Salivary Gland Inflammation (Sialadenitis): Causes

Pathogenesis (development of disease)

Bacterial sialadenitis.

Acute bacterial sialadenitis is usually favored by the presence of hyposialia (decreased salivary flow) and triggered by hemolytic streptococci (group A) and staphylococci (S. aureus). In ascending inflammatory mechanism, sialangitis (inflammation of the ductal system) is followed by invasion of the glandular parenchyma and consecutive hyposialia. Chronic sialadenitis

• Obstructive electrolyte sialadenitis – Due to disturbance of electrolyte balance (salt balance) viscosity change of saliva. Tougher saliva leads to mucus obstruction (outflow obstruction) and consecutive formation of sialoliths (stone formation). Inorganic and organic material accumulates on an inorganic core and leads to an increase in the volume of the stone: sialolithiasis; increase in volume as organic and inorganic material accumulates in layers on an inorganic core. The ductal epithelia play a central role as a target of the inflammatory process. Obstructive electrolyte sialadenitis never affects the parotid and submandibular glandules simultaneously.
• Obstructive sialadenitis – In addition to sialoliths, other obstructions may be causative in the development of sialadenitis:
  • Sialodochitis (primary inflammation of the ductal epithelium).
  • Induction of obstruction by radioiodine therapy.
  • Stenosis (narrowing) or stricture (high-grade narrowing) – post-traumatic, post-inflammatory or tumor-related scarring of the ductal system.
  • Compression of an excretory duct by a tumor with inflammatory and immunological changes resulting from
  • Anomalies – mostly congenital polycystic changes with sometimes massive dilatations (expansion) of the excretory duct (synonyms: mega-Stenon’s duct, sialectase).
• Chronic recurrent sialadenitis of the submandibular gland (Küttner tumor) – Secretory dysfunction and obstructive electrolyte sialadenitis are followed by periductal fibrosis, secretory thickening, and proliferation. Immune responses (IgA, IgG, lactoferrin, lysozyme) with extensive immunological destruction of parenchyma and ductal epithelium are followed by ascending infections.
• Chronic recurrent parotitis – Predisposing (“favoring”) congenital gangectasias (ductal dilatation) are suspected, an immunological genesis is also discussed.
• Chronic myoepithelial sialadenitis in Sjögren’s or Sicca syndrome – inflammatory-degenerative autoimmune disease; antinuclear autoantibodies are found in 60 to 100%, as well as antibodies against cytoplasm of the ganglion cells. Consecutive, relapsing loss of glandular function.
• Chronic epithelioid cell sialadenitis of the parotid gland (synonyms: Heerfordt syndrome; febris uveo-parotidea) – extrapulmonary manifestation of sarcoidosis (M. Boeck).
• Radiation sialadenitis – radiogenic (radiation-induced) induced damage to the serous acini (acinus: berry-shaped, secretory end piece of glands) and inflammation of the ductal epithelium with subsequent apoptosis (controlled cell death) and fibrotic remodeling of the glandular parenchyma.

Etiology (causes)

Biographical causes

• Congenital ductal ectasia
  • Suspected as a predisposing factor for the development of chronic recurrent parotitis.

Behavioral causes

• Nutrition
  • Decreased fluid intake
    • Saliva reduction caused by exsiccosis (dehydration) and associated bacterial infection; in overall Marantic situation (protein deficiency situation), the parotid gland (parotid gland) is typically affected – Marantic parotitis, Marantic sialadenitis.
  • Disturbed electrolyte balance (salt balance).
• Consumption of stimulants
  • Alcohol (woman: > 20 g/day; man: > 30 g/day).

