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Sialolithiasis
Sialolithiasis
Sialolithiasis
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Sialolithiasis
Calculi (salivary gland stones) removed from the sublingual gland
SpecialtyDental surgery Edit this on Wikidata

Sialolithiasis (also termed salivary calculi,[1] or salivary stones)[1] is a crystallopathy where a calcified mass or sialolith forms within a salivary gland, usually in the duct of the submandibular gland (also termed "Wharton's duct"). Less commonly the parotid gland or rarely the sublingual gland or a minor salivary gland may develop salivary stones.

The usual symptoms are pain and swelling of the affected salivary gland, both of which get worse when salivary flow is stimulated, e.g. with the sight, thought, smell or taste of food, or with hunger or chewing. This is often termed "mealtime syndrome."[2] Inflammation or infection of the gland may develop as a result. Sialolithiasis may also develop because of the presence of existing chronic infection of the glands, dehydration (e.g. use of phenothiazines), Sjögren's syndrome and/or increased local levels of calcium, but in many instances the cause is idiopathic (unknown).

The condition is usually managed by removing the stone, and several different techniques are available. Rarely, removal of the submandibular gland may become necessary in cases of recurrent stone formation. Sialolithiasis is common, accounting for about 50% of all disease occurring in the major salivary glands and causing symptoms in about 0.45% of the general population. Persons aged 30–60 and males are more likely to develop sialolithiasis.[2]

Classification

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The term is derived from the Greek words sialon (σίαλον, saliva) and lithos (stone), and the Greek -iasis meaning "process" or "morbid condition". A calculus (plural calculi) is a hard, stone-like concretion that forms within an organ or duct inside the body. They are usually made from mineral salts, and other types of calculi include tonsiloliths (tonsil stones) and renal calculi (kidney stones). Sialolithiasis refers to the formation of calculi within a salivary gland. If a calculus forms in the duct that drains the saliva from a salivary gland into the mouth, then saliva will be trapped in the gland. This may cause painful swelling and inflammation of the gland. Inflammation of a salivary gland is termed sialadenitis. Inflammation associated with blockage of the duct is sometimes termed "obstructive sialadenitis". Because saliva is stimulated to flow more with the thought, sight or smell of food, or with chewing, pain and swelling will often get suddenly worse just before and during a meal ("peri-prandial"), and then slowly decrease after eating, this is termed meal time syndrome. However, calculi are not the only reasons that a salivary gland may become blocked and give rise to the meal time syndrome. Obstructive salivary gland disease, or obstructive sialadenitis, may also occur due to fibromucinous plugs, duct stenosis, foreign bodies, anatomic variations, or malformations of the duct system leading to a mechanical obstruction associated with stasis of saliva in the duct.[2]

Salivary stones may be divided according to which gland they form in. About 85% of stones occur in the submandibular gland,[3] and 5–10% occur in the parotid gland.[2] In about 0–5% of cases, the sublingual gland or a minor salivary gland is affected.[2] When minor glands are rarely involved, caliculi are more likely in the minor glands of the buccal mucosa and the maxillary labial mucosa.[4] Submandibular stones are further classified as anterior or posterior in relation to an imaginary transverse line drawn between the mandibular first molar teeth. Stones may be radiopaque, i.e. they will show up on conventional radiographs, or radiolucent, where they not be visible on radiographs (although some of their effects on the gland may still be visible). They may also symptomatic or asymptomatic, according to whether they cause any problems or not.

Signs and symptoms

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Swelling of the submandibular gland as seen from the outside
The stone seen in the submandibular duct on the person's right side

Signs and symptoms are variable and depend largely upon whether the obstruction of the duct is complete or partial, and how much resultant pressure is created within the gland.[1] The development of infection in the gland also influences the signs and symptoms.

