• Kaposi sarcoma (KS) is an indolent angio-proliferative spindle-cell tumor derived from endothelial and immune cells infected with human herpes virus type 8 (HHV-8)[1]
• It is a multifocal neoplasm
• This is a systemic angiomatosis of malignant evolution which is primarily manifested as multiple vascular nodules in the skin and the organs
• It was first described by Moritz Kaposi, a Hungarian dermatologist in 1872[2]
• It is the most common malignancy in HIV patients
• It is identified as AIDS defining illness

• Etiology:
  • HHV8
  • Sustained by cytokines and growth factors
  • It leads to angioproliferation especially in skin.
  • HIV is a predisposing factor to KS.
  • It spreads mainly through saliva, such as during sexual contact or in interactions between a mother and child.
  • People with healthy immune systems can carry the virus without any problems. But it triggers cancers in people with weakened immune systems

• Pathology:
  • HHV-8 invades endothelial cells causing lytic and/or latent infection of the spindle shaped endothelial cells
  • Endothelial cells infected with HHV8 undergo altered lymphatic differentiation and manufacture cytokines creating a favorable environment for angiogenesis
  • Spread to viscera by dissemination of the involved lymph nodes

• Epidemiology and survival rate:
  • It occurs more in men.
  • HIV-1 associated Kaposi’s sarcoma has a high occurrence in homosexual men of over 30%. Overall, almost 75% of people who have KS live at least 5 years after diagnosis. If the cancer hasn’t spread, about 82% live at least 5 more years. In people whose cancer has spread to nearby areas, the 5-year survival rate is 60%. The rate is 38% if the cancer has spread farther away

• Origin: Endothelial cells

• Clinical:
  • Early lesion – Blue flat macule
  • Late lesion – Nodular red blue mass

Picture

• Types:

	Epidemiology	Age	Site	Prognosis
Classical	Mediterranean	Old men	Skin Lower extremities	Fair prognosis
Endemic	Africa	Children and adults	Skin Extremities	Fair prognosis
Immunodeficiency	HIV and transplant patients	Young adults	Skin Mucosa Internal organs	Poor prognosis

• Diagnosis:
  • P24 ELISA
  • Viral load
  • CD4 count
  • CD4 : CD8
  • PCR
  • HHV8 immunohistochemistry

• Histology: Neoplastic proliferation of endothelial cell origin

• Management:
  • The chemotherapy most commonly used for KS is Interferon alpha with didanosine for slowly progressive disease.
  • Radiation therapy-for skin lesions.
  • In AIDS-related Kaposi’s sarcoma, the first step in treatment is to start or switch to an antiviral drug (ART) combination that will reduce the amount of the virus causing AIDS.
  • EG. Chemotherapeutic drugs (Doxorubicin and paclitaxel) with ART.
  • Although, KS remains to be controlled than cured.
  • Sclerotherapy eg alcohol, propanol, Vinca-alkaloids

• Prevention:
  • There’s no vaccine to protect against HHV-8.
  • Avoid unprotected sex.
  • Avoid injecting drugs with used needles.
  • Medications called pre-exposure prophylaxis can also make you less likely to get HIV.
  • If you have HIV, antiretroviral therapy (ART) should prevent KS, especially if you start it when your CD4 count is still high. If you’ve had an organ transplant, some anti-rejection drugs can also lower your chance of getting KS

• Etiology:
  • Tobacco, smoking
  • Age 50+

• Clinical: Persistent red patch

• Histology: Dysplasia

• Management:
  • Biopsy
  • Close patient follow up

Pictures

Benign proliferation of fibroblasts and multinucleated giant cells (osteoclastic) occurring almost always in the jaws

Peripheral giant cell granuloma

• Gingival overgrowth
• Multinucleated giant cells

• Etiology:
  • Trauma
  • Chronic irritation
  • Not by hormones/drug

• Location:
  • Exclusively gingival
  • Size < 2cm

• Clinical:
  • Pedunculated/ sessile swelling – various size
  • Dark red colour
  • Typically ulcerated

• Radiograph:
  • Saucerization/ spooning
  • Superficial erosion of alveolar bone

• Histology: 
  • Foci of multinucleated osteoclast-like giant cells
  • in cellular, richly vascular stroma of plump spindle shaped cells
  • Hyperplastic fibroblasts

• Management: 
  • Surgical excision
  • Full mouth scaling
  • Underlying bone curetted

• Recurrence: Some, no malignant potential

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Central giant cell granuloma

Called central giant cell granuloma (CGCG) if it lies within the jaw bone

Common sites: Mand > max, ant > post

Radiology: Poorly defined radiolucency.

