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Abstracts presented at the Forty-fifth Annual Meeting of the American Academy of Oral Medicine, April 21–28, 1991, New Orleans, La.
Abstracts presented at the Forty-fifth Annual Meeting of the American Academy of Oral Medicine, April 21-28, 1991, New Orleans, La.
THE PREVALENCE OF ORAL CARCINOMA IN SALTlMORE CITY’S ELDERLY SLACK POPULATION. Streckfus CF. University of Maryland, Baltimore An elderly black population residing in Baltimore City consisting of 10,819 patients was examined for oral pathology. A total of 247 patients required biopsies from the total population that was examined. Fourteen of the 247 biopsied patients were reported to have oral cancer, representing a prevalence rate of I .3 per 1000 people. Eight patients had squamous cell carcinoma, three adenosarcoma, and one basal cell plasmacytoma. Nine of the patients were edentulous. emphasizing the need for frequent oral examinations among the edentulous population. This report represents the only study ever performed on this population.
EVALUATION OF A SYNTHETIC ANALOG OF VITAMIN A AND BETA CAROTENE ON THE CLINICAL AND HISTOLOGIC APPEARANCE AND BIOLOGIC MARKERS IN HUMAN, PREMALIGNANT ORAL LESIONS. Hays G, Lippman S, Toth B. Weber Hong W. UTHSCH-Dental
R, Batsakis
J, Wargovich
M,
Branch and M. D. Anderson Cancer Center, Houston, Tex. The purpose of this study is to evaluate I3-cis-retinoic acid (13~ RA) and P-carotene (BC) in the treatment of premalignant oral lesions. Fifty-six patients with premalignant oral mucosal lesions were examined at baseline with respect to medical history. clinical examination, biopsy, and cytology. Biopsies were evaluated in reference to keratin, involucrin. and transglutaminase. Cytology was used to evaluate micronuclei. Three-month induction therapy was begun with each subject taking 13~ RA at a dosage of I .5 mg/kg/ day. After 3 months lesions were evaluated as at baseline. All subjects with lesions that responded or remained stable were randomly placed in either a low-dose l3c RA regimen (0.5 mg/kg/day) treatment group or a BC (30 mg/day) treatment group. After another 9 months, lesions were evaluated once again. Fifty-six subjects initiated treatment and 46 completed the 12-month trial. Sixty-two percent of the patients showed clinical improvement of the lesions after 3 months. The I3c RA low-dose treatment group showed significant improvement compared with the BC treatment group. Complete and partial remission rates at 12 months for l3c RA were 75% versus 27% for BC (p < 0.05). The relapse rates were more frequent in the BC group (54% vs 10%; p < 0.01). Micronuclei frequency patterns paralleled clinical data with more effective suppression in 13~ RA group. In conclusion, a regimen of lowdose l3c RA was significantly more effective than BC in maintenance therapy for premalignant oral mucosal lesions after l3c RA induction therapy.
HORMONAL RESPONSE OF LOW-DOSAGE MUCOSAL APPLICATION OF FLUOCINONIDE IN AN ANIMAL MODEL. Cade JE, Wright B, Lang C, Porter JR. Louisiana State University School of Dentistry, New Orleans The purpose of this study is to evaluate high, medium and low doses of fluocinonide
rat oral mucosa. Two-week time-release pellets were implanted into the buccal mucosa of 400 gm Holtzman rats in doses of 0.5, 0.05, and 0.005 mg. Control animals received placebo pellets in the same manner. Animals were sacrificed at baseline and at I, 4, and 9 days. Body, anterior pituitary, and adrenal weights were determined. Plasma corticosterone, ACTH, insulin, and glucose were measured. The results demonstrated several systemic effects in a comparison of the placebo-controlled group with the active treatment groups. ACTH was significantly inhibited at day I (high, middle doses) and day 4 (low dose). Corticosterone was significantly suppressed on days I, 4, and 9 (high dose); days I and 4 (middle dose); and days I, 4, and 9 (low dose). Insulin level was significantly increased on days I, 4, and 9 (high. middle doses, but only on day I of the low dose). Glucose levels were elevated at days I and 4 (high dose); day 1 (middle dose); and day 4 (low dose). Body weights and adrenal weights were reduced in several of the active drug treatment groups. In conclusion, these results indicate significant systemic physiologic effects secondary to mucosal implantation of fluocinonide in an animal model.