  • Pain, which is intermittent, and may suddenly get worse before mealtimes, and then slowly get better (partial obstruction).[3]
  • Swelling of the gland, also usually intermittent, often suddenly appearing or increasing before mealtimes, and then slowly going down (partial obstruction).[3]
  • Tenderness of the involved gland.[3]
  • Palpable hard lump, if the stone is located near the end of the duct.[1][3] If the stone is near the submandibular duct orifice, the lump may be felt under the tongue.
  • Lack of saliva coming from the duct (total obstruction).[3]
  • Erythema (redness) of the floor of the mouth (infection).[3]
  • Pus discharging from the duct (infection).[3]
  • Cervical lymphadenitis (infection).[3]
  • In advanced cases, a fistula may form to the skin of the neck or cheek.[5] See adjacent image demonstrating cutaneous fistulization.
  • Bad breath.[3]
Chronic submandibular sialadenitis with skin fistula formation on the neck
Acute parotid sialadenitis with skin fistula formation on the cheek

Rarely, when stones form in the minor salivary glands, there is usually only slight local swelling in the form of a small nodule and tenderness.[1]

Causes

[edit]
The major salivary glands (paired on each side). 1. Parotid gland, 2. Submandibular gland, 3. Sublingual gland.

There are thought to be a series of stages that lead to the formation of a calculus (lithogenesis). Initially, factors such as abnormalities in calcium metabolism,[3] dehydration,[2] reduced salivary flow rate,[2] altered acidity (pH) of saliva caused by oropharyngeal infections,[2] and altered solubility of crystalloids,[2] leading to precipitation of mineral salts, are involved. Other sources state that no systemic abnormality of calcium or phosphate metabolism is responsible.[1]

The next stage involves the formation of a nidus which is successively layered with organic and inorganic material, eventually forming a calcified mass.[2][3] In about 15-20% of cases the sialolith will not be sufficiently calcified to appear radiopaque on a radiograph,[3] and will therefore be difficult to detect.

Other sources suggest a retrograde theory of lithogenesis, where food debris, bacteria or foreign bodies from the mouth enter the ducts of a salivary gland and are trapped by abnormalities in the sphincter mechanism of the duct opening (the papilla), which are reported in 90% of cases. Fragments of bacteria from salivary calculi were reported to be Streptococci species which are part of the normal oral microbiota and are present in dental plaque.[2]

Stone formation occurs most commonly in the submandibular gland for several reasons. The concentration of calcium in saliva produced by the submandibular gland is twice that of the saliva produced by the parotid gland.[3] The submandibular gland saliva is also relatively alkaline and mucous. The submandibular duct (Wharton's duct) is long, meaning that saliva secretions must travel further before being discharged into the mouth.[3] The duct possesses two bends, the first at the posterior border of the mylohyoid muscle and the second near the duct orifice.[3] The flow of saliva from the submandibular gland is often against gravity due to variations in the location of the duct orifice.[3] The orifice itself is smaller than that of the parotid.[3] These factors all promote slowing and stasis of saliva in the submandibular duct, making the formation of an obstruction with subsequent calcification more likely.

Salivary calculi sometimes are associated with other salivary diseases, e.g. sialoliths occur in two thirds of cases of chronic sialadenitis,[4] although obstructive sialadenitis is often a consequence of sialolithiasis. Gout may also cause salivary stones,[4] although in this case they are composed of uric acid crystals rather than the normal composition of salivary stones.

Diagnosis

[edit]
Ultrasound image of sialolithiasis
Stone resulting in inflammation and dilation of the duct[6]

Diagnosis is usually made by characteristic history and physical examination. Diagnosis can be confirmed by x-ray (80% of salivary gland calculi are visible on x-ray), by sialogram, or by ultrasound.

Treatment

[edit]
Salivary gland stone and the hole left behind from the operation

Some current treatment options are:

Non-invasive:

Minimally invasive:

Surgical:

  • An ENT or oral/maxillofacial surgeon may cannulate the duct to remove the stone (sialectomy).
  • A surgeon may make a small incision near the stone to remove it.
  • In some cases when stones continually reoccur the offending salivary duct is removed.

Supporting treatment:

  • To prevent infection while the stone is lodged in the duct, antibiotics are sometimes used.

Epidemiology

[edit]

The prevalence of salivary stones in the general population is about 1.2% according to post mortem studies, but the prevalence of salivary stones which cause symptoms is about 0.45% in the general population.[2] Sialolithiasis accounts for about 50% of all disease occurring in major salivary glands, and for about 66% of all obstructive salivary gland diseases. Salivary gland stones are twice as common in males as in females. The most common age range in which they occur is between 30 and 60, and they are uncommon in children.[2]

References

[edit]
[edit]
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Sialolithiasis

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Sialolithiasis is a benign condition characterized by the formation of calcified stones, known as sialoliths, within the ductal system of the major s, including the parotid, submandibular, and sublingual glands. These stones, primarily composed of and other minerals, obstruct flow, leading to recurrent episodes of glandular swelling and pain, especially during meals when salivary secretion increases. It represents the most common cause of salivary gland pathology, accounting for approximately 50% of cases of salivary gland swelling. Epidemiologically, sialolithiasis has an estimated incidence of 1 in 10,000 to 1 in 30,000 individuals annually, predominantly affecting adults aged 30 to 60 years, more commonly in males according to some studies. Approximately 80-85% of sialoliths occur in the due to its tortuous duct anatomy and higher calcium concentration in its secretions, while 10-15% form in the and fewer than 5% in the sublingual or minor glands. The condition is rare in children and bilateral in 1-3% of cases, with multiple stones present in about 25% of affected patients. The etiology remains multifactorial and not fully elucidated, but key contributing factors include salivary stasis from dehydration, reduced fluid intake, or medications with anticholinergic effects, as well as local inflammation, duct strictures, and metabolic alterations leading to supersaturation of minerals in saliva. Tobacco smoking is a recognized risk factor, potentially exacerbating compositional changes in saliva, while underlying conditions such as gout may contribute through elevated uric acid levels in stone formation. Pathophysiologically, a nidus of bacteria, desquamated cells, or foreign material initiates crystallization around a core, growing via concentric deposition during periods of low salivary flow. Clinically, patients often present with acute, intermittent swelling and tenderness over the affected gland, accompanied by dry mouth or a bad taste if infection develops; symptoms typically resolve spontaneously but recur without intervention. Diagnosis is primarily clinical, supported by imaging modalities such as ultrasonography (with 60-95% sensitivity), computed tomography for stone detection, or sialendoscopy for direct visualization. Treatment begins conservatively with hydration, sialogogues to stimulate saliva flow, warm compresses, and massage to facilitate stone expulsion, which succeeds in many cases for smaller stones (<7 mm). For persistent or larger sialoliths, minimally invasive options like sialendoscopy or extracorporeal shock wave lithotripsy are preferred, with surgical excision reserved for refractory cases or glandular complications such as chronic sialadenitis. The prognosis is generally excellent, with low recurrence rates following removal, though untreated obstruction can lead to glandular atrophy or secondary bacterial infection.

Background

Definition and Overview

Sialolithiasis is a benign condition characterized by the pathological formation of calcified stones, known as sialoliths, within the ducts or of the major salivary glands, resulting in obstruction of salivary flow. The term sialolithiasis is derived from the Greek words sialon () and lithos (stone), combined with the -iasis indicating a pathological process. This obstruction disrupts normal salivary secretion, potentially leading to acute glandular swelling—especially during stimulation of saliva production, such as eating—and increasing the risk of secondary bacterial infection if the blockage persists. In contrast to sialadenitis, which encompasses inflammation of the salivary glands from diverse etiologies including but not limited to obstruction, sialolithiasis is distinguished as a primary obstructive disorder due specifically to the presence of calculi.