Histology: Fibroblastic matrix + variable numbers and sizes of giant cells.

Management: Excision + calcitonin (osteoblast inhibitor)

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• Exuberant connective tissue proliferation
• Misnomer – No pus or granulation

• Etiology:
  • Trauma
  • Chronic irritation
  • Female reproductive hormones/drugs

• Epidemiology: Females of child bearing age

• Clinical:
  • Soft deep red purple swelling
  • Often ulcerated

• Location:
  • Predominantly gingival
  • Traumatized soft tissues

• Histology:
  • Solid sheets of endothelial cells ± canalization
  • Numerous small vessels + large dilated thin walled vascular spaces
  • Hyperplastic granulation tissue

• Management: Excision

Picture

Type	Hemangioma	Vascular malformations
1. Definition	Hamartoma endothelial cell proliferation	Errors in blood vessel morphogenesis
2. Elements	Increased number of capillaries/ sinusoidal spaces	Mix of arteries, veins and capillaries
3. Classification	– Superficial (capillary) – Deep (cavernous) – Compound (both)	1. Simple lesion a) Low flow: – Capillary malformation – Venous malformation – Lymphatic malformation (Lymphangioma) b) High flow: – Arterial malformation 2. Combined lesions – AV malformation – Lymphovenous malformation
4. Growth	Rapid congenital growth	Grows with patient
5. Boundaries	Circumscribed, rarely affecting bone	Poorly circumscribed, may affect bone
6. Thrill & bruit	No	May have
7. Involution (shrink)	Spontaneously Responds to oral steroids	Does not involute
8. Resection	Persistent lesions resectable	Difficult – surgical hemorrhage
9. Recurrence	Uncommon	Common

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Hemangioma

Clinical:

• Purple, flat/nodular lesion – blanch on pressure
• Painless swelling
• Resorb overlying bone
• Bleeds
• Loosens teeth

Associated syndromes:

• Sturge Weber syndrome
• Rendu Osler Weber syndrome

Diagnosis: Angiogram hemangioma – in head and neck, inject radiopaque material into external carotid artery

Radiology:

• Well circumscribed radiolucency
• Unilocular or multilocular (honeycomb appearance)

Histology:

• Fibrous connective tissue network – contains endothelial lined capillaries containing RCB
• Sinusoids with endothelial cells

NB:

1. Infantile hemangioma

• Superficial overlying patch of redness
• Appears weeks/months after birth
• Natural course:
  • 1. Proliferate – first year
  • 2. Involuting – few years
  • 3. Involuted – most resolved by age 10

2. Congenital hemangioma

• Present at birth – blue/gray hue with pale halo

• RICH – Rapidly involuting congenital hemangioma
  • Reach maximum size by birth and involute within 12-18 months
• NICH – Non involuting congenital hemangioma
  • Continue to grow in size in proportion to patient and do not involute
• PICH – Partially involuting congenital hemangioma
  • Evolve from RICH to persistent NICH like lesions

• Complications: Ulceration, bleeding, infection, obstruct/displace organs

Management:

1. Watchful neglect – if congenital, most involute
2. Surgical excision – contraindicated in large lesions
   • Need for surgery: Trauma, hemorrhage, ulceration, 2ry infection, psychosocial effect
3. Laser therapy
4. Pharmacologic – steroids, propranolol, vincristine
5. Sclerotherapy – induction of fibrosis to control bleeding with absolute (95%) alcohol and then surgical removal
   • Sclerosants: Doxycycline, bleomycin, OK-432, sodium tetradecyl sulphate
6. Embolic therapy
7. Cryotherapy

AKA Hereditary hemorrhagic telangiectasia

• Etiology: AD – Dilation of small blood vessels on skin, mucosa and viscera (lungs, brain, liver)

• Clinical:
  • Nose bleeds
  • Lesions on lips, nose, finger, skin – especially in sun exposed areas

Hereditary

1. Leukoedema

Incidental finding in non Caucasians

• Clinical: Generalized opacification on buccal mucosa, symmetrical

• Histology:
  • Parakeratosis
  • Acanthosis
  • Basket weave appearance – intracellular edema of stratum spinosum
  • Enlarged cells + pyknotic nuclei