the systemic effects of (Lidex) implanted in
ORAL HAIRY LEUKOPLAKIA: ETIOPATHOGENETIC CONSIDERATIONS. Ficarra G. Adler-Storthz K, Romagnoli P, Pimpinelli N, Shillitoe EJ. University of Florence and USL IO/D. Florence, Italy, and the University of Texas Dental Branch, Houston The purpose of this study is to report the prevalence of EpsteinBarr virus (EBV) and human papillomavirus (HPV) in oral hairy leukoplakia (OHL) and normal buccal mucosa. Alterations of the epithelial microenvironment that may be relevant to the pathogenesis of OHL will be discussed. Initial studies suggested an association of OHL with both EBV and HPV. Evidence of association with HPV is demonstrated by staining with antiserum to common HPV antigens and sporadic reports of HPV-positive OHL as detected by in situ DNA hybridization. In addition, a decrease in the number of Langerhans cells in the epithelial microenvironment of OHL may facilitate the appearance of OHL. The prevalence of EBV DNA, HPV structural antigens, and HPV DNA in OHL were studied with DNA in situ hybridization, polymerase chain reaction PCR and avidin-biotin peroxidase immunostaining. respectively. Studies on nonlymphoid accessory cells (NLACs) were done using electron microscopy and immunohistochemistry. EBV DNA was detected in 47 of 58 samples of OHL and in I of IO biopsy specimens of normal buccal mucosa of HIV-seropositive patients. Positive staining with antibody to papillomavirus common structural antigens was demonstrated in 26 of 43 OHL specimens. HPV DNA was detected by PCR amplification and dot blot hybridization in I I of 20 OHL specimens and in 5 of IO normal buccal mucosa specimens. Lack of CD4+ cells and reduced number and incomplete differentiation of NLACs were found in OHL epithelium. Retrovirus-like particles were seen within NLACs. In conclusion, our results showed that EBV can be found in normal mucosa also. Thus the etiology of OHL remains undefined. EBV and HPV both may act as cofactors in the etiology of OHL. The impairment of local cellular immunity may contribute to the development of OHL.
311
3 I 2 Proceedings and abstracts
ORAL SURC ORAL MED ORAL PATHOI. September 1991
MISDIAGNOSIS OF FACIAL PAIN IN FOUR CASES SALIVARY PATHOSIS. Abramovitch K, Flaitz CM.
Diagnostic Sciences, UTHSCH-Dental Tex.
OF
Oral Branch, Houston,
Diagnosing pain in the lower third of the face is a frequent dilemma for dental clinicians. If the teeth and the periodontium are ruled out as sources of pain, the diagnostic process becomes more challenging. Because of the proximity of the parotid and submandibular gland to the posterior dentition and temporomandibular joint, salivary gland disease must be considered in the differential diagnosis. Four cases of facial swelling and pain that were originally diagnosed as either odontogenic or arthrogenic are presented. The ages of the patients (three female, one male) ranged from 27 to 67 years, with a mean of 43 years. Two of the caseswere initially diagnosed by the referring dentists as dental abscesses.In one case careful evaluation of Stensen’s duct revealed an inflamed orifice with suppuration. In the other a parotid sialogram demonstrated findings consistent with sialadenitis. The other two casesoriginally presented as regressive casesof temporomandibular disorders. One was a unilateral acute sialadenitis secondary to Sjiigren’s syndrome. In the other case a sialogram demonstrated a nonfunctioning gland with tumor involvement. Squamous cell carcinoma was diagnosed at parotidectomy. All four patients initially presented with facial swelling and pain. Because of the similarity of signs and symptoms, it may be difficult for the dental practitioner to differentiate from several potential oral disease entities including inflammatory/infectious, neuromuscular, and neoplastic conditions in this region of the head and neck. Parotid gland pathosis needs to be considered when a patient presents with posterior facial pain and swelling. GINGIVAL SYNDROME.
FIBROMATOSIS
IN EHLER-DANLOS
Moghadam BK, Daryabegi P. University of Missouri-Kansas City School of Dentistry and Tufts University School of Dentistry, Boston, Mass. Various oral abnormalities have been reported in association with the Ehler-Danlos syndrome (EDS). Among these, gingival fibromatosis without extensive alveolar hone loss is relatively rare. This is a report of such a case that provided the initial clue for the diagnosis of EDS in a 22-year-old female patient. The patient’s chief complaint was gingival bleeding during toothbrushing. Intraoral examination showed extensive gingival fibromatosis of posterior maxillary and mandibular teeth. Dental radiographs showed a generalized mild alveolar bone loss without extensive in-
volvement of the posterior teeth. No structural abnormalities ot enamel or dentin were noted. Further physical examination showed a mild hyperextensibility of the joints and the skin, with a tendency for bruising. Family history indicated that the patient’s older brother had similar joint and skin problems. These findings, together with the gingival fibromatosis, suggested the diagnosis of EDS. Dental treatment was initiated with deep scaling and curettage followed by gingivectomy. Histologic examination of the gingiva showed nonspecific chronic inflammatory reaction with masses of eosinophilic components. The presence of uncommon oral abnormalities linked to connective tissue disorders may provide clues for the diagnosis of the generalized disorders of EDS or other
related
EVALUATION HIV-INFECTED
disorders. OF HIV-1 PATIENT.
IN SALIVA
OF AN
Yeh C-K, Fox PC, Goto Y, Fox CH. UPC& LOM, National Institute of Dental Research, LIR, NIAID, National Institutes of Health, Bethesda, Md. The purpose of this report is to present a case demonstrating human immunodeficiency virus (HIV) in salivary tissue, whole saliva, and individual major salivary gland secretions. We studied a 22year-old woman with a diagnosis of systemic lupus erythematosus who was infected with HIV via a blood transfusion and who subsequently developed bilateral parotid gland enlargement. HIV viral RNA (vRNA) was localized using in situ hybridization to mononuclear cells recovered from whole saliva. DNA was extracted from salivary samples for detection of HIV by the polymerase chain reaction. Glandular saliva (parotid and submandibular/sublingual) failed to show vRNA. Both whole saliva and major gland saliva were positive for HIV proviral sequences. Parotid gland tissue, obtained at biopsy, revealed multiple cysts with infiltrating lymphoid tissue containing large amounts of HIV vRNA. No vRNA was demonstrated in secretory epitheiial cells. In general, HIV recovery from saliva has been infrequent and the quantity of HIV in saliva has been extremely low compared with other body fluids. Previous reports have demonstrated the presence of infectious HIV in whole saliva and in a single sample of parotid saliva. HIV p24 antigen has been found in lymphocytes isolated from whole saliva. HIV proviral genome was detected in whole saliva. Additionally, HIV has been demonstrated in infiltrating mononuclear cells within salivary glands of patients with HIVassociated salivary gland disease. The present findings plus the observed salivary inhibition of HIV infectivity may explain the lack of significant transmission of HIV by the salivary route.
THE PREVALENCE OF ORAL CARCINOMA IN SALTlMORE CITY’S ELDERLY SLACK POPULATION. Streckfus CF. University of Maryland, Baltimore An elderly black population residing in Baltimore City consisting of 10,819 patients was examined for oral pathology. A total of 247 patients required biopsies from the total population that was examined. Fourteen of the 247 biopsied patients were reported to have oral cancer, representing a prevalence rate of I .3 per 1000 people. Eight patients had squamous cell carcinoma, three adenosarcoma, and one basal cell plasmacytoma. Nine of the patients were edentulous. emphasizing the need for frequent oral examinations among the edentulous population. This report represents the only study ever performed on this population.
EVALUATION OF A SYNTHETIC ANALOG OF VITAMIN A AND BETA CAROTENE ON THE CLINICAL AND HISTOLOGIC APPEARANCE AND BIOLOGIC MARKERS IN HUMAN, PREMALIGNANT ORAL LESIONS. Hays G, Lippman S, Toth B. Weber Hong W. UTHSCH-Dental
R, Batsakis
J, Wargovich
M,
Branch and M. D. Anderson Cancer Center, Houston, Tex. The purpose of this study is to evaluate I3-cis-retinoic acid (13~ RA) and P-carotene (BC) in the treatment of premalignant oral lesions. Fifty-six patients with premalignant oral mucosal lesions were examined at baseline with respect to medical history. clinical examination, biopsy, and cytology. Biopsies were evaluated in reference to keratin, involucrin. and transglutaminase. Cytology was used to evaluate micronuclei. Three-month induction therapy was begun with each subject taking 13~ RA at a dosage of I .5 mg/kg/ day. After 3 months lesions were evaluated as at baseline. All subjects with lesions that responded or remained stable were randomly placed in either a low-dose l3c RA regimen (0.5 mg/kg/day) treatment group or a BC (30 mg/day) treatment group. After another 9 months, lesions were evaluated once again. Fifty-six subjects initiated treatment and 46 completed the 12-month trial. Sixty-two percent of the patients showed clinical improvement of the lesions after 3 months. The I3c RA low-dose treatment group showed significant improvement compared with the BC treatment group. Complete and partial remission rates at 12 months for l3c RA were 75% versus 27% for BC (p < 0.05). The relapse rates were more frequent in the BC group (54% vs 10%; p < 0.01). Micronuclei frequency patterns paralleled clinical data with more effective suppression in 13~ RA group. In conclusion, a regimen of lowdose l3c RA was significantly more effective than BC in maintenance therapy for premalignant oral mucosal lesions after l3c RA induction therapy.
