fibrin and Dilatation--Pathologic

Here we report a case of Kussmaul's disease, or sialodochitis fibrinosa. This rare disease is characterized by recurrent swelling of the salivary glands, which then discharge clots of fibrin into the oral cavity. An 80-year-old man with a history of allergic rhinitis visited our department with the chief complaint of pain in the bilateral parotid gland area on eating. An initial examination revealed mild swelling and tenderness in this region, and indurations could be felt around the bilateral parotid papillae. Pressure on the parotid glands induced discharge of gelatinous plugs from the parotid papillae. No pus was discharged, and there were no palpable hard objects. Panoramic X-ray showed no obvious focus of dental infection, and there was no calcification in the parotid gland region. Magnetic resonance imaging revealed segmental dilatation of the main ducts of both parotid ducts, with no signs of displacement due to sialoliths or tumors, or of abnormal saliva leakage. Two courses of antibiotic therapy resulted in no improvement. During treatment, gelatinous plugs (fibrin clots) obstructing the left parotid duct were dislodged by massage, which prevented further blockage by encouraging salivary outflow. The obstruction persisted in the right parotid duct, however. Therefore, the distal portion of the right parotid duct was partially resected and the opening into the mouth enlarged, which, in combination with massage, prevented further obstruction. The pain and swelling of the parotid gland and discharge of gelatinous plugs improved, with no further recurrence at 12 months postoperatively. This case is presented along with a review of the relevant literature.

Topics: Aged, 80 and over; Diagnosis, Differential; Dilatation, Pathologic; Fibrin; Humans; Magnetic Resonance Imaging; Male; Massage; Parotid Diseases; Parotid Gland; Radiography, Panoramic; Salivary Ducts; Tomography, X-Ray Computed

To evaluate the influence of impaired masseter function during growth on the development of temporomandibular synovitis.. Sixteen 3-week-old male Wistar rats were classified into four groups. The first group served as control; and in the second group, jaw opening was forced for 3 hours when the rats were 9 weeks old. In the third and fourth groups, the masseter muscles were bilaterally resected at 3 weeks of age, and the rats in the fourth group were additionally forced to open their jaw at 9 weeks of age. All rats were sacrificed at 9 weeks. Temporomandibular joint (TMJ) tissue samples were processed for histology, and evaluated for cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions by immunohistochemistry to examine the inflammatory changes in the synovial membrane.. The control group showed noninflammatory changes. In the jaw-opening group, vascular dilation and weak COX-2 immunoreactivity were induced by jaw opening in the synovium. In the masseter-resection group, the masseter-resected rats exhibited moderate synovial changes while in the resection with opening group, the masseter-resected rats revealed more significant inflammatory changes including synovial hyperplasia, dilated vasculature, fibrin deposits, and intense immunoreactivity for COX-2 and iNOS, all caused by jaw opening.. These results suggest that masseter activity in the growth period is an important factor in the induction of temporomandibular synovitis.

Topics: Animals; Cyclooxygenase 2; Dilatation, Pathologic; Fibrin; Hyperplasia; Immunohistochemistry; Male; Masseter Muscle; Muscle Weakness; Nitric Oxide Synthase Type II; Range of Motion, Articular; Rats; Rats, Wistar; Stress, Mechanical; Synovial Membrane; Synovitis; Temporomandibular Joint; Temporomandibular Joint Disorders; Vascular Diseases

Cardiovascular implants of fresh autologous pericardium produced mixed results including fibrosis with retraction or thinning and dilatation. The reasons for these differences are unknown but may involve activation of cells intrinsic to the tissue implant. To better understand the behavior of autologous pericardial implants, we studied the outcomes of vital pericardium (fresh) versus ethanol-killed pericardium.. Fresh and ethanol-killed autologous pericardium was transplanted as a patch, a conduit, or a rectangular flap bisecting the lumen in the descending aorta of sheep. The implants, recovered at 1, 5, 10, 15, and 30 days, were evaluated macroscopically and microscopically and by immunohistologic studies.. Fresh implants showed good preservation with fibrin deposition on day 15. Microscopically, cells positive for alpha-actin and von Willebrand-related antigen appeared in the fibrin by day 10. By day 30 the flap was fibrotic and retracted whereas the patch and conduit retained their original appearance on the luminal aspect. An endothelium-like layer expressing von Willebrand-related antigen was present in the patch and conduit but absent in the flap. In contrast, the ethanol-killed implants were free of fibrin by day 10. By day 30, there were no signs of fibrosis or retraction, and a surface layer of cells expressing von Willebrand-related antigen, characteristic of endothelial cells, was present on all implants. All ethanol-killed implants were repopulated by host cells.. The transluminal flap is an interesting model for studying the behavior of intraluminal autologous pericardial cardiovascular implants. Killing of the pericardial implants alleviated the fibrosis and tissue retraction observed with fresh flap implants.

Topics: Actins; Animals; Aorta, Thoracic; Blood Vessel Prosthesis Implantation; Collagen; Dilatation, Pathologic; Endothelium, Vascular; Ethanol; Fibrin; Fibrosis; Fixatives; Follow-Up Studies; Immunohistochemistry; Neutrophils; Pericardium; Sheep; Surgical Flaps; Tissue Preservation; Transplantation, Autologous; von Willebrand Factor

Indirect immunoperoxidase staining for fibrinogen/fibrin and fibronectin was performed on normal and healing arterial tissue of muscular and smaller elastic arteries. Fibronectin was observed in the wall of the normal arteries, whereas fibrinogen/fibrin could not be demonstrated. Fibronectin was observed in the intima as well as the media deposited in a similar fashion in the femoral and carotid artery during repair. Apart from the early occurrence of fibrin/fibrinogen in the media of both arteries the distribution of fibrinogen/fibrin and degradation products differed. In the femoral artery a progressively weakening positive reaction for fibrinogen/fibrin and degradation products towards the lumen was observed in the intima and the media 7 and 14 days after the lesion. By 28 days the reaction in the media was negative. No thrombus formation was observed. In contrast, all the specimens examined from the common carotid arteries were obliterated by luminal thrombi 28 days after the lesion. The thrombus as well as the damaged intimal thickening and the compressed media were loaded with fibrinogen/fibrin and degradation products. The deposition of fibronectin, fibrinogen, and degradation products in the carotid artery was similar to that previously reported in experimental aortic arteriosclerosis in rabbits as well as in giant cell arteritis.

Topics: Animals; Carotid Arteries; Dilatation, Pathologic; Femoral Artery; Fibrin; Fibrinogen; Fibronectins; Immunohistochemistry; Rabbits