• Management: No intervention needed

Picture

2. White sponge naevus

• Etiology: AD, Keratin 4 and 13 point mutations

• Clinical:
  • White areas, lack sharp borders
  • Spongy white lesion
  • Other mucosal surfaces
  • Symmetrical

• Histology:
  • Parakeratosis
  • Acanthosis
  • Basket weave appearance
  • Hyperkeratosis
  • Marked spongiosis

• Management: No intervention needed

Picture

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Reactive

1. Frictional keratosis

• Etiology:
  • Chronic rubbing or friction against a mucosal surface
  • Ill fitting dentures or prosthesis, line of occlusion – Linea alba

• Histology:
  • Hyperkeratosis
  • Chronic inflammatory cells in epithelium

• Management: Observe for any clinical change that may suggest neoplastic change

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2. Nicotine stomatitis

• Etiology: Smoking

• Clinical:
  • Keratin opacification of palate
  • Inflamed minor salivary glands (reddened and enlarged)

• Histology:
  • Hyperkeratosis
  • Inflamed minor glands
  • Epithelial hyperplasia

• Management:
  • Encorage patient to quit
  • Observe for neoplastic changes

Picture

3. Hairy leukoplakia

• Etiology:
  • EBV
  • HIV, Immunosuppression

• Clinical:
  • Lateral surface of tongue in male homosexuals
  • Flat plaque like of filiform (corrugated)

• Histology:
  • Hyperkeratosis
  • Viral cytopathy – Inclusion bodies in superficial cells of epithelium
  • Ballooning degeneration of cells
  • Scanty subepithelial infiltrate and Langerhans cells

• Management:
  • Acyclovir, ganciclovir
  • Tretinoin
  • Podophyllum

Picture

4. Burns

• Etiology:
  • Thermal burns
    • Dorsum of tongue, palate – Hot food/drink
    • Erosive lesion – erythematous border surrounding white damaged mucosa
  • Chemical burns:
    • Dorsum of tongue, palate – toxic chemical/ suicide
    • Muccobuccal fold: Etching process, aspirin placed near decayed tooth
    • Mild white filmy desquamation in oral mucosa

• Clinical:
  • Transient non keratotic appearance
  • Superficial membrane composed on coagulated tissue within inflammatory exudate

• Histology:
  • Inflammatory infiltrate
  • Coagulative necrosis of epithelium

• Management:
  • Heal without scarring in 7-10 days
  • Palliative care
  • Topical anesthetics (benzocaine gel)
  • Topical corticosteroids (triamcinolone ointments)
  • Bonjela
  • Sodium bicarbonate mouthwash

Picture

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Preneoplastic and neoplastic

1. Actinic cheilitis

• Etiology: Chronic exposure to the sun (UVB rays)

• Clinical: Accelerated tissue degeneration of vermillion of lips

• Histology:
  • Hyperkeratotic epithelium
  • Atrophic epithelium
  • Basophilic change of collagen
  • Telangiectasia

• Management: PABA lip balm (para-aminobenzoic acid)

Types of chelitis

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2. Leukoplakia

• Etiology:
  • Tobacco
  • Alcohol
  • Nutrition deficiency
  • Idiopathic
  • Age: 40+

• Clinical:
  • White patch on oral mucosa that cannot be scraped off
  • Vestibule buccal > palate, alveolar ridge, lip, tongue, floor of mouth

• Histology:
  • Hyperkeratosis
  • Dysplasia
  • Carcinoma in situ

• Management: 10 – 15% turn malignant

Picture

3. Lichen planus

• Etiology:
  • Chronic mucocutaneous disease
  • Abnormal cellular adhesion molecules (CAM) – bind to T-lymphocyte receptors (LFA) – which destroy skin and mucosal tissue
  • Therefore lymphocytic destruction of basal keratinocytes

• Subtypes:
  • Reticular
  • Plaque like
  • Atrophic
  • Erosive/ulcerative
  • Bullous

• Histology:
  • Orthokeratosis/ parakeratosis
  • Acanthosis
  • Epithelial atrophy
  • Missing rete-ridges/ saw tooth appearance

• Diagnosis: +ve for fibrinogen immune fluorescence

• Management: Long term follow up

• NB: Koebner phenomenon – occurