New models of experimental parotitis and parotid gland distension in rats.

A significant reduction of the escape threshold to mechanical stimulation of the lateral facial skin was observed bilaterally at days 2 and 3 after unilateral complete Freund's adjuvant (CFA) administration into parotid gland. A slight reduction of mechanical escape threshold was also observed in rats with saline administration. The parotid gland inflammation was verified and quantified by measuring the tissue Evans' blue dye extravasation. The Evans' blue concentration in the parotid gland tissues was significantly greater in the CFA-injected rats than that of the saline-injected rats at 72 h after treatment. On day 10 after CFA administration into the parotid gland, the Evans' blue concentration was recovered to the control level. The administration of capsaicin into the parotid gland did not alter neuronal activities in the transition zone between the trigeminal spinal subnucleus interpolaris and caudalis (Vi/Vc). In contrast, capsaicin administration induced significant increases in the receptive field size and mechanical and cold responses of neurons located in superficial laminae of the C1/C2. The subgroup of C1/C2 neurons responded to mechanical distension of the parotid gland, whereas no Vi/Vc neurons responded to parotid distension.

Aprendiendo de los errores: fenómeno EDTA / Learning from errors: EDTA phenomenon

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Molecular alterations of parotid saliva in infantile chronic recurrent parotitis.

Infantile chronic recurrent parotitis (ICRP) is an insidious disease whose etiopathogenesis remains an enigma. Alterations in the physical appearance of parotid saliva from ICRP patients have been frequently reported. However, sialochemical studies in regard to ICRP are very rare. The aim of this study was to determine whether saliva of ICRP patients presents major physicochemical and biochemical alterations compared with saliva from paired healthy controls. Parotid, whole, and submandibular/sublingual saliva was collected at an asymptomatic stage from 33 ICRP patients (5-16 y old, both sexes) and from 33 sex- and age-matched healthy controls. Saliva was analyzed for protein concentration, mode of protein diffusion on cellulose membranes, unidimensional sodium dodecylsulfate (SDS)-polyacrylamide gel electrophoresis protein profiles and zymographic profiles of metalloproteinase 2 (MMP-2) and metalloproteinase 9 (MMP-9). Parotid saliva of ICRP patients showed an increased protein concentration, altered mode of protein diffusion, a higher frequency of polypeptide bands of 43, 37, 33, 29, 26, 16, and 10 kD, higher asymmetry in the polypeptide profiles of both contralateral parotid saliva, and an increase in the frequency of MMP-2 and MMP-9. Parotid saliva of patients with ICRP is molecularly altered with respect to normal saliva. Some of the molecular differences could be related to the etiopathogenesis of the disease.

Lipopolysaccharide induced-in vivo increases in beta-defensins of the rat parotid gland.

Antimicrobial beta-defensins are thought to protect epithelial surfaces. Their mobilization in response to inflammation was studied in the rat parotid gland using an ELISA assay. Bacterial lipopolysaccharide (LPS), injected into the parotid duct on one side, induced a marked local inflammatory response in the parotid gland as judged by several fold increases in myeloperoxidase activity and, in histological sections, infiltration of neutrophils. Three hours after the injection, beta-defensin 1 and 3 were increased (by 41% and 15%, respectively, P<0.01) as compared to the contralateral gland. Though still elevated 6h after the injection, the percentage figures for beta-defensin 1 were, at this time, somewhat lower (30%) compared to the situation at 3h, while those for defensin 3 were significantly higher 65% (P<0.01); neither at the early nor at the late time of observation were any changes in the level of beta-defensin 2 observed. The beta-defensins under study were not detected in submandibular and sublingual glands, neither were they detected in the inflamed submandibular gland, showing also here several fold increases in myeloperoxidase activity and, in addition, the presence of inflammatory cells, following ductal injection of LPS towards the gland.

Chronic parotitis: not another SPINKosis.

INTRODUCTION: Pancreatitis and parotitis share several etiological, pathohistological and functional similarities. It arose from recent pancreatitis research that some cases of chronic pancreatitis are associated with mutations of the serine protease inhibitor, Kazal type-1 (SPINK1). We tested the hypothesis that the pancreatitis-associated N34S mutation of SPINK1 is also a risk factor for chronic parotitis. METHODS: Reverse-transcriptase polymerase chain reaction was used to investigate SPINK1 transcription in the parotid gland. Forty-five blocks of formalin-fixed, paraffin wax-embedded tissues with chronic parotitis of unknown cause were analyzed for the SPINK1-N34S mutation. RESULTS: The SPINK1 gene is transcribed in the parotid gland. Two of the 45 patients (4.4%) with chronic parotitis carried the N34S mutation heterozygously. Of 82 healthy blood donors, 3 subjects (3.7%) were identified as carrying this mutation heterozygously (p = 0.83). CONCLUSION: The SPINK1-N34S mutation is not associated with chronic parotitis.