Anatomy of Salivary Glands

The salivary glands are exocrine glands responsible for producing , which aids in lubrication, digestion, and oral health. There are three pairs of major salivary glands—the parotid, submandibular, and sublingual—and numerous minor salivary glands distributed throughout the . These glands are composed of acini that secrete and a ductal system that transports it to the oral cavity. The parotid glands are the largest of the major salivary glands, each weighing approximately 25–30 grams, and are located anterior to the ear, overlying the masseter muscle and extending between the mandible's ramus and the sternocleidomastoid muscle. They produce purely serous saliva, which is watery and enzyme-rich, contributing about 25–30% of total daily saliva output. Saliva from the parotid gland drains via Stensen's duct (also known as the parotid duct), a 5–7 cm structure that courses over the masseter muscle and opens into the oral cavity opposite the second upper molar tooth. The submandibular glands, the second largest at 7–15 grams each, lie in the submandibular triangle beneath the mandible, with superficial and deep lobes wrapping around the mylohyoid muscle. These glands secrete mixed saliva that is predominantly serous, with mucous acini comprising approximately 10%, accounting for roughly 70% of daily saliva production. Their secretions exit through Wharton's duct (submandibular duct), the longest salivary duct at about 5 cm, which is relatively narrow and travels along the floor of the mouth to open at the sublingual papilla near the lingual frenulum. The sublingual glands, the smallest major glands at around 3 grams each, are situated in the anterior floor of the mouth beneath the tongue and mylohyoid muscle, embedded in the sublingual fold. They primarily produce mucous saliva, which is viscous and lubricating, contributing about 5% of total saliva. Multiple small ducts, including Bartholin's duct and up to 20 other minor ducts, drain directly into the oral floor along the sublingual folds. Minor salivary glands, numbering 600–1,000, are small, unencapsulated structures scattered in the of the , cheeks, soft and , , and other oral regions (excluding the gingiva). Unlike the major glands, they lack prominent ducts and secrete mainly mucous for local , producing less than 10% of total saliva volume. The ductal systems of all salivary glands consist of intercalated ducts (short, cuboidal-lined segments adjacent to acini), striated ducts (columnar that modifies saliva ion content), and excretory ducts (pseudostratified leading to the oral cavity). composition across glands is approximately 99.5% water with electrolytes, enzymes like , mucins, and agents; serous types from the parotid are enzyme-focused for , while mixed and mucous types from submandibular and sublingual glands emphasize and . Vascular supply to the major salivary glands derives primarily from branches of the : the parotid from the superficial temporal and maxillary arteries, the submandibular from the and lingual arteries, and the sublingual from the lingual and submental arteries; venous drainage parallels via the retromandibular, , and . Neural innervation is predominantly parasympathetic for secretory control—the parotid via the (CN IX) through the , and the submandibular and sublingual via the (CN VII) through the —while sympathetic fibers from the modulate and reduce secretion, influencing glandular blood flow and potential responses to stimuli like swelling. The length and relative narrowness of Wharton's duct contribute to its vulnerability in conditions like sialolithiasis.

Pathophysiology

Formation of Sialoliths

Sialoliths form through a process of heterogeneous in supersaturated , where initial occurs around an organic nidus such as , desquamated epithelial cells, or foreign material within the salivary ducts or glands. This nidus serves as a scaffold for the deposition of inorganic salts, primarily calcium phosphates, initiating the development of microliths—small, subclinical calculi that arise from secretory granules in acinar cells and are released into the ductal system. Over time, these microliths aggregate and grow via successive layering, evolving into macroscopic stones through a two-stage process involving core formation and peripheral accretion. The composition of sialoliths reflects this layered genesis, with a central core often comprising loosely organized calcium apatite crystals intertwined with organic elements like bacterial biofilms and inflammatory exosomes, surrounded by denser intermediate zones of and whitlockite. Scanning electron microscopy reveals an onion-like with alternating concentric layers of mineralized (radiodense) inorganic material and radiolucent organic matrix, including mucins, glycoproteins, cellular debris, and carbonates that constitute up to 20-40% of the stone's volume. This organic-inorganic interplay stabilizes the growing , with the peripheral multilayers showing granule-shaped crystals and exfoliated epithelial cells embedded in bacterial colonies. Physical factors such as salivary stagnation, often due to or reduced flow rates, promote and precipitation by concentrating ions in the ducts, particularly in the where viscous, mucinous and an upward ductal trajectory exacerbate stasis. Changes in salivary toward further facilitate , as higher levels reduce the of calcium phosphates, enabling their deposition onto the evolving nidus over weeks to months. This progression from microliths to clinical sialoliths underscores the dynamic biochemical environment of as a key driver in stone .

Causes and Risk Factors

Sialolithiasis arises from a combination of metabolic disturbances that alter salivary composition, increasing the likelihood of mineral precipitation. Conditions such as are implicated due to their role in elevating salivary calcium and levels, which contribute to stone formation. Similarly, hypercalcemia has been linked to salivary with calcium, a key factor in lithogenesis, though animal studies show mixed evidence for direct causation. These metabolic factors may provide the biochemical milieu for an initial nidus in sialolith development. Iatrogenic factors, particularly those reducing salivary flow, heighten the risk of sialolithiasis. for head and neck cancers can diminish function, leading to stasis and stone formation. Medications that cause or , such as diuretics, anticholinergics, and antihistamines, further promote salivary stagnation by decreasing fluid intake or output. Infectious processes contribute by creating an inflammatory environment conducive to nidus formation. Chronic bacterial , often involving pathogens like , can lead to ductal irritation and mineral deposition. Lifestyle and demographic elements also play a role in predisposing individuals to sialolithiasis. induces ductal and reduces salivary , facilitating stone genesis, while poor exacerbates salivary stagnation. from low fluid intake compounds these effects.

Classification

Types of Sialoliths

Sialoliths are primarily classified by their composition, which influences their formation, detectability, and clinical behavior. Most sialoliths are mixed types, consisting of layered organic and inorganic materials around an initial nidus or core. The inorganic components, which dominate in many cases, include calcium salts such as (the most common), whitlockite, and octacalcium phosphate. Organic elements comprise glycoproteins, mucopolysaccharides, cellular debris, and like species. Pure inorganic sialoliths, rich in calcium salts with minimal organic matrix, are less common but more radiopaque due to their mineral density. Organic-matrix rich sialoliths feature higher proportions of mucoproteins and proteins, often resulting in softer, less calcified structures. Rarely, -based sialoliths form, primarily composed of lipids including , phospholipids, triglycerides, and esters, which may mimic compositions in their lipid profile. Size classifications help predict clinical impact and treatment approaches for sialoliths. Microliths, typically smaller than 2 mm (including intracellular forms up to 25 μm or acinar ones up to 70 μm), often remain undetected and may contribute to larger stone development without causing acute symptoms. Small sialoliths measure 2-5 mm and are frequently mobile within ducts. Large sialoliths exceed 10 mm, with giants over 15 mm occurring in about 7.6% of cases; these can weigh up to 5 g on average 300 mg and lead to severe obstruction due to their bulk. Morphological variants of sialoliths vary based on their site of formation and growth patterns. They can present with smooth, cylindrical surfaces, especially those in ductal locations, or irregular, rough, ovoid, rounded, spheroidal, ellipsoidal, or globular shapes. Single sialoliths account for 70-80% of cases, while multiple stones per are rarer but can complicate by increasing obstruction risk. Clinical subtypes further categorize sialoliths by their behavior and visibility. Impacted sialoliths are lodged firmly in ducts, causing persistent obstruction, whereas free-floating ones are mobile, typically under 5-7 mm, and may migrate or pass spontaneously. Radiolucent sialoliths, comprising about 20% of cases and often organic-heavy, are invisible on plain X-rays, while radiopaque variants (around 80%) contain sufficient inorganic minerals for radiographic detection. Larger radiopaque stones are more commonly found in submandibular ducts.

Affected Glands and Locations

Sialolithiasis predominantly affects the , accounting for 80-90% of cases, primarily due to the length and tortuosity of Wharton's duct, which promotes salivary stasis and stone formation. The posterior portion of Wharton's duct, near the hilum, serves as the most common site of impaction within this gland. The is involved in 10-20% of cases, with stones typically forming in Stensen's duct, often near the ductal punctum, and less frequently due to the gland's production of serous , which is less viscous than the mucous secretions of the submandibular gland. Involvement of the and minor salivary glands is rare, comprising approximately 1-5% of cases, and usually occurs in Bartholin's duct for the or in sites such as the buccal mucosa for minor glands. Stones are classified as intraglandular or extraglandular based on location, with the majority being extraglandular in the main ducts, while intraglandular stones within the acini or are uncommon. In the , intraglandular locations are more frequent compared to the .

Clinical Presentation

Signs and Symptoms

Sialolithiasis typically presents with acute intermittent swelling and pain in the affected , most commonly the , which worsens during or shortly after meals due to stimulation of salivary flow—a phenomenon known as "mealtime ." This swelling is usually unilateral and may involve facial edema in the submandibular or parotid regions, lasting from minutes to hours before subsiding. Patients often report a dull, aching pain that intensifies postprandially, accompanied by reduced salivary flow on the affected side. Chronic manifestations include recurrent episodes of low-grade swelling and , resulting from persistent obstruction and diminished saliva production. A foul in the may arise from secondary bacterial , particularly if stasis allows overgrowth. Associated discomfort can include to the or , reflecting the innervation of the salivary glands. Physical signs encompass a palpable firm mass along the duct or in the or floor of the mouth, with tenderness on bimanual of the gland. In infected cases, purulent discharge may express from the duct orifice upon massage, though fever is typically absent unless acute develops. If untreated, such infections can rarely progress to complications like formation.

Complications

Untreated or recurrent sialolithiasis can lead to obstructive complications, primarily acute bacterial , where ductal blockage promotes bacterial stasis and , often presenting as suppurative with fever, , and discharge from the affected . Secondary can occur in association with sialoliths. Salivary formation represents another obstructive , arising from chronic ductal pressure and , resulting in abnormal tracts between the gland or duct and surrounding tissues, such as the oral cavity or skin. Prolonged obstruction from sialoliths contributes to chronic sequelae, including recurrent or persistent that induces glandular scarring and through ongoing and acinar . Over time, this can progress to irreversible gland , characterized by parenchymal loss, ductal dilation, and replacement with fibrotic tissue, impairing salivary function. Rare but severe outcomes include sialolith-induced abscess formation or cellulitis, where infection extends beyond the gland into adjacent soft tissues, potentially involving deep neck spaces and leading to systemic sepsis. In submandibular gland cases, the anatomical proximity to the airway raises the risk of compromise, manifesting as stridor or respiratory distress in advanced infections. Long-term risks encompass altered salivary composition and reduced flow due to partial obstruction or glandular dysfunction, which heightens susceptibility to dental caries and secondary oral infections by diminishing the protective buffering and properties of . Additionally, the recurrent pain associated with episodic obstruction can impose a psychological burden, contributing to discomfort, anxiety, and diminished health-related .

Diagnosis

History and Physical Examination

The diagnosis of sialolithiasis begins with a detailed patient to elicit characteristic symptoms and potential risk factors. Clinicians inquire about unilateral swelling and pain in the affected , particularly episodes that intensify during meals due to increased salivary stimulation, often resolving partially afterward. The also explores the duration and recurrence of symptoms, such as prior similar episodes suggesting chronic obstruction, as well as contributing factors like recent dehydration from illness or inadequate fluid intake, use of medications that reduce salivary flow (e.g., diuretics or anticholinergics), smoking , and assessment of dental or oral hygiene practices that may promote bacterial involvement in stone formation. Physical examination focuses on targeted intraoral and extraoral evaluation to identify signs of obstruction or . Intraoral reveals potential or at the ductal orifice, such as the (Wharton's duct) or Stensen's duct for the , with possible visible calculi appearing as white or yellow oval structures. Bimanual of the gland and duct—from posterior to anterior—assesses for tenderness, a palpable mass, or stone mobility, while gentle massage or expression attempts may yield turbid , , or even dislodge small stones. Extraoral of the or parotid region detects asymmetric swelling or induration, confirming localized involvement. Key elements in the history and exam help differentiate sialolithiasis from mimics. Meal-time exacerbation and unilateral presentation distinguish it from bilateral viral conditions like , which often include a prodromal viral illness. Palpable, mobile stones without fixed induration or pulsatility suggest benign calculi over neoplasms, which may present as firm, nontender masses. Red flags include systemic symptoms such as fever, , or purulent discharge indicating secondary infection (), or persistent/recurrent episodes with hypercalcemia clues (e.g., , ) hinting at underlying as a .

Imaging and Diagnostic Tests

Diagnosis of sialolithiasis often relies on imaging modalities to confirm the presence, location, and characteristics of salivary stones following clinical suspicion from findings such as gland swelling or tenderness. Plain , including orthopantomography (OPG), serves as an initial imaging tool, effectively detecting radiopaque sialoliths, which comprise approximately 80% of submandibular stones but only 60% of parotid stones. However, its utility is limited for radiolucent stones, which account for 10-20% of cases and may require more advanced techniques for visualization. Ultrasound has emerged as the first-line non-invasive method due to its accessibility, lack of , and high diagnostic accuracy. It demonstrates hyperechoic stones with posterior acoustic shadowing, ductal dilation proximal to the obstruction, and associated through Doppler assessment, achieving a sensitivity of approximately 90% for submandibular sialolithiasis. This modality is particularly effective for superficial glands like the submandibular, with specificity exceeding 95% in meta-analyses. For complex cases, computed tomography (CT) provides precise localization, sizing, and compositional analysis of sialoliths, serving as the gold standard for detailed evaluation when is inconclusive. Non-contrast CT scans detect even small or radiolucent stones with high sensitivity, often using thin slices (0.2-0.5 mm) to minimize artifacts. Sialography, involving contrast injection into the salivary duct, was historically the gold standard but is now less commonly used due to risks such as exacerbation of infection, pain, and exposure to and iodine contrast. Magnetic resonance imaging (MRI), particularly MR sialography, is valuable for assessing involvement, ductal , and radiolucent stones without , offering non-invasive visualization of gland parenchyma and obstruction effects. Sialendoscopy, a minimally invasive endoscopic procedure, allows direct visualization of the salivary ducts and can confirm the presence of sialoliths, assess ductal , and often facilitate immediate treatment. It is particularly useful when non-invasive is inconclusive or for therapeutic planning. Laboratory tests may be considered in specific contexts. If is suspected due to purulent discharge, culture and sensitivity testing can guide therapy for secondary bacterial . Serum calcium levels may be assessed in cases of recurrent sialolithiasis with suspicion of underlying metabolic disorders such as , though this is not routine.