HORMONAL RESPONSE OF LOW-DOSAGE MUCOSAL APPLICATION OF FLUOCINONIDE IN AN ANIMAL MODEL. Cade JE, Wright B, Lang C, Porter JR. Louisiana State University School of Dentistry, New Orleans The purpose of this study is to evaluate high, medium and low doses of fluocinonide
rat oral mucosa. Two-week time-release pellets were implanted into the buccal mucosa of 400 gm Holtzman rats in doses of 0.5, 0.05, and 0.005 mg. Control animals received placebo pellets in the same manner. Animals were sacrificed at baseline and at I, 4, and 9 days. Body, anterior pituitary, and adrenal weights were determined. Plasma corticosterone, ACTH, insulin, and glucose were measured. The results demonstrated several systemic effects in a comparison of the placebo-controlled group with the active treatment groups. ACTH was significantly inhibited at day I (high, middle doses) and day 4 (low dose). Corticosterone was significantly suppressed on days I, 4, and 9 (high dose); days I and 4 (middle dose); and days I, 4, and 9 (low dose). Insulin level was significantly increased on days I, 4, and 9 (high. middle doses, but only on day I of the low dose). Glucose levels were elevated at days I and 4 (high dose); day 1 (middle dose); and day 4 (low dose). Body weights and adrenal weights were reduced in several of the active drug treatment groups. In conclusion, these results indicate significant systemic physiologic effects secondary to mucosal implantation of fluocinonide in an animal model.
the systemic effects of (Lidex) implanted in
ORAL HAIRY LEUKOPLAKIA: ETIOPATHOGENETIC CONSIDERATIONS. Ficarra G. Adler-Storthz K, Romagnoli P, Pimpinelli N, Shillitoe EJ. University of Florence and USL IO/D. Florence, Italy, and the University of Texas Dental Branch, Houston The purpose of this study is to report the prevalence of EpsteinBarr virus (EBV) and human papillomavirus (HPV) in oral hairy leukoplakia (OHL) and normal buccal mucosa. Alterations of the epithelial microenvironment that may be relevant to the pathogenesis of OHL will be discussed. Initial studies suggested an association of OHL with both EBV and HPV. Evidence of association with HPV is demonstrated by staining with antiserum to common HPV antigens and sporadic reports of HPV-positive OHL as detected by in situ DNA hybridization. In addition, a decrease in the number of Langerhans cells in the epithelial microenvironment of OHL may facilitate the appearance of OHL. The prevalence of EBV DNA, HPV structural antigens, and HPV DNA in OHL were studied with DNA in situ hybridization, polymerase chain reaction PCR and avidin-biotin peroxidase immunostaining. respectively. Studies on nonlymphoid accessory cells (NLACs) were done using electron microscopy and immunohistochemistry. EBV DNA was detected in 47 of 58 samples of OHL and in I of IO biopsy specimens of normal buccal mucosa of HIV-seropositive patients. Positive staining with antibody to papillomavirus common structural antigens was demonstrated in 26 of 43 OHL specimens. HPV DNA was detected by PCR amplification and dot blot hybridization in I I of 20 OHL specimens and in 5 of IO normal buccal mucosa specimens. Lack of CD4+ cells and reduced number and incomplete differentiation of NLACs were found in OHL epithelium. Retrovirus-like particles were seen within NLACs. In conclusion, our results showed that EBV can be found in normal mucosa also. Thus the etiology of OHL remains undefined. EBV and HPV both may act as cofactors in the etiology of OHL. The impairment of local cellular immunity may contribute to the development of OHL.
311
3 I 2 Proceedings and abstracts
ORAL SURC ORAL MED ORAL PATHOI. September 1991
MISDIAGNOSIS OF FACIAL PAIN IN FOUR CASES SALIVARY PATHOSIS. Abramovitch K, Flaitz CM.
Diagnostic Sciences, UTHSCH-Dental Tex.
