This document discusses several conditions that can affect the salivary glands, including congenital absence of salivary glands, sialolithiasis (salivary stones), sialadenitis (inflammation of salivary glands), and pleomorphic adenoma (benign salivary gland tumor). It provides details on the clinical features, histopathology, imaging findings, causes, and treatment for each condition.

1. HAGIR ABD RAHMAN

3.  Congenital absence of an organ or tissue.
 rare developmental anomaly that can affect one or
more of the major salivary glands.
 The condition may occur alone, or as a component of
syndrome:
 mandibulofacial dysostosis (Treacher Collins syndrome)
 hemifacial microsomia
 lacrimo-auriculo-dento-digital (LADD) syndrome.

4. Clinical Features
 agenesis of any one or all of the largest glands
 Can be associated with absence of the lacrimal glands
 males > females by a 2 : 1 ratio
 severe xerostomia.

5. LADD syndrome
 autosomal dominant, caused by mutations in the fibroblast
growth factor 10 (FGF10) gene.
 aplasia or hypoplasia of the lacrimal and salivary glands
 cup-shaped ears, hearing loss
 digital anomalies.
 hypodontia, microdontia, and mild enamel hypoplasia.

7.  Sialoliths are calcified
structures that develop
within the salivary ductal
system.

8.  arise from deposition of calcium salts around a nidus
of debris within the duct lumen.
 This debris may include inspissated mucus, bacteria,
ductal epithelial cells, or foreign bodies.

9. Clinical Features
 young and middle-aged adults.
 80% develop within the ductal system of the
submandibular gland.
 In minor gland mostly in upper lip or buccal mucosa

10. Opening of
Wharton’s duct is
narrower than the
diameter of the whole
duct
the duct ascends
towards its opening,
which is also
conducive to saliva
retention
It produces a viscous,
mucous and more
alkaline saliva, with a
relatively high
concentration of
hydroxyapatites and
phosphates. This
predisposes to the
precipitation of salts
Why submandibular gland

11. Clinical Features
 Episodic pain or swelling of the affected gland,
especially at meal time.
 If the stone is located toward the terminal portion of
the duct, then a hard mass may be palpated beneath
the mucosa.

12. Hard mass at the orifice of Wharton duct.

13. Radiographic Features
 radiopaque masses.
 Multiple parotid stones
radiographically can
mimic calcified parotid
lymph nodes such as
might occur in
tuberculosis.

15. Minor salivary gland sialolith
presenting as a hard nodule
in the upper lip.
soft tissue radiograph of the
same lesion revealed a
laminated calcified mass.

16. Histopathologic Features
 On gross examination, sialoliths appear as hard masses
that are round oval, or cylindrical
 Yellow, although they may be white or yellowish-
brown.
 the calcified mass exhibits concentric laminations that
may surround a nidus of amorphous debris

17. Histopathologic Features
 associated duct often demonstrates squamous,
oncocytic, or mucous cell metaplasia.
 acute or chronic sialadenitis of the feeding gland.

18.  Intraductal calcified mass showing concentric
laminations

19. Treatment
 Small sialolith: massage of the gland in an effort to milk the
stone toward the duct orifice.
 Sialagogues , moist heat, and increased fluid intake.
 Large sialoliths: surgical removal.
 Minor gland sialoliths are best treated by surgical removal,
including the associated gland.
 Lithotripsy (an ultrasonic shock wave) and interventional
sialendoscopy

21.  Inflammation of the salivary glands

22. inflammation
bacterial
streptococci
E. coli
Staff. aureus
viral
cytomegalovirus
ECHO
Coxsackie A
Mumps

24. Predisposing factors of bacterial
infections
ductal obstruction
congenital strictures
sialolithiasis
Compression by an
adjacent tumor
decreased saliva
debilitation
dehydration
medications that
inhibit secretions

25. Acute sialadenitis
 is most common in the parotid gland.
 The affected gland is swollen and painful, and the
overlying skin is erythematous.
 A purulent discharge often is observed from the duct
orifice when the gland is massaged.

26. chronic sialadenitis
 Periodic swelling and pain
 usually developing at meal time when salivary flow is
stimulated.

27. Subacute necrotizing sialadenitis
 teenagers and young adults.
 minor salivary glands of the hard or soft palate,
presenting as a painful nodule that is covered by
intact, erythematous mucosa.

29. tender swelling of the
submandibular gland.
A purulent exudate
arising from Stensen
duct when the parotid
gland is massaged.

30.  Parotid sialogram demonstrating ductal dilatation
proximal to an area of obstruction

31. Histopathologic Features
 acute sialadenitis: accumulation of neutrophils.
 Chronic sialadenitis is characterized by scattered or
patchy infiltration of the salivary parenchyma by
lymphocytes and plasma cells.
 Atrophy or necrosis of the acini is common, as is
ductal dilatation.

