Clinical assessment of oral dryness: development of a scoring system related to salivary flow and mucosal wetness.

OBJECTIVE: The aim of this study was to develop a clinical oral dryness score (CODS) for routine use in assessment of xerostomia patients and determine its relationship with salivary flow rates and mucosal wetness. STUDY DESIGN: CODS was determined from 10 features of oral dryness, each scoring as 1 point for a total score of 0-10. CODS, salivary flow rates, and mucosal wetness were measured in 100 patients and 50 healthy control subjects. The reproducibility of CODS was 0.89-0.96 (intraclass correlation coefficient). RESULTS: The mean ± SD CODS in patients was 6.0 ± 1.6 compared with 1.0 ± 0.9 for control subjects (P < .001), and the highest mean value was in the primary Sjögren syndrome group. There was a general inverse relationship in patients between mean CODS and salivary flow rate (P < .01) and mean CODS and mucosal wetness (P < .01). CONCLUSIONS: The CODS was found to be useful, easy to use, and reliable for routine assessment of the severity of dry mouth.

Investigating the relationship between hyposalivation and mucosal wetness.

BACKGROUND: Mucosal wetness (MW) reflects the layer of residual saliva that covers the oral mucosal surfaces. OBJECTIVES: The aim of this study was to determine MW at different oral mucosa sites and to investigate the relationship between MW, unstimulated whole salivary flow rates (UWS) and Clinical Oral Dryness Score (CODS). METHOD: A total of 100 dry mouth patients and 50 healthy subjects participated in the study. MW was sampled with filter paper strips at four sites inside the mouth; anterior hard palate (AHP), buccal mucosa (BUC), anterior tongue (AT), lower lip (LL) and measured with a micro-moisture meter. Reproducibility was assessed by repeated sampling and diurnal variation was examined. RESULTS: Mucosal wetness in healthy subjects differed according to site and means±SD were; AHP (11± 11.7µm), BUC (32±14.8µm), AT (65±17.2µm), and LL (25 ±13.5µm). Dry mouth patients with reduced UWS showed increased CODS. MW at all four sites was significantly reduced (P<0.05) in dry mouth patients compared with the healthy subjects. Reproducibility of MW measurement using the intra-class correlation coefficient showed agreement at different visits within subject. MW of the AT showed a positive correlation with UWS (P<0.05). CONCLUSION: Mucosal wetness is a reliable measure of oral dryness and had a positive correlation with UWS.

Altered plasticity of the parasympathetic innervation in the recovering rat submandibular gland following extensive atrophy.

Adult rat submandibular glands have a rich autonomic innervation, with parasympathetic and sympathetic nerves working in synergy rather than antagonistically. Ligation of the secretory duct rapidly causes atrophy and the loss of most acini, which are the main target cell for parasympathetic nerves. Following deligation, there is a recovery of gland structure and function, as assessed by autonomimetic stimulation. This study examines whether the parasympathetic nerves reattach to new target cells to form functional neuro-effector junctions. Under recovery anaesthesia, the submandibular duct of adult male rats was ligated via an intra-oral approach to avoid damaging the chorda-lingual nerve. Four weeks later, rats were either killed or anaesthetized and the ligation clip removed. Following a further 8 weeks, both submandibular ducts were cannulated under terminal anaesthesia. Salivary flows were then stimulated electrically (chorda-lingual nerve at 2, 5 and 10 Hz) and subsequently by methacholine (whole-body infusion at two doses). Glands were excised, weighed and divided for further in vitro studies or fixed for histological examination. Ligation of ducts caused 75% loss of gland weight, with the loss of most acinar cells. Of the remaining acini, only 50% were innervated despite unchanged choline acetyltransferase activity, suggesting few parasympathetic nerves had died. Following deligation, submandibular glands recovered half their weight and had normal morphology. Salivary flows from both glands (per unit of gland tissue) were similar when evoked by methacholine but greater from the deligated glands when evoked by nerve stimulation. This suggests that parasympathetic nerves had reattached to new target cells in the recovered glands at a greater ratio than normal, confirming reinnervation of the regenerating gland.

Acute salivary gland hypofunction in the duct ligation model in the absence of inflammation.

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. MATERIALS AND 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. CONCLUSION: 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.

Rat salivary gland ligation causes reversible secretory hypofunction.

AIM: To determine the influence of inflammation on salivary secretion. Secretion by salivary glands involves interactions between nerves, blood vessels and salivary cells. The present study investigated the effects of inflammation on rat submandibular gland function following acute ductal obstruction. METHODS: Under recovery anaesthesia a metal clip was placed on the main duct of the submandibular gland. After 24 h salivary secretion was evoked by nerve and methacholine stimulation. For recovery experiments the clip was removed after 24 h and the animal left to recover for 3 days when salivary function was again assessed. RESULTS: By 24 h of obstruction an inflammatory infiltrate had developed within the obstructed gland and stimulated salivary flows were just 20% of the normal secretion, whilst protein secretion and ion reabsorption were also severely impaired. If ductal obstruction was removed after 24 h the salivary function returned to normal after 3 days of recovery. In vitro analysis of cells from 24-h ligated glands revealed normal changes in intracellular calcium (the main secondary messenger involved in fluid secretion) in response to methacholine stimulation. Protein secretion from isolated cells indicated some changes in particular to methacholine-induced protein secretion although a significant protein secretion was still seen in response to isoprenaline - the main stimulus for protein secretion. CONCLUSION: This report demonstrates reversible salivary inhibition associated with an inflammatory infiltrate within the salivary gland.

Glandular function after intraoral removal of salivary calculi from the hilum of the submandibular gland.

We studied 43 patients (25 women and 18 men) who had salivary calculi removed from the hilum of the submandibular gland. Preoperatively they had clinical and radiographic examinations, and glandular function was measured scintigraphically in 38 patients. Postoperative follow-up was based on history, clinical examination, structured questionnaire, and scintigraphy. Stone(s) were removed successfully in 42 patients (97%). During the follow-up of a mean of 24 months (range 4-47), 37 patients were symptom-free and 2 patients had mild obstructive symptoms that did not require intervention. The other 4 patients had repeated infections that necessitated removal of the gland under general anaesthesia. Preoperative and postoperative scintigraphic assessments were made in 37 patients (88%). There was a significant increase in the functional fraction and the excretion rate in the gland after removal of the calculus. We conclude that glandular function improves to varying degrees in most patients after the removal of a salivary calculus.