Sialodacryoadenitis in the rat. A light and electron microscopic study.
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From personal observations, I review the genetic disorders of salivary gland development and function, including the lacrimo-auriculodentodigital (LADD) syndrome, autosomal dominant hypoplasia/agenesis of salivary and/or lacrimal glands, chronic recurrent sialadenitis, polycystic-dysgenetic disease of the parotids and salivary calculi.
Necrotizing sialometaplasia is a self-healing nonneoplastic disease of the hard and soft palate characterized by one or two deeply excavating ulcers. Histologically, there is necrosis of the mucous cells of the minor salivary gland tissue with partial replacement by squamous epithelium. The deeply situated squamous epithelium intermixed with mucous cells may lead to the erroneous diagnosis of squamous carcinoma or mucoepidermoid carcinoma. The confinement of cytologically benign squamous epithelium to the pre-existing lobular pattern of the salivary gland should permit an accurate histologic diagnosis by biopsy and avert further surgical intervention.
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A review of the literature and a report of a case of necrotizing sialometaplasia of the hard palate is presented. Because necrotizing sialometaplasia may be misdiagnosed as squamous cell carcinoma or mucoepidermoid carcinoma, it is important that the clinician and pathologist take the necessary precautions to prevent any further mutilative surgery for this benign disease entity.
Computerized assays on cultured cells ex vivo have been used to screen thousands of compounds for their effectiveness in correcting the basic physiological defect in cystic fibrosis (CF). While a number of these compounds appear promising, their effectiveness will almost certainly need to be demonstrated in animals before therapeutic tests in humans will be possible. We show herein that the function of salivary secretion in the mouse model for CF could be used as a simple, easy and rapid in vivo assay for drug effects. We demonstrate that salivary secretory capacity stimulated with a beta-adrenergic agonist closely reflects the genotype of origin. Specifically, the mean maximal secretory rate of saliva in normal wild type (+/+) mice was about 1.5 times higher than that of the mean rate in heterozygote (+/-) mice and more than 50 times greater than in CF (-/-) mice. Total saliva secreted per stimulated period obeyed a similar phenotype-genotype segregation. The data indicate that salivary secretory rates in CF mice could be used to assay potential drugs for their effectiveness in correcting the secretory defect in cystic fibrosis.
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Opportunistic DNA viruses, particularly members of the herpesvirus family, are frequently the aetiological agents of HIV-associated oral lesions. Oral lesions common to the early phase of the AIDS epidemic, including Kaposi's sarcoma (KS), oral aphthous ulceration, AIDS-associated oral lymphoma, and oral hairy leukoplakia (OHL), have been tested for the prevalence of Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV). While EBV DNA is detected by PCR in all of these lesions, abundant viral replication can only be detected in OHL. In OHL, a novel state of EBV infection has been discovered with concurrent expression of replicative and transforming proteins, with all of these proteins contributing to the development of the lesion. Activation of signalling pathways and up-regulation of the viral receptor, proliferative and antiapoptotic genes by these proteins induce several of the histological features common to OHL, such as acanthosis and hyperproliferation. In contrast to other permissive herpesvirus infections, expression of EBV transforming proteins within the permissively infected OHL tissue enables epithelial cell survival and may enhance viral replication. Detection of KSHV in these HIV-infected individuals has been localized only to their saliva. Replicative and latent KSHV gene products have been detected in association with the development of oral KS lesions. EBV, but not human cytomegalovirus (HCMV), has been detected by PCR in minor salivary gland biopsies of HIV-associated salivary gland disease. Human papillomaviruses (HPV) are associated with oral warts in HIV-positive individuals; a diagnosis that appears to be increasing in frequency in the era of highly active antiretroviral therapy. To date, there appears to be little increase in the incidence of HPV-associated oral cancer. The mechanisms of interaction between HIV and HPV are not fully understood. Expression of viral gene products is clearly important and necessary for the development of multiple AIDS-associated oral lesions.
This study reports the results of an interdisciplinary approach to the diagnosis of Sjögren's syndrome in 100 patients. Ocular and systemic diagnoses and oral features from the history and physical examination are correlated with measurements of stimulated parotid flow rate and labial salivary gland histopathology. A new diagnostic criterion is introduced whereby labial salivary gland focus scores are used to establish the presence of the oral component of Sjögren's syndrome in place of the subjective evaluation of xerostomia. The differential diagnosis of the oral clinical features of Sjögren's syndrome and the clinical management of the oral component of this disease are discussed.
