electrolytes, which accounts for the volume of saliva produced, results from a complex set of stimuli which are largely parasympathetic. The active secretion of proteins into the saliva depends upon the relative levels of both sympathetic and parasympathetic stimulation.
Although the ducts are less densely innervated than secretory acini, they do influence the composition of the saliva. Adrenal aldosterone promotes resorption of sodium and secretion of potassium into the saliva by striated ductal cells. Myoepithelial cell contraction is stimulated predominantly by adrenergic fibers although there may be an additional role for cholinergic axons.
The cholinergic parasympathetic nerves release acetylcholine that binds to M3 and to a lesser extent M1 muscarinic receptors which result in the secretion of saliva by the acinar cells in the endpieces of the duct trees. The sympathetic nerves release noradrenaline that results in the release of stored protein from both the acinar cells and the ductal cells. There is also cross talk between the calcium and cyclic AMP intracellular pathways. Additionally, other non‐adrenergic and non‐cholinergic neuropeptides released from the autonomic nerves evoke saliva secretion and parasympathetically derived vasointestinal peptide acting through endothelial cell‐derived nitric oxide. These neuropeptides play a role in the reflex vasodilatation that accompanies salivary secretion (as seen dramatically in Frey syndrome). Neuronal type, calcium activated, soluble nitric oxide within salivary cells seems to play a role in mediating salivary protein secretion in response to autonomimetics. The fluid secretion involves aquaporin 5 and the extent to which its expression on apical acinar cell membranes is upregulated by cholimimetics remains obscure (Proctor and Carpenter 2007).
Summary
Although embryologically the parotid consists of a single lobe, anatomically the facial nerve lies in a distinct plane between the anatomical superficial and deep lobes.
The parotid capsule is attenuated and incomplete where the gland lies in intimate contact with the branches of the facial nerve.
There are fixed anatomical landmarks indicating the origin of the extracranial facial nerve as it leaves the stylomastoid foramen.
The lower pole of the parotid gland is separated from the posterior pole of the submandibular gland by only thin fascia. This can lead to diagnostic confusion in determining the origin of a swelling in this area.
The relationship of the submandibular salivary duct to the lingual nerve is critical to the safe removal of stones within the duct.
Great care must be taken to identify the lingual nerve when excising the submandibular gland. The lingual nerve is attached to the gland by the parasympathetic fibers synapsing in the submandibular (sublingual) ganglion.
The sublingual gland may drain into the submandibular duct or it may drain directly into the floor of the mouth via multiple secretory ducts.
Case Presentation – Wait, What?
A 67‐year‐old man presented to the emergency department with an abrupt onset of acute left visual loss. The patient had a known history of multiple cerebrovascular accidents and had chronic right visual loss and a chronic mild aphasia.
Past Medical History
The patient had a history of hypercoagulable state with methylenetetrahydrofolate reductase (MTHFR) mutation, hypertension, hyperlipidemia, peripheral vascular disease, and gastroesophageal reflux disease. He had undergone a left carotid endarterectomy in the past and a bypass surgery for peripheral vascular disease. He was taking a baby aspirin daily, atorvastatin, hydrochlorothiazide, metoprolol, niacin, ranitidine, and warfarin that was on hold for five days for a planned vascular surgery procedure.
Imaging
The patient underwent a CT of the head that demonstrated multiple remote infarcts with no acute findings. A CT angiogram of the brain and neck revealed occlusive disease of the left internal carotid artery and absence of his left submandibular gland (Figure 1.15a and b).
Figure 1.15. Axial (a) and coronal (b) CT angiogram of the neck demonstrating agenesis of the left submandibular gland. Hypertrophy of the right submandibular gland is noted.
Diagnosis
Congenital absence of the left submandibular gland. The patient's operative report for his left carotid endarterectomy made no mention of encountering or removing the left submandibular gland.
TAKE HOME POINTS
1 Unilateral or bilateral agenesis of the submandibular glands is extremely rare.
2 Unilateral submandibular gland agenesis is typically asymptomatic and discovered incidentally through imaging of the neck. Bilateral agenesis is more likely to produce symptoms in affected patients such as xerostomia, dysphagia, and dental problems.
3 Submandibular gland agenesis may be accompanied by genetic syndromes such as Treacher Collins syndrome, hemifacial microsomia, ectodermal dysplasia, and lacrimo‐dento‐digital syndrome.
4 Physical examination of the neck might not disclose unilateral or bilateral agenesis of the submandibular glands. It becomes necessary, therefore, to examine the oral cavity where the unilateral Wharton duct opening may not be present. CT or MR imaging of the neck will unequivocally establish the diagnosis of agenesis of the submandibular gland as this case demonstrated.
References
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