The effects of ductal obstruction on the acinar cells of the parotid of cat

Harrison, J. D.; Fouad, H M A; Garrett, J. R.

doi:10.1016/s0003-9969(00)00076-5

Cited by 24 publications

(11 citation statements)

References 22 publications

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“…By avoiding any possible damage of the chorda-lingual the complications of a denervation-induced atrophy are avoided (Harrison et al 2001). In addition, the 24-h time point precedes any obvious acinar protein degranulation that is often regarded as the starting point of atrophy (Ohlin & Perec 1967, Scott et al 1999, Harrison et al 2000, 2001, Osailan et al 2006). The ligated glands were oedematous which was reduced following methacholine stimulation suggesting it was partially caused by the build up of saliva within the gland in addition to inflammation-related oedema.…”

Section: Discussionmentioning

confidence: 99%

Rat salivary gland ligation causes reversible secretory hypofunction

et al. 2007

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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.

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Section: Discussionmentioning

confidence: 99%

Rat salivary gland ligation causes reversible secretory hypofunction

et al. 2007

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“…In patients with therapy-resistant ductal stenosis, repeat injection of Botulinum toxin into the gland parenchyma may arrest symptoms 79 - 81 . Duct ligation has reported to be unsuccessful in not more than 50% of cases and is therefore not a preferred procedure 12 18 37 65 70 71 82 - 84 .…”

Section: Treatmentmentioning

confidence: 99%

Salivary duct stenosis: diagnosis and treatment

Koch

Iro

2017

Acta Otorhinolaryngol Ital

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La gestione delle stenosi delle ghiandole salivari maggiori ha subito un cambiamento significativo nel corso degli ultimi 15-20 anni. Lelemento fondamentale che sta alla base di una scelta terapeutica minimamente invasiva è rappresentato da unaccurata diagnosi. La scialografia convenzionale e la scialo-RM possono essere utili strumenti per la diagnosi delle stenosi salivare, senza dimenticare il ruolo basilare e centrale dellecografia qualora si sospetti che un processo stenotico a carico dei dotti salivari sia la causa dellostruzione. Tuttavia, ad oggi, la scialoendoscopia rappresenta la scelta diagnostica migliore, permettendo una corretta pianificazione terapeutica attraverso una quanto più precisa caratterizzazione della stenosi. Sia a livello sottomandibolare che parotideo è possibile distinguere le stenosi infiammatorie da quelle secondarie a processi fibrotici e, inoltre, a carico dei dotti salivari parotidei è stata descritta una stenosi associata a varie anomalie del sistema duttale. Nella maggior parte dei casi la sola terapia conservativa non è sufficiente per la risoluzione della sintomatologia ostruttiva, tuttavia lo sviluppo di trattamenti minimamente invasivi, prima fra tutte la scialoendoscopia, ha permesso di ottenere un tasso di conservazione della funzione ghiandolare di oltre il 90% dei casi. Se a livello sottomandibolare la principale misura terapeutica nella gestione delle stenosi del dotto ghiandolare rimane lincisione duttale (eccezion fatta per il crescente ruolo della scialoendoscopia nelle stenosi centrali), viceversa a livello del dotto parotideo la stenosi viene preminentemente gestita mediante la scialoendoscopia. Va comunque sottolineato che nel 10-15% dei casi il successo terapeutico viene ottenuto attraverso un trattamento di tipo combinato. La seguente review si propone di fornire una panoramica circa lepidemiologia, la diagnostica e lattuale stato dellarte del trattamento delle stenosi salivari.

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“…Salivary gland atrophy can be recreated experimentally in rodents via ligation of the main excretory duct of the submandibular gland, which creates a histological appearance comparable with that which occurs in humans, 4 which involves deletion of acinar cells through apoptosis 5 and autophagy, 6 as well as mitotic proliferation of ductal cells. 5 …”

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confidence: 99%

Rapamycin delays salivary gland atrophy following ductal ligation

2014

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Salivary gland atrophy is a frequent consequence of head and neck cancer irradiation therapy but can potentially be regulated through the mammalian target of rapamycin (mTOR). Excretory duct ligation of the mouse submandibular gland provokes severe glandular atrophy causing activation of mTOR. This study aims to discover the effects of blocking mTOR signaling in ligation-induced atrophic salivary glands. Following 1 week of unilateral submandibular excretory duct ligation: gland weights were significantly reduced, 4E-BP1 and S6rp were activated, and tissue morphology revealed typical signs of atrophy. However, 3 days following ligation with rapamycin treatment, a selective mTOR inhibitor, gland weights were maintained, 4E-BP1 and S6rp phosphorylation was inhibited, and there were morphological signs of recovery from atrophy. However, following 5 and 7 days of ligation and rapamycin treatment, glands expressed active mTOR and showed signs of considerable atrophy. This evidence suggests that inhibition of mTOR by rapamycin delays ligation-induced atrophy of salivary glands.

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The effects of ductal obstruction on the acinar cells of the parotid of cat

Cited by 24 publications

References 22 publications

Rat salivary gland ligation causes reversible secretory hypofunction

Rat salivary gland ligation causes reversible secretory hypofunction

Salivary duct stenosis: diagnosis and treatment

Rapamycin delays salivary gland atrophy following ductal ligation

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