title: Acute salivary gland hypofunction in the duct ligation model in the absence of inflammation.
abstract: OBJECTIVE
  The commonly associated aetiology of salivary gland inflammation and salivary hypofunction has led to the widely held belief that inflammation causes salivary gland hypofunction. Indeed, our own recent study seemed to support this contention. Here, we tested the hypothesis that, in an acute duct ligation model, eliminating inflammation the submandibular gland would recover normal function.
  
  
  METHODS
  Ligation of the rat submandibular gland excretory duct for 24 h was used to induce inflammation and salivary gland hypofunction. A group of duct ligated rats was compared with a second group given dexamethasone, on the day of duct ligation. Twenty-four hours later salivary gland function was assessed and salivary glands were collected.
  
  
  RESULTS
  Histology and myeloperoxidase activity assay revealed a profound decrease in inflammatory cell infiltration of ligated glands from rats given dexamethasone, compared with ligated glands in the absence of dexamethasone. Salivary flow rate evoked by methacholine was decreased (P < 0.01) by approximately 56% (ligated vs control, 79 +/- 9 microl min(-1) g(-1)vs 177 +/- 11 microl min(-1) g(-1)) and salivary flow from ligated dexamethasone-treated and ligated glands was similar.
  
  
  CONCLUSIONS
  Despite eliminating the inflammatory reaction in the ligated gland, salivary hypofunction was not reversed, suggesting that other mechanisms must be at work in the ligation-induced salivary hypofunction.
authors.affiliation: Salivary Research Unit, King's College London Dental Institute at Guy's, King's College and St Thomas' Hospitals, London, UK. patricia.correia@kcl.ac.uk
authors.forename: P N
authors.initials: PN
authors.lastname: Correia
authors.forename: G H
authors.initials: GH
authors.lastname: Carpenter
authors.forename: S M
authors.initials: SM
authors.lastname: Osailan
authors.forename: K L
authors.initials: KL
authors.lastname: Paterson
authors.forename: G B
authors.initials: GB
authors.lastname: Proctor
mesh_terms: D000208:Acute Disease; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D003907:Dexamethasone / Q000627:therapeutic use; D004195:Disease Models, Animal; D005938:Glucocorticoids / Q000627:therapeutic use; D008026:Ligation; D008264:Macrophages / Q000473:pathology; D016210:Methacholine Chloride / Q000494:pharmacology; D009504:Neutrophils / Q000473:pathology; D010277:Parasympathomimetics / Q000494:pharmacology; D009195:Peroxidase / Q000032:analysis; D011199:Potentiometry; D051381:Rats; D017208:Rats, Wistar; D012463:Saliva / Q000187:drug effects / Q000378:metabolism; D018987:Salivary Ducts / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D012471:Salivary Proteins and Peptides / Q000032:analysis; D012636:Secretory Rate / Q000187:drug effects / Q000502:physiology; D012793:Sialadenitis / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D013363:Submandibular Gland / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D013364:Submandibular Gland Diseases / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors; D014987:Xerostomia / Q000473:pathology / Q000503:physiopathology*
chemical_list: D000893:Anti-Inflammatory Agents; D005938:Glucocorticoids; D010277:Parasympathomimetics; D012471:Salivary Proteins and Peptides; D016210:Methacholine Chloride; D003907:Dexamethasone; D009195:Peroxidase