjo¨gren’s syndrome which had been proven negative. She was symptomatically treated for dry eyes and nose. Extraoral examination was significant for bilateral parotid and submandibular gland enlargement. Her oral mucosa was extremely dry with wrinkled erythematous tissues. Major salivary glands were tender on palpation with clear sluggish flow from Stenson’s and Whartons’s ducts with and without gustatory stimulation. Her tongue was fissured with a brownish coating. She was dentate with no obvious clinical caries. Our differential diagnosis included Sjo¨gren’s syndrome, sarcoidosis, benign lymphoepithelial lesion, Warthin tumor, and medicationinduced xerostomia. Recommendations for symptomatic relief of xerostomia, dysphagia, and burning as well as preventative oral health care were provided. SSA, SSB, ANA and RF serology work-up for Sjogren’s syndrome was negative. Minor salivary gland biopsy was consistent with granulomatous sialadenitis. PAS, AFB, and Gram stains for microorganisms were negative, and there was no evidence of foreign body implantation. The patient was advised to be evaluated for sarcoidosis as the possible systemic cause for her salivary gland enlargement and xerostomia. The patient was subsequently diagnosed with sarcoidosis based on findings of hilar infiltrate in the chest x-ray and CT. She was also found to have elevated serum angiotensinconverting enzyme (ACE). On her follow-up visit to the Oral Medicine clinic 6 months later, she reported her oral symptoms (xerostomia, dysphagia, burning, and dental sensitivity) had substantially improved. Cclinical examination showed that the bilateral parotid swellings had resolved and the salivary glands were nontender and secretory. Intraorally, tissues were moist and wet. The mere knowledge of a specific diagnosis seemed to have significantly alleviated her stress and depression enabling her to be weaned off many of her antidepressant medications. The patient was extremely appreciative about our contribution to the diagnosis of her underlying systemic condition and its appropriate management by a rheumatologist.
PRESENCE OF LEUKOPLAKIA AT PREVIOUS CANCER SITE PREDICTS TUMOR RECURRENCE. M. Williams, A. Hovan, J. Epstein, L. Zhang, M. Rosin, British Columbia Cancer Agency, Vancouver, Canada, Fraser Valley Cancer Centre, Surrey, Canada, and University of British Columbia, Vancouver , Canada. Background. Clinical evaluation of malignant risk of oral leukoplakia is based mainly on the clinical appearance (homogeneous vs. nonhomogeneous), size, and site of the lesion(s). However, these clinical risk predictors have been mainly derived from studies of primary oral leukoplakia. Their value in assessing cancer risk of leukoplakia at previous cancer sites is not clear. Understanding the
A COMPARISON OF ORAL GRAFT VS. HOST DISEASE (GVHD) BETWEEN NONMYELOABLATIVE STEM CELL TRANSPLANTATION (NST) AND MYELOABLATIVE HEMATOPOIETIC STEM CELL TRANSPLANTATION (HSCT). S. Elad, R. Or, D. Almog, A. Hirschhorn, M. Y. Shapiram, Hebrew University Hadassah School of Dental Medicine, Jerusalem, Israel, and University of Rochester, Rochester, NY. Objective. In recent years the nonmyeloablative stem cell transplantation (NST) became a common hematopoietic stem cell transplantation (HSCT) conditioning protocol. The NST is based on the concept that graft vs. leukemia (GVL) effect will compensate for the nonablation and the ablation-related toxicities will be avoided. The objective of this study was to evaluate the oral prevalence and manifestations of acute graft versus host disease (aGVHD) in patients undergoing NST compared to patients undergoing myeloablative HSCT. Study design. A prospective longitudinal study including 32 patients undergoing HSCT was undertaken. Patients were classified into 3 groups: NST, ablative HSCT, and autologous HSCT (used as a control group). Oral tissues were examined once every 3 weeks, starting 2 weeks post-HSCT and ending on day 100 post-HSCT. Clinical signs typical to oral GVHD were documented. The examiner was blinded in regard to patient classification. Comparison of systemic GVHD incidence and oral GVHD incidence was done using Pearson’s chi-square test and Fisher’s exact test. Results. The incidence of oral GVHD was 29.4% in the NST group and 75% in the myeloablative HSCT group (P\.08). The mean onset time of oral GVHD was 17 days post-HSCT in the NST group and 21.5 days post-HSCT in the myeloablative HSCT group (P\.76). There were no patients with systemic or oral GVHD in the autologous HSCT control group. Conclusions. There is a trend for a decreased incidence of oral involvement typical for aGVHD in NST compared to myeloablative HSCT. Large-scale studies are warranted to confirm this result.