Treatment

Conservative Management

Conservative management of sialolithiasis focuses on non-invasive strategies to alleviate symptoms, promote salivary flow, and facilitate the spontaneous passage of small stones (typically <7 mm), with reported success rates varying from 20-60% depending on stone size and location. Increased fluid intake is a of conservative therapy, encouraging patients to consume at least 1.5-2 liters of daily to enhance saliva production and reduce stagnation within the ducts, thereby aiding stone dislodgement. Sialogogues, such as lemon drops, sour candies, or lemon wedges, are recommended to stimulate salivary secretion; these agents increase gland activity and can be used multiple times daily, often in combination with hydration to maximize flow. Pharmacotherapy supports symptom control and addresses secondary issues. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, are prescribed for pain relief and to reduce glandular , typically at standard doses. In cases of associated or , indicated by fever or purulent discharge, antibiotics like amoxicillin or anti-staphylococcal agents are administered for 7-10 days to prevent formation. For significant swelling without contraindications, short-term corticosteroids may be used to decrease and restore exocrine function. Physiotherapeutic techniques involve gentle external massage of the affected , performed several times daily, particularly after meals or sialogogue use, to "milk" the duct and encourage stone movement toward the oral cavity. Manual probing of the duct orifice with a blunt instrument may be attempted in clinical settings to dislodge proximal stones, though this requires caution to avoid trauma. Patients are monitored with clinical follow-up within 1-2 weeks to evaluate symptom resolution and stone passage, often using for non-invasive assessment if needed; lack of improvement prompts escalation to more invasive options. Early conservative intervention helps avert complications such as chronic or .

Interventional and Surgical Options

When conservative management fails to resolve sialolithiasis, interventional and surgical options are employed to remove stones or address glandular dysfunction, prioritizing gland preservation where possible. Minimally invasive techniques include intraoral duct incision (transoral duct surgery, TDS) and basket extraction, suitable for accessible stones in the submandibular or parotid ducts. TDS involves a small incision at Wharton's or Stensen's duct papilla to extract stones up to 10 mm in the distal or hilar regions, achieving high success rates due to direct visualization and accessibility. Basket extraction, often performed under sialendoscopy guidance, uses wire baskets to retrieve small, mobile stones (≤3-5 mm) in the distal duct, frequently combined with papillotomy for complete removal. Extracorporeal shock wave lithotripsy (ESWL) employs ultrasound-guided shock waves to fragment stones, particularly those <8 mm in intraparenchymal or proximal locations, with success rates of 70-80% for complete stone clearance when used alone or in combination with other methods. Note that ESWL is not FDA-approved in the United States and may have limited availability in some regions. Endoscopic approaches, such as sialendoscopy, provide visualization of the ductal system using microendoscopes (0.8-1.6 mm diameter) inserted via the papilla, allowing for stone retrieval with microinstruments like or baskets. This technique yields a pooled success rate of 80.9% for sialolithiasis cases, with 88.3% for submandibular stones and 81.2% for parotid stones across 91 studies involving 8,218 patients. For larger or adherent intraductal stones, via sialendoscopy (e.g., :YAG laser) fragments calculi with success rates exceeding 80%, minimizing tissue damage in narrow ducts. Open surgical interventions are reserved for recurrent or therapy-resistant cases where minimally invasive methods fail. excision via transcervical or intraoral approach removes the gland and associated stones, indicated for chronic or multiple calculi, with near-complete resolution but risks including marginal mandibular nerve injury (up to 15.6% temporary). is rarely performed due to the high risk of damage, limited to exceptional cases of severe, intractable parotid sialolithiasis. Postoperative care typically involves antibiotics to prevent , wound monitoring for or dehiscence, and salivary massage to promote drainage, with stents occasionally placed to maintain ductal patency. Recurrence rates following these interventions range from 5-10%, prompting removal in persistent symptomatic cases.