Cheilitis glandularis (CG) is an uncommon disease that usually affects the lower lip of adults. It is characterized by enlargement and eversion of the lip in association with excretory duct dilatation. The presence of minor salivary gland hyperplasia is controversial. Three types of CG have been described in the literature; the classification is based on the common clinical and histopathologic findings (ie, simple, superficial, and deep). This report is of an unusual case of CG simplex for which the initial histopathologic diagnosis was papillary cystadenoma, a neoplastic process. The lesion was completely excised, and final microscopic review of a larger specimen revealed chronic sclerosing sialadenitis, dilated salivary secretory ducts with oncocytic change and periductal inflammation, and foci of adenomatous hyperplasia consisting of enlarged ducts exhibiting squamous epithelial metaplasia and hyperplasia with papillary architecture. The latter proliferative pattern is an unusual finding in what is otherwise clinically diagnosed as CG.
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Tumour-like lesions must be distinguished from true tumours of the salivary glands. In the new WHO classification of salivary gland tumours seven entities were considered: sialadenosis, oncocytosis (diffuse oncocytosis and focal adenomatous oncocytic hyperplasia), necrotizing sialometaplasia (salivary gland infarction), benign lymphoepithelial lesion (chronic myoepithelial sialadenitis), salivary duct cysts (mucoceles of the minor salivary glands of extravasation or retention type, cysts of the major salivary glands, ranula and dysgenetic polycystic disease of the parotid gland), chronic sclerosing sialadenitis of the submandibular gland (Küttner tumour), and cystic lymphoid hyperplasia in AIDS. The main topics of clinical data and pathohistology were described and documented by the results of the Salivary Gland Register in Hamburg (1965-1989).
The epidemiology of HIV-related oral disease in industrialized nations has evolved following the initial manifestations described in 1982. Studies from both the Americas and Europe report a decreased frequency of HIV-related oral manifestations of 10-50% following the introduction of HAART (highly active antiretroviral therapy). Evidence suggests that HAART plays an important role in controlling the occurrence of oral candidosis. The effect of HAART on reducing the incidence of oral lesions, other than oral candidosis, does not appear as significant, possibly as a result of low lesion prevalence in industrialized countries. In contrast to other oral manifestations of HIV, an increased prevalence of oral warts in patients on HAART has been reported from the USA and the UK. HIV-related salivary gland disease may show a trend of rising prevalence in the USA and Europe. The re-emergence of HIV-related oral disease may be indicative of failing therapy. A range of orofacial iatrogenic consequences of HAART has been reported, and it is often difficult to distinguish between true HIV-related oral disease manifestations and the adverse effects of HAART. A possible association between an increased risk of oral squamous cell carcinoma and HIV infection has been suggested by at least three epidemiological studies, with reference to the lip and tongue. These substantial and intensive research efforts directed toward enhancing knowledge regarding the orofacial consequences of HIV infection in the industrialized nations require dissemination in the wider health care environment.
It is well known that the incidence of malignant lymphomas (non-Hodgkin type) is increased in patients with Sjögren's syndrome. The occurrence of malignant diseases was retrospectively studied in 62 patients. In the course of the disease two patients developed a non-Hodgkin lymphoma, one patient developed a transitional-cell carcinoma located in the nasopharynx and three patients developed a squamous-cell carcinoma located in the salivary glands. The large quantity of epithelial carcinomas seems to be remarkable, especially compared with the number of non-Hodgkin lymphomas. It might be possible that early surgical treatment of persistent or progressive swelling of the salivary glands helps to prevent the occurrence of malignant lymphoma in patients with known myoepithelial sialadenitis.
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AIM: The vast majority of oral diseases are confined to oral tissues, but numerous underlying systemic conditions may present with signs and symptoms within the oral cavity. Since the epidemiology of diseases is variable between regions, the authors carried out Europe's first paediatric-based survey of oral and maxillofacial pathology specimens submitted for diagnosis. DESIGN: All entries for specimens from children between the ages of 0 and 16 years during the 30-year period from 1973 to 2002 were retrieved and compiled into 12 diagnostic categories. RESULTS: During the study period, 4406 (8.2%) specimens came from children between the ages of 0 and 16 years, with a male to female ratio of 1.01. The diagnostic category with the largest number of specimens was tooth pathology (22.1%), followed by salivary gland disease (19.1%) and mucosal pathology (12.1%). In all, there were 114 benign tumours of nonodontogenic origin, 43 odontogenic tumours and 31 malignant tumours. The most frequently diagnosed lesions were mucous extravasation cysts, which accounted for over 16% of cases. Periapical pathology in the form of a radicular cyst, residual cyst or chronic periapical granuloma formed almost 13% of all cases. CONCLUSIONS: This survey shows that, while nearly 10% of specimens submitted to the authors' laboratory are from children under 16 years of age, the majority of lesions are of a benign nature, requiring minimal intervention; less than 1% of cases comprise malignant lesions. Odontogenic tumours are relatively rare in this age group; however, certain lesions such as adenomatoid odontogenic tumour and ameloblastic fibroma occur predominantly in children and, therefore, remain an important diagnostic consideration.