DIAGNOSIS OF SYSTEMIC SARCOIDOSIS BASED ON ORAL MANIFESTATIONS: A CASE REPORT. M. Fatahzadeh, J. Rinaggio, University of Medicine and Dentistry of New Jersey-New Jersey Dental School, Newark, and New Jersey Dental School. Background. Sarcoidosis is a multifocal systemic disorder of unknown etiology presenting with a constellation of signs and symptoms and characterized histologically by the presence of noncaseating granulomas in the affected organs. Because some symptoms of sarcoidosis are known to manifest within the head and neck, dentists may play an important role in the diagnosis of sarcoidosis. We describe a patient who presented with xerostomia, xerophthalmia, and parotid enlargement but minimal respiratory complaints who subsequently was found to have sarcoidosis, based on the initial histopathological findings of labial minor salivary gland biopsy and further diagnostic evaluations. Case study. A 47-year-old white female presented to the University Oral Medicine Service with complaints of severe dry mouth, burning tongue, and dysgeusia. Her symptoms started several years prior to the appointment, but had exacerbated over the previous months. She also complained of dysphagia, tooth sensitivity on
Abstracts
457
exposure to cold as well as diminished acuity for sweet and salty tastes. She had tried a myriad of products including Biotene gel, Mouth Kote, artificial saliva, and dry mouth lozenges for symptomatic relief. Her past medical history was significant for thyroidectomy, gastroesophageal reflux disease (GERD), asthma, narcolepsy, depression, and chronic sinusitis. Her medications included thyroxine and liothyronine as thyroid hormone replacement, omeprazole for GERD, albuterol for asthma, zaleplon, methylphenidale, and lorazepam for sleep disorder , doxepin and venlafaxine for depression, and montelukast, fexofenidine, and mometasone furoate for seasonal allergy. She was allergic to sulfa drugs. The patient had a distant history of 4 pack-years smoking but quit 15 years prior to presentation. She denied any alcohol or recreational drug abuse. Review of systems was significant for dry skin, mouth, nose and eyes, generalized weakness, occasional shortness of breath and heaviness of chest as well as intolerance to heat. Her eye symptoms had started a few years ago and she had been evaluated by a rheumatologist for Sjo¨gren’s syndrome which had been proven negative. She was symptomatically treated for dry eyes and nose. Extraoral examination was significant for bilateral parotid and submandibular gland enlargement. Her oral mucosa was extremely dry with wrinkled erythematous tissues. Major salivary glands were tender on palpation with clear sluggish flow from Stenson’s and Whartons’s ducts with and without gustatory stimulation. Her tongue was fissured with a brownish coating. She was dentate with no obvious clinical caries. Our differential diagnosis included Sjo¨gren’s syndrome, sarcoidosis, benign lymphoepithelial lesion, Warthin tumor, and medicationinduced xerostomia. Recommendations for symptomatic relief of xerostomia, dysphagia, and burning as well as preventative oral health care were provided. SSA, SSB, ANA and RF serology work-up for Sjogren’s syndrome was negative. Minor salivary gland biopsy was consistent with granulomatous sialadenitis. PAS, AFB, and Gram stains for microorganisms were negative, and there was no evidence of foreign body implantation. The patient was advised to be evaluated for sarcoidosis as the possible systemic cause for her salivary gland enlargement and xerostomia. The patient was subsequently diagnosed with sarcoidosis based on findings of hilar infiltrate in the chest x-ray and CT. She was also found to have elevated serum angiotensinconverting enzyme (ACE). On her follow-up visit to the Oral Medicine clinic 6 months later, she reported her oral symptoms (xerostomia, dysphagia, burning, and dental sensitivity) had substantially improved. Cclinical examination showed that the bilateral parotid swellings had resolved and the salivary glands were nontender and secretory. Intraorally, tissues were moist and wet. The mere knowledge of a specific diagnosis seemed to have significantly alleviated her stress and depression enabling her to be weaned off many of her antidepressant medications. The patient was extremely appreciative about our contribution to the diagnosis of her underlying systemic condition and its appropriate management by a rheumatologist.
PRESENCE OF LEUKOPLAKIA AT PREVIOUS CANCER SITE PREDICTS TUMOR RECURRENCE. M. Williams, A. Hovan, J. Epstein, L. Zhang, M. Rosin, British Columbia Cancer Agency, Vancouver, Canada, Fraser Valley Cancer Centre, Surrey, Canada, and University of British Columbia, Vancouver , Canada. Background. Clinical evaluation of malignant risk of oral leukoplakia is based mainly on the clinical appearance (homogeneous vs. nonhomogeneous), size, and site of the lesion(s). However, these clinical risk predictors have been mainly derived from studies of primary oral leukoplakia. Their value in assessing cancer risk of leukoplakia at previous cancer sites is not clear. Understanding the