A new model of experimental parotitis in rats and its implication for trigeminal nociception.

A rat model of chronic parotitis was developed following a direct injection of Complete Freund's adjuvant (CFA) into the unilateral parotid gland via the parotid duct without skin incision. The nocifensive behavior, plasma extravasation in the parotid gland, and trigeminal Fos protein expression, a marker of neuronal activation, were analyzed in this model and compared to that of the saline-injected rats. A significant reduction of the escape threshold to mechanical stimulation of the lateral face on the ipsilateral side to the CFA injection was observed at 1-6 days after CFA injection as compared to that of the pre-CFA control ( P<0.01). The lateral face region contralateral to the CFA injection also showed mechanical hyperalgesia at 1-6 days after injection ( P<0.05). The plasma extravasation was significantly increased in the parotid gland ipsilateral to CFA injection as compared to that of the parotid gland with saline injection at 3 days after injection as shown by Evans' blue dye extravasation ( P<0.05). Bilateral expression of Fos protein-like immunoreactive cells was observed in the transition zone between the trigeminal spinal nucleus interpolaris (Vi) and caudalis (Vc) and paratrigeminal nucleus (Pa5). On the other hand, a significant unilateral expression of Fos protein-positive cells was observed on the ipsilateral side of the upper cervical (C2) dorsal horn ( P<0.05). This model of parotitis can be used to study trigeminal pain mechanisms associated with sialadenitis. A unique feature of this preparation is that the inflammation was limited to the parotid gland after intraductal injection of CFA, allowing analysis of peripheral input from a defined orofacial region. The model will be useful in developing new strategies to treat chronic orofacial pain.

Epstein-Barr virus status and the histopathological changes of parotid gland lymphoid infiltrates in HIV-positive children.

This study examined the EBV status and the morphology in parotid glands of a large cohort of HIV-positive pediatric patients. Nineteen children with vertically acquired HIV infection, ranging in age from three months to seven years and two months, were analyzed. Seventeen patients were assessed for serological evidence of EBV infection; nine showed evidence of past infection, one each re-activation and current infection and six did not have serological evidence of EBV. Immunohistochemistry and in situ hybridization for EBER 1 and 2 were performed on formalin-fixed, paraffin-embedded tissue. Fourteen of the 19 cases were classified as severe or established myoepithelial sialadenitis (MESA) and five were regarded as having mild MESA. The majority of intraepithelial lymphocytes were of B-cell lineage, while the pericystic infiltrate contained CD8-positive T-lymphocytes. p24 immunohistochemistry for HIV showed positive follicular dendritic cells, lymphoid cells and macrophages. Ten of 14 cases were positive for EBER 1 and 2. These included cases that were serologically negative for EBV. This study confirms that the morphology and immunophenotype of pediatric HIV-associated parotid lesions are similar to those seen in adults. Ten of 14 cases with evidence of EBV within the lymphoid infiltrate showed the same morphology and immunophenotype as cases in which EBV was not detected either by serology or by in situ hybridization. These findings indicate that EBV is not uniformly found in either the tissue or serum of these patients, and may not have a pathogenetic role in HIV-associated lymphoepithelial lesions in the pediatric age group.

Clinical and immunohistochemical analyses of parotid gland tumors.

Clinical, histological and immunohistochemical data on 71 parotid gland tumors were analyzed. Benign neoplasms accounted for 71.8% of the case material and malignant tumors 22.6%. Chronic parotitis occurred in 5.6% of the total case number. Pleomorphic adenomas and mucoepidermoid carcinomas were the most frequently occurring benign and malignant neoplasms. Pleomorphic adenomas stained positive for S-100 protein, tenascin, smooth muscle actin, synaptophysin and chromogranin A. This immunohistochemical, histological and clinical analysis was believed to be of potential assistance in the diagnosis, treatment and prognosis of parotid gland tumors.

[Sialochemistry in nonneoplastic diseases of parotid gland: immunoglobulins and electrolytes].

The concentration and total value of immunoglobulins (SIgA, IgG) and electrolytes (sodium, potassium, chlorine, calcium and phosphorus) in mixed saliva were examined in 28 patients with Sjögren's syndrome (SS), 25 with chronic obstructive parotitis (COP), 32 with sialadenosis and 32 normal controls. The results showed that in SS group, total saliva flow rate was decreased: concentration of SIgA, IgG, electrolytes was significantly elevated; but total value of SIgA, IgG, electrolytes was markedly decreased. Decreased total value of sodium, potassium, chlorine and calcium was revealed in COP group. Elevated concentration and total value of phosphorus was found in sialadenosis group. This study indicates that examination of total value of immunoglobins and electrolytes has greater value than that of concentration. The possible mechanism of changes observed is discussed.

