Search PubMed⌕ Search

Biomedical subjects

K Donath

Publications and source records attributed to K Donath.

At least 181 records · Page 10Linked to original sources
PubMed1976

[Morphology of salivary gland diseases].

The human salivary glands represent a functional system with manifold responsibilities and interactions to the organism. The major and minor salivary glands show a common construction schedule consisting of an acinar functional system for the production of an enzyme- and mucin-containing primary saliva and a ductal functional system with manifold secretory, resorptive and regulatory responsibilities for the transport and the definitive composition of the saliva. The cyclic AMP and calcium iones localized in the glandular acini have an exceptional importance for the course of the secretory process. The neurohormonal control of the salivary secretion results by adrenergic and cholinergic transmitter substances. Moreover the secretory process shows a daily cycle combined with morphological alterations of the glandular cells (so called circadian structures). The fluid secretion of the salivary duct system (the output of sodium-, potassium- and chlorine-iones) represents an active energy-consumed transport process which will be regulated by several factors (autonomic nervous system, quantity of perfusion, hydrostatic pressure in the blood capillaries, transepithelial active transport by ATP-consumed pump systems). The striated ducts are the functional most important sector of the duct system for a rapid fluid- and electrolyte excretion. The terminal axons of the postganglionic sympathic and parasympathic neurits are characterized by spindle-shaped enlargements (varicosities) which contain neurosecretory granules. In the region of the acinar and intercalated duct cells a direct synaptic contact exists for the stimulation transmission, in the course of which the terminal axon contacts immediately with the effector cell by penetration of the basement membrane. The salivary glands form a part of the stabil tissues with reversible postmitotic cells in regard of the tissue regeneration. Under pathological conditions (inflammations, impediment of secretion fluid, radiation effects etc.) metaplasias and proliferations of the duct system arise with development of indifferent duct formations analogous to the type of an embryonal salivary gland. The terminal zone between intercalated and striated ducts represents an indifferent zone with large regeneratory potency. A special behaviour shows the myoepithelial cells which are developed as well to the outside of primitive embryonic duct buds as differentiated intercalated and striated ducts. Morphologically three types of diseases can be classified in the salivary glands: sialadenosis, sialadenitis and tumours.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1976

Classification of the pathohistology of diseases of the salivary glands - review of 2,600 cases in the Salivary Gland Register.

Three major disease groups emerge from a classification of the pathohistology of 2,600 salivary gland preparations in the salivary gland register (from 1965 to 1974): salivary gland tumors (41%), salivary gland inflammations (26%), and sialadenosis (6%). Mucoceles (2%) and salivary gland cysts (1.5%) are seen less often. It is diagnostically important that lymph node changes in the area of the salivary glands (lymphadenitis, lymphomas, etc.) are worked up under suspicion of a primary salivary gland disease. Sialadenosis involves a primary, vegetative neuropathy, which is accompanied by enlargement of acinar cells. Under the heading of chronic sialdenitis, we fine 50% socalled Küttner tumors of the submandibular gland, 21% chronic relapsing parotitis, 14% chronic inflammations of the minor salivary glands and the sublingual gland, and 12% immune sialadenitis (myoepithelial sialadenitis in Sjögren's syndrome and epitheloid cell sialadenitis in Heerfordts syndrome). A more than average number of immune sialadenitis cases develop into malignant lymphomas (4 cases in the salivary gland register). The 1,067 tumor cases containing of 929 epithelial tumors (87%), 89 mesenchymal tumors (hemangiomas, lymphangiomas, lipomas, neurofibromas, sarcomas) and 49 metastases or periglandular tumors. Epithelial tumors were grouped on the basis of the World Health Organization (WHO) classification. Benign tumors (71.5%) consisted of pleomorphic adenomas (51.5%) and monomorphic adenomas (50%). After the pleomorphic adenomas, cystadenolymphomas (over 10%) represented the most frequent benign salivary gland tumor. On the basis of epithelial and stromal differentiation, pleomorphic adenomas were subdividied into four subtypes (stroma-rich and stroma-poor adenomas). The malignant tumors consisted of acinar cell tumors (2.5%), mucoepidermoid tumors (6%), and carcinomas at various levels of differentiation (adenoid-cystic carcinomas, 6.5%; adenocarcinomas, 2%; squamous cell carcinomas, 2%; carcinomas in pleomorphic adenomas, 4%; miscellaneous carcinomas - salivary duct carcinomas, clear-cell carcinomas, undifferentiated carcinomas, 5.5%). Differences in age and sex distribution, localization, malignity metastases, recidivism, et

Adenoma↗
PubMed1976

[A pathological classification of pleomorphic adenoma of the salivary glands (author's transl)].