32. Histopathologic Features
 Subacute necrotizing sialadenitis: a heavy mixed
inflammatory infiltrate consisting of neutrophils,
lymphocytes, histiocytes, and eosinophils.
 There is loss of most of the acinar cells, and many of
the remaining ones exhibit necrosis.
 The ducts tend to be atrophic

33. Chronic inflammatory infiltrate with associated acinar
atrophy, and ductal dilatation

34. Treatment
 antibiotic therapy and rehydration of the patient to
stimulate salivary flow.
 Surgical drainage if there is abscess formation.
 Subacute necrotizing sialadenitis is a self-limiting
condition that usually resolves within 2 weeks of
diagnosis without treatment.

36.  Paramyxovirus.
 direct contact with salivary droplets
 incubation period of about 21 days
 Headache, malaise, fever and tense, painful and tender
swelling of the parotids.
 reduction of swelling occur 10 days after the onset of
symptoms.

37.  unilateral parotitis

39.  an uncommon, locally destructive inflammatory
condition of the salivary glands.
 ischemia of the salivary tissue that leads to local
infarction
 predisposing factors:
 Traumatic and Dental injuries
 Ill-fitting dentures
 Upper respiratory infections
 Adjacent tumors
 Previous surgery

40. Clinical Features
 75% of all cases occur on the posterior hard palate.
 Adults.
 Males are affected twice as often as females.
 initially appears as a nonulcerated swelling, often associated
with pain or paresthesia.
 Within 2 - 3 weeks, necrotic tissue sloughs out, leaving a
craterlike ulcer

41. Early lesion
demonstrating
swelling of the
posterior lateral hard
palate.
Later-stage lesion
showing craterlike
defect of the
posterior palate

43. Histopathologic Features
 acinar necrosis
 squamous metaplasia of the salivary ducts.
 pseudoepitheliomatous hyperplasia of the overlying
epithelium
 The lobular architecture of salivary glands is preserved

44.  Necrotic mucous acini. and adjacent ductal squamous
metaplasia

45. Treatment
 Once the diagnosis has been established, no specific
treatment is indicated
 The lesion typically resolves on its own, with an
average healing time of 5 - 6 weeks.

47.  is a rare inflammatory condition of minor salivary
glands.
 several etiologic factors have been suggested:
 actinic damage
 Tobacco
 poor hygiene
 heredity.

48. Clinical Features
 lower lip vermilion .
 middle-aged and older men.
 swelling and eversion of the lower lip as a result of
hypertrophy and inflammation of the glands.
 The openings of the minor salivary ducts are inflamed
and dilated with muco-purulent secretions.

49. Prominent lower lip with inflamed openings of the minor
salivary gland ducts.

50. Clinical Features
Classified into three types:
 Simple
 Superficial suppurative (Baelz's disease)
 Deep suppurative (cheilitis glandularis apostematosa).
increasing inflammation, suppuration, ulceration.

51. Histopathologic Features
 chronic sialadenitis and ductal dilatation.
 dysplastic changes may be observed in the overlying
surface epithelium

52. Treatment
 Vermilionectomy (lip shave)

54.  unusual non-inflammatory disorder characterized by
salivary gland enlargement particularly involving the
parotid gland.
 excessive accumulation of secretary granules, with
marked enlargement of the acinar cells.

55. ENDOCRINE
Acromegaly
Diabetes
Pregnancy
Hypothyroidism
NUTRITIONAL
Bulimia
Anorexia nervosa
Cirrhosis
Alcoholism
malnutrition
NEUROGENIC
MEDICATIONS
Psychotropic
Antihypertensive
Sympathomimetic

56. Clinical Features
 slowly swelling of the
parotid glands, which may
or may not be painful.
 usually bilateral, but it
also can be unilateral.
 Decreased salivary
secretion may occur.

57. Radiographic Features
 Sialography
demonstrates a "
leafless tree" pattern,
which is thought to be
caused by compression
of the finer ducts by
hypertrophic acinar
cells .

58. Histopathologic Features
 hypertrophy of the acinar cells sometimes 2-3 times
greater than normal size.
 The nuclei are displaced to the cell base, and the
cytoplasm is engorged with zymogen granules.
 In cases associated with long-standing diabetes or
alcoholism, there may be acinar atrophy and fatty
infiltration.

60. Treatment
 control of the underlying cause.
 partial parotidectomy

62.  excessive salivation with drooling.
 may lead to macerated sores around the mouth, chin,
and neck that can become secondarily infected.

63. causes
local irritations
new dentures
ill-fitting dentures
aphthous ulcersrabies
Gastroesophageal reflux disease
medications
Cholinergic agonists
antipsychotic
heavy-metal poisoning
poor neuromuscular control
Parkinson disease
cerebral palsy
resection of the mandible
Mental retardation

64. Treatment
 management of the gastroesophageal reflux
 Anticholinergic medications