Epidemiology

Prevalence and Demographics

The of sialolithiasis based on diagnosed cases is low, estimated at approximately 1-2 per in studied populations such as . The annual incidence is estimated at 1 in 10,000 to 1 in 30,000 individuals, corresponding to roughly 3 to 10 cases per population in various Western cohorts. The is the most commonly affected site, accounting for 80% to 90% of cases, while the is involved in 10% to 15%, and the sublingual or minor glands in fewer than 5%. The condition predominantly affects adults aged 30 to 60 years, with a mean age at around 55 years in recent large-scale analyses. Earlier literature described a male predominance with a 2:1 ratio, but contemporary studies indicate a more balanced distribution or slight female majority (approximately 57%). It appears more frequent in Western populations compared to Asian cohorts, potentially linked to dietary and hydration differences; for example, prevalence in (1996-2013) averaged 1.9 per 100,000, lower than reported incidences in Western countries such as 7-14 per 100,000 in , though direct comparative data remain limited. Geographic variations show increased risk in regions prone to , such as arid climates, where reduced salivary flow may contribute to stone formation. Differences between urban and rural settings are minimal, with no significant disparities reported in available epidemiological data. Recent trends indicate a stable underlying incidence, but rising detection rates—averaging 6% annual increase in diagnoses in from 2010-2019—likely stem from improved imaging modalities like ultrasonography and computed tomography introduced post-2000. This enhanced diagnostic capability has led to better identification of asymptomatic or incidental cases. Sialolithiasis also shows associations with metabolic conditions like , which may influence demographic patterns in affected populations. Sialolithiasis, the formation of calcified masses within salivary gland ducts, was first systematically described in the late 19th century by German physician Hermann Küttner in 1896, during his investigations of chronically swollen submandibular glands associated with stone formation. Earlier anecdotal references to salivary calculi appear in medical literature, but detailed pathological recognition emerged with improved anatomical understanding of salivary structures in the 1800s. Surgical interventions for stone removal began in the 18th and 19th centuries among European physicians, often involving invasive intraoral or external approaches to the submandibular gland, though these carried high risks of infection and gland damage due to limited diagnostic precision at the time. Key diagnostic and therapeutic advancements marked the . Sialography, involving contrast injection into salivary ducts for radiographic visualization, was introduced in the early , with the first reported clinical use by Pierre Arcelin in 1913 to identify a in Wharton's duct. This technique became the gold standard for duct imaging until the late . In the , extracorporeal shock wave lithotripsy (ESWL), initially developed for renal stones, was adapted for sialolithiasis; the first successful application in humans was reported by Iro et al. in 1989, offering a non-invasive option for fragmenting stones under 10 mm. Sialendoscopy, a minimally invasive endoscopic approach for direct duct visualization and intervention, was pioneered in the early by Francis Marchal and colleagues, who in 2000 described its use for treating ductal pathologies while preserving gland function. Treatment paradigms have evolved dramatically toward gland-preserving, minimally invasive methods, reducing the need for open surgery and gland excision. Prior to the 1990s, submandibular gland resection was performed in 40–50% of cases due to inaccessible or recurrent stones; by the 2010s, adoption of ESWL, transoral duct surgery, and sialendoscopy lowered this rate to under 5%, with overall success rates exceeding 80% for stone clearance. Diagnostic imaging has paralleled this shift, with ultrasound emerging post-1980s as a first-line, radiation-free tool for detecting sialoliths, as evidenced by early studies in 1982 demonstrating its efficacy in parotid gland cases. These trends reflect broader advances in otolaryngology, emphasizing outpatient procedures and reduced morbidity. Despite progress, gaps persist in global understanding and management as of 2025. Underreporting is likely in developing regions, where limited access to sialendoscopy or advanced may lead to reliance on conservative measures or misdiagnosis as , as suggested by regional case series from resource-constrained settings. Ongoing into genetic predispositions remains limited, with studies indicating no strong familial patterns or specific loci, though multifactorial influences like metabolic disorders are under investigation without conclusive evidence.

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