Pleomorphic adenomas of the salivary glands show, despite their pleomorphism, certain histological characteristics. These are based onthe differentiation of the epithelial cell and the amount and nature of the stroma. A systematic histological analysis of 310 pleomorphic adenomas of the parotid gland resulted in the following findings and classification. 1. The most frequent epithelial cell forms were salivary duct and myoepithelial cells (75-90%) seen as epidermoid cell groups (75%). Rarer forms of differentiation were striated duct cells (5%), keratinised squamous epithelium (2,5%), oncocytes (1%), basal cells (1%), and sebaceous gland cells or goblet cells (less than 1%). 2. A myxomatous stroma represented the prototype of stromal differentiation (80%). A chondroid stroma was found in 10% of cases examined and a mixed mucochondroid stroma in 3%. Further differentiation included hyaline stroma (25%) and fibrous stroma (15%) especially in the older tumour or after irradiation. Rarely was a fascicular (0,5%) or osseous (1%) stromal change found. 3. Four subgroups of pleomorphic adenoma can be classified from consideration of the epithelial and stromal changes. Subgroup 1 (30,5%) is the classical pleomorphic adenoma with a stroma content of 30-50%; subgroup 2 (55%) has a stroma content of 80%; subgroup 3 (9%) has a poor stroma content of 20-30% or less and an epitaelial differentiation similar to subgroup 1; and subgroup 4 has also a poor stroma content (6%) with a relatively monomorphic epithelial structure. 4. Recurrences (13,5%) were seen more in stroma-rich pleomorphic adenomas than in stroma-poor tumours. 5. On the basis of cytological differentiation, pleomorphic adenomas develop from indifferent tissue adjacent to salivary intercalated or striated ducts.

Adenoma↗
PubMed1976

[Sialadenosis of the parotid gland. Ultrastructural, clinical and experimental findings in disturbances of secretion (author's transl)].

Among the secretory disturbances ("Dyschylien") of salivary glands the sialadenosis of the parotid gland is a clinic and a morphologic definited entity. The typical clinical symptom is a bilateral, often recurrent, and painless swelling of the parotid gland. The characteristic pathological findings consist in an acinar cell hypertrophy without any inflammatory signs. According to this definition, sialadenosis has to be separated from those diseases of salivary glands, which are primarily altered by inflammation of the salivary tissue with secondary secretory disturbances. From flinical point of view it is possible to distinguish the following kinds of sialadenosis according to the syntropy with various diseases: Endocrine sialadenosis (in diabetes mellitus, dysfunction of gonads, pituitary gland, thyroid gland etc.); dystrophic-metabolic sialadenosis (malnutrition, avitaminosis, alcohilsm, chronic liver diseases etc.), and neurogenic sialadenosis (dysfunction of the vegetative nervous system, drug damages e.g. antihypertensive agents). The question arises, whether all forms of sialadenosis have a common etiology and a coincidental pathogenic factor. The following studies were carried out with the aim to find further details concerning the etiology and pathogenesis of sialadenosis. The study is based on the following material: a) 126 Biopsies of parotid glands from patients with sialadenosis (Register of salivary gland diseases at the Institute of Pathology, University of Hamburg, supported by Deutsche Forschungsgemeinschaft). This material was collected from 1965 to 1973. b) 80 Biopsies of parotid glands from patients with other diseases (parotitis [4]; acinic cell carcinoma [4]; other parotid and oral tumors [72]; for comparison. c) Experimental studies on the parotid salivary glands of Wistar-rats. The biopsies of the parotid glands were studied histologically, morphometrically, and ultrastructurally. The investigations centered on the ultrastruct of sialadenosis. Before interpreting the ultrastructural findings in view of etiology and pathogenesis of sialadenosis, it was primarily necessary to study the normal ultrastructure of the human parotid gland including the vegetative nervous system. Furthermore it was necessary to elucidate details of a functional morphology of the secretory cycle and to integrade the findings into a concept of general pathology of secretory disturbances. The following results were achieved by our investigations: 1. Normal ultrastructure of human parotid gland: The architecture of the acinar cells is identical with these of other animal species (cytoplasm with a basal standing nucleus, rough endoplasmatic reticulum, Golgi-apparatus, secretory granules etc.). Further identical elements are intercalated and striated ducts, myoepithelial cells, and the vegetative nervous system (postganglionic sympathetic and parasympathetic neurites, however no ganglionic cells in the parotid gland)...