OF
Oral Branch, Houston,
Diagnosing pain in the lower third of the face is a frequent dilemma for dental clinicians. If the teeth and the periodontium are ruled out as sources of pain, the diagnostic process becomes more challenging. Because of the proximity of the parotid and submandibular gland to the posterior dentition and temporomandibular joint, salivary gland disease must be considered in the differential diagnosis. Four cases of facial swelling and pain that were originally diagnosed as either odontogenic or arthrogenic are presented. The ages of the patients (three female, one male) ranged from 27 to 67 years, with a mean of 43 years. Two of the caseswere initially diagnosed by the referring dentists as dental abscesses.In one case careful evaluation of Stensen’s duct revealed an inflamed orifice with suppuration. In the other a parotid sialogram demonstrated findings consistent with sialadenitis. The other two casesoriginally presented as regressive casesof temporomandibular disorders. One was a unilateral acute sialadenitis secondary to Sjiigren’s syndrome. In the other case a sialogram demonstrated a nonfunctioning gland with tumor involvement. Squamous cell carcinoma was diagnosed at parotidectomy. All four patients initially presented with facial swelling and pain. Because of the similarity of signs and symptoms, it may be difficult for the dental practitioner to differentiate from several potential oral disease entities including inflammatory/infectious, neuromuscular, and neoplastic conditions in this region of the head and neck. Parotid gland pathosis needs to be considered when a patient presents with posterior facial pain and swelling. GINGIVAL SYNDROME.
FIBROMATOSIS
IN EHLER-DANLOS
Moghadam BK, Daryabegi P. University of Missouri-Kansas City School of Dentistry and Tufts University School of Dentistry, Boston, Mass. Various oral abnormalities have been reported in association with the Ehler-Danlos syndrome (EDS). Among these, gingival fibromatosis without extensive alveolar hone loss is relatively rare. This is a report of such a case that provided the initial clue for the diagnosis of EDS in a 22-year-old female patient. The patient’s chief complaint was gingival bleeding during toothbrushing. Intraoral examination showed extensive gingival fibromatosis of posterior maxillary and mandibular teeth. Dental radiographs showed a generalized mild alveolar bone loss without extensive in-
volvement of the posterior teeth. No structural abnormalities ot enamel or dentin were noted. Further physical examination showed a mild hyperextensibility of the joints and the skin, with a tendency for bruising. Family history indicated that the patient’s older brother had similar joint and skin problems. These findings, together with the gingival fibromatosis, suggested the diagnosis of EDS. Dental treatment was initiated with deep scaling and curettage followed by gingivectomy. Histologic examination of the gingiva showed nonspecific chronic inflammatory reaction with masses of eosinophilic components. The presence of uncommon oral abnormalities linked to connective tissue disorders may provide clues for the diagnosis of the generalized disorders of EDS or other
related
EVALUATION HIV-INFECTED
disorders. OF HIV-1 PATIENT.
IN SALIVA
OF AN
Yeh C-K, Fox PC, Goto Y, Fox CH. UPC& LOM, National Institute of Dental Research, LIR, NIAID, National Institutes of Health, Bethesda, Md. The purpose of this report is to present a case demonstrating human immunodeficiency virus (HIV) in salivary tissue, whole saliva, and individual major salivary gland secretions. We studied a 22year-old woman with a diagnosis of systemic lupus erythematosus who was infected with HIV via a blood transfusion and who subsequently developed bilateral parotid gland enlargement. HIV viral RNA (vRNA) was localized using in situ hybridization to mononuclear cells recovered from whole saliva. DNA was extracted from salivary samples for detection of HIV by the polymerase chain reaction. Glandular saliva (parotid and submandibular/sublingual) failed to show vRNA. Both whole saliva and major gland saliva were positive for HIV proviral sequences. Parotid gland tissue, obtained at biopsy, revealed multiple cysts with infiltrating lymphoid tissue containing large amounts of HIV vRNA. No vRNA was demonstrated in secretory epitheiial cells. In general, HIV recovery from saliva has been infrequent and the quantity of HIV in saliva has been extremely low compared with other body fluids. Previous reports have demonstrated the presence of infectious HIV in whole saliva and in a single sample of parotid saliva. HIV p24 antigen has been found in lymphocytes isolated from whole saliva. HIV proviral genome was detected in whole saliva. Additionally, HIV has been demonstrated in infiltrating mononuclear cells within salivary glands of patients with HIVassociated salivary gland disease. The present findings plus the observed salivary inhibition of HIV infectivity may explain the lack of significant transmission of HIV by the salivary route.