Salivary factors in children with recurrent parotitis. Part 2: Protein, albumin, amylase, IgA, lactoferrin lysozyme and kallikrein concentrations.

The concentrations of total protein, albumin, amylase, IgA, lactoferrin, lysozyme and kallikrein in parotid saliva from 17 children with juvenile recurrent parotitis (JRP) in a non-active phase of disease and in healthy controls of the same number, sex and age were analysed after gustatory stimulation with 1%, 2% and 6% citric acid. There was a great individual variation in all analysed variables, especially in saliva from the diseased glands. Significantly raised levels of albumin, IgA, lactoferrin and kallikrein were found in the saliva from the JRP-children compared with the controls (p < 0.01-0.001), while total protein and alpha-amylase did not differ significantly. The sialo-chemical findings are discussed in the light of histological and bacteriological findings and support the hypothesis that the etiology of juvenile recurrent parotitis is a combination of congenital malformation of portions of the salivary ducts and a set-in infection.

Nodular fasciitis of the parotid gland. Report of a case with presentation in an unusual location and cytologic differential diagnosis.

The histomorphology of nodular fasciitis (NF), a benign proliferation of myofibroblasts, is well described in the surgical pathology literature. The cytomorphology, however, has been reported infrequently. Cytologic interpretation of this pseudosarcomatous lesion is subject to the same pitfalls so frequently reported for histologic material. NF arises most commonly in the extremities or trunk; occurrence in the parotid gland is relatively uncommon. We describe a case of NF arising in association with the parotid gland; review the clinical, cytologic, histologic and immunohistochemical features of NF; and offer a differential diagnosis, based on cytologic features, of other benign and malignant lesions likely to be encountered at this location.

Increased beta 2-microglobulin in both parotid and submandibular/sublingual saliva from patients with Sjögren's syndrome.

Samples of unstimulated saliva from patients with sialoadenopathy were collected by microcapillary tube (1 microliter), and their beta 2-microglobulin (B2-MG) content determined by a sandwich enzyme immunoassay. A higher than normal (control) concentration of the globulin was present in both parotid and submandibular/sublingual saliva from the patients with Sjögren's syndrome but not in the samples from the patients with sialoadenitis or diabetes mellitus. The increase in B2-MG in saliva from patients with Sjögren's syndrome may reflect that immunolopathological events are important in the degeneration of both glands in this disease. Therefore, the determination of B2-MG in saliva may be a simple, non-invasive technique for confirming the diagnosis of Sjögren's syndrome as an autoimmune disease.

[The participation of prostaglandin F2 in the peroxidation damages and antiperoxidation protection of the parotid gland in acute nonepidemic parotitis]. / Uchastie prostaglandina F2 v perekisnykh povrezhdeniiakh i antiperekisnoi zashchite okoloushnoi sliunnoi zhelezy pri ostrom neépidemicheskom parotite.

Effects of prostaglandin F2 on the major components of the antioxidative system (levels of malonic dialdehyde and lipid peroxides, activities and content of glutathione enzymes and nonenzymes (glutathione peroxidase, glutathione reductase, and NADPH (NADH), oxidized and reduced glutathione) were studied in experiments with 60 dogs in which acute nonepidemic parotitis was modeled. A varying capacity of the cells of the parotid gland to resist the detrimental effects of the disease and specific features of prostaglandin F2 effect on this capacity were revealed: injection of prostaglandin F2 stimulated both lipid peroxidation and the activity of the antioxidative system and led to cellular injury in the presence of a relatively high level of cellular metabolism, preserving cellular viability on condition of inhibited rate of metabolic reactions, this being the principal factor for the parotid gland, among other factors determining the cytoprotective effect.

[The auto-oxidative system of the acinar cells in acute postoperative parotitis]. / Autookislitel'naia sistema atsinarnykh kletok pri ostrom posleoperatsionnom parotite.

The major constituents of acinar cell auto-oxidative system in acute postoperative parotitis were determined in experiments on 32 dogs. Two types of cellular reactions were identified: free-radical processes with increased levels of lipid peroxidation products and insufficiency of enzymatic and nonenzymatic glutathion antioxidants and reaction of defense metabolism inhibition. A conclusion is made about the necessity of altering the current methods for prevention and therapy of postoperative parotitis.

[Relapsing parotiditis: its etiopathology and treatment]. / La parotiditis recidivante. Su etiopatogenia y tratamiento.

In this paper 85 cases of relapsing Parotiditis are presented, with the aim to ascertain the degree of accuracy provided by treatments with vitamin B complex, anti-inflammatory drugs or catchers of free radicals. Perusal of the bibliography and proposal of considering the malady divided in two stages. The first one would be characterized for metabolic alterations of the saccharoid cycle with scarce yielding of energy (ATP). Therefore failure of the Na/L bomb, which phenomenon is linked to an enzymatic protein deficiency and/or coenzyme of the B complex vitamins, being this condition provoked for a dietetic deficiencies, intestinal malabsorption due to alcoholic oedema, excessive expenditure of energy among drug-addicts, anemia, diabetes, etc. From this moment on appears the second stage--the inflammatory--with the whole metabolic and biochemical courtship of structural and functional irreversible damages.

Two-dimensional electrophoresis of human salivary proteins from patients with sialoadenopathy.

Unstimulated saliva was fractionated by micro two-dimensional gel electrophoresis, and the proteins visualized by silver staining and immunostaining. The subjects with Sjögren's syndrome exhibited both quantitative and qualitative alterations in the protein composition of the saliva not only from the parotid gland but also from the submandibular/sublingual glands.

Recurrent parotitis in children. A report of 102 cases.

This article presents 102 cases of recurrent parotitis in children with studies of clinical findings, sialographic manifestations, dynamic functions of the parotid gland examined with radionuclide, laboratory findings and follow-up studies of 28 cases with sialography. The following conclusions are reached: 1. Retrograde infection induced by the mumps virus and upper respiratory infection seem to play a major role in the etiology of recurrent parotitis. Familial abnormalities are potential factors. Incomplete immune functions of the children are factors related to the pathogenesis, and following growth and development of the immune system, this disease will undergo remission; 2. Sequential scintigraphy shows normal uptake and retarded excretion function of the parotid; 3. Long-term follow-up studies demonstrate that the patients are free from symptoms for many years, but the punctate dilatation in sialography may diminish, disappear, or be unchanged; and 4. If the disease is not cured in childhood, it may continue into adulthood and healing will take place eventually. Relationship with Sjogren's syndrome has not been revealed.

Chronic sialadenitis. An immunocytochemical study in humans.

The cellular changes in salivary gland parenchyma with chronic inflammation were studied immunocytochemically with a panel of antibodies. Myoepithelial cells were labelled with antimyosin, duct cells with a polyclonal anti-callus prekeratin, a monoclonal anti-keratin CAM 5.2 and a monoclonal anti-keratin 7 (RPN 1162), and a subpopulation of basal duct cells with a monoclonal anti-keratin 16a. The wide range of changes observed were similar to those described following experimental duct ligation. One of the most striking features was the survival of myoepithelial cells surrounding persisting acini and ductal structures. Most of these ductal structures appeared to be either surviving intercalated ducts or were altered acinar cells. There was no evidence of myoepithelial or ductal hyperplasia. The 16a positive basally located duct cells which are conspicuous in normal glands, pleomorphic adenomas and in the epithelial islands in lymphoepithelial lesions (Palmer et al. 1985; 1986) were virtually absent, except in one specimen with mild inflammatory changes. If this cell type represents a reserve cell, then loss of it may preclude recovery of the remaining parenchyma following resolution of inflammation.

Crystalloids with calcareous deposition in the parotid gland: one of the possible causes of development of salivary calculi.

Aggregated crystalloids and calculi, up to 600 to 700 micron in diameter, found in the parotid gland tissue taken from a patient with chronic recurrent parotitis were examined histopathologically and microanalytically. In part of the periphery of calculi which had lamellated structure, layers of crystalloids in continuation with calculi were observed; and diffuse deposition of von Kossa-positive fine granules was seen in the innermost area of the crystalloid-layers. By electron probe x-ray microanalysis, phosphorus, sulphur and calcium were principally detected within the innermost area of the crystalloid-layers. The result of the present study lends support to the possibility that crystalloids have some relation to the development of salivary calculi in the human parotid gland.

Quantitation of human salivary acidic proline-rich proteins in oral diseases.

Acidic proline-rich proteins (APRP) were quantitated immunochemically in salivary secretions from groups of: caries-resistant (CR) and caries-susceptible (CS) subjects; heavy- and light-calculus-formers; and patients with Sjögren's Syndrome, drug-induced xerostomia, and recurrent parotitis. In all groups except the parotitis patients, there were comparable levels of APRP, about 40-50 mg%, with similar values in parotid and submandibular saliva. In chronic recurrent parotitis, the values were somewhat higher (about 60 mg%). There were no differences in the proportion of APRP-A to C in a subset of CR and CS. Taken as a whole, the data support the view that the secretion of APRP is stable and that caries status and propensity to calculus formation are not associated with abnormal levels of these phosphoproteins.