Disease-related causes

• Congenital anomalies – usually congenital polycystic changes with sometimes massive dilatations (dilations) of the excretory duct (synonyms: mega-Stenon’s duct, sialectasis).
• Autoimmune disease
  • Primary biliary cholangitis (PBC, synonyms: nonpurulent destructive cholangitis; formerly primary biliary cirrhosis) – relatively rare autoimmune disease of the liver (affects women in approximately 90% of cases); begins primarily biliary, i.e., at the intrahepatic and extrahepatic (“inside and outside the liver“) bile ducts, which are destroyed by inflammation (= chronic nonpurulent destructive cholangitis). In the longer course, the inflammation spreads to the entire liver tissue and eventually leads to scarring and even cirrhosis; detection of antimitochondrial antibodies (AMA); PBC is often associated with autoimmune diseases (autoimmune thyroiditis, polymyositis, systemic lupus erythematosus (SLE), progressive systemic sclerosis, rheumatoid arthritis); Associated with ulcerative colitis (inflammatory bowel disease) in 80% of cases; long-term risk of cholangiocellular carcinoma (CCC; bile duct carcinoma, bile duct cancer) is 7-15%.
  • Sarcoidosis (synonyms: Boeck’s disease; Schaumann-Besnier’s disease) – systemic disease of connective tissue with granuloma formation (skin, lungs and lymph nodes).
  • Sjögren’s or Sicca syndrome
• Blood loss
• Diabetes insipidus (hormone deficiency-related disorder in hydrogen metabolism leading to extremely high urine excretion (polyuria; 5-25 l/day) due to impaired concentration capacity of the kidneys).
• Diabetes mellitus
• Diarrhea (diarrhea)
• Nausea (nausea)
• Immunodeficiency / immunodeficiency
• Immunological genesis for chronic recurrent parotitis under discussion.
• Infections
  • Viral sialadenitis
    • Mumps virus – ss-RNA virus of the paramyxovirus family, belonging to the rubulavirus genus; only one human pathogenic serotype known; causative agent of parotitis epidemica (mumps).
    • Cytomegalovirus (synonyms: CMV, cytomegalovirus) – DNA virus from the subgroup of human herpesviruses (HHV 5). The virus induces the formation of giant cells from the ductal epithelium of the salivary glands.
    • Coxsackie viruses – RNA viruses, belonging to the genus enteroviruses, the family of picornaviruses. Known are serotype A and B.
    • Echo viruses
    • HI virus (HIV)
    • Influenza viruses – triggers influenza (flu).
    • Parainfluenza viruses
  • Bacterial sialadenitis
    • Acute bacterial sialadenitis often underlies hyposialia (decreased salivation), favoring ascending infection.
      • Β-hemolytic streptococci (group A).
      • Cat scratch disease – bacterial lymph gland disease caused by pathogen Bartonellae henselae; sialadenitis as an atypical course.
      • Staphylococcus (S. aureus)
  • Infectious-granulomatous sialadenitis.
    • Actinomycosis (radiation mycosis).
    • Atypical mycobacterioses
    • Syphilis (lues; venereal disease) – very rare, but must be ruled out in granulomatous sialadenitis.
    • Tuberculosis
• Marasmus – most severe form of malnutrition; also referred to as protein-energy malnutrition (PEM).
• Stenosis (narrowing) or stricture (high-grade narrowing) of the ductal system
  • Post-inflammatory (following inflammation).
  • Post-traumatic (after trauma/injury).
  • Tumor-related
• Tuberculosis, atypical mycobacterioses.
• Tumors – compression of the ductal system and glandular parenchyma.
• Burns

Medication

• Sixty-three percent of the 200 most prescribed medications have salivation-inhibiting (salivation-inhibiting) effects. The use of xerogenic (dry mouth-related) medications for long periods of time favors the development of sialadenitis due to hyposialia (secretion of insufficient amounts of saliva) and (ascending) ascending infection. About 400 such drugs are known. They belong to the following groups:
  • Antiadiposita
  • Anoretics
  • Antiarrhythmics
  • Anticholinergics
  • Antiepileptic drugs
  • Antidepressants
  • Antihistamines
  • Antihypertensives
  • Antiparkinsonian drugs
  • Antipsychotics (neuroleptics)
  • Anxiolytics
  • Ataractics
  • Diuretics
  • Hypnotics
  • Muscle relaxants
  • Sedatives
  • Spasmolytics
• Induction by radioiodine therapy

X-rays

• Radiogenic sialadenitis (radiation sialadenitis) – during radiotherapy in the head and neck region and associated damage to soft tissues.

Chemotherapies

• Immunosuppression (suppression of immunological processes) → ascending (ascending) infection.

Operations

• Head and neck surgery and associated damage to the salivary glands (strictures and stenoses).
• Postoperative parotitis after major surgery such as laparotomy (abdominal incision).