Action Potentials↗
PubMed1976

[Malignant lymphomas and immunosialadenitis (author's transl].

Immune sialadenitis with or without clinical symptoms of Sjögren's syndrome represents an inflammation of the salivary duct system with considerable proliferation of the immunoactive lymphoproliferative system. By prolonged stimulation the immune system can turn into malignant lymphoma, mainly of immunocytoma or immunoblastic sarcoma type. In four out of 77 cases from the salivary gland register of the Institute of Pathology, University of Hamburg, showing myoepithelial sialadenitis, malignant lymphomas associated with chronic myoepithelial lymphadenitis were observed. According to the new "Kiel-classification" (Lennert) of malignant lymphomas two of the cases represented a diffuse germinoblastoma (lymphoblastoma Brill-Symmers), one a immunocytic lymphoma and one a immunoblastic sarcoma (reticulum cell sarcoma). From literature 16 further observations of malignant lymphoma occuring in the area of the major salivary glands in association with immune sialadenitis (Sjögren's syndrome) were collected, likewise 25 other cases with lymphomas outside of the major salivary glands and Sjögren's syndrome. It is suggested that the above average frequency of malignant lymphomas in immune sialadenitis may result from a secondary malignant transformation of immune cells due to prolonged stimulation. Local rapidly appearing tumorous alterations of the salivary glands in chronic immune sialadenitis are, therefore, always be suspicious of the development of a malignant lymphoma and demand adequate therapy.

Adult↗
PubMed1975

Ultrastructural studies of the parotid glands in sialadenosis.

30 parotid biopsies of patients with sialadenosis--a symmetrical, painless, non-inflammatory, recurrent parotid swelling--were studied by electron microscopy. The patients suffered from different diseases, such as diabetes mellitus, liver diseases, hypertension and other affections. Parotid biopsies from 25 patients with slight parotitis or with oral cancer were used as controls. Morphometric studies reveal that the parotid swelling is caused by an enlargement of acinar cells. In controls the average diameters of the acinar cells are 30 to 40 mu. In sialadenosis the diameters are enlarged to 50 to 70 mu, in some cases to a maximum of 100 mu. Histologically the cytoplasm of the enlarged acinar cells shows either a granular pattern due to a numerical increase in secretory granules or a vacuolar transformation. Ultrastructurally the vacuolar transformed acinar cells also contain an increased number of granules with less electron density than the surrounding cytoplasm. Three types of sialadenosis can be distinguished with regard to the electron density of the acinar granules: a) a dark granular type, b) a pale granular type and c) a mixed granular type. The mixed granular type probably develops from the dark granular form. Alterations leading to the destruction of the myoepithelial cells were observed in all three types of sialadenosis with minimal changes in the dark granular type. Degenerative alterations of the autonomic nervous system are evident in all three groups with most pronounced changes in the pale granular type of sialadenosis. The ultrastructural alterations are interpreted as a disturbance of secretion, probably primarily caused by the degeneration of the autonomic nervous system. The alteration of the autonomic nervous system is suggested to be the common pathogenetic principle in all types of human sialadenosis occurring with different basic diseases. The enlargement of the acinar cells is the result of an intracellular disturbance in the secretory process due to the preceding defect of the autonomous nerval structures.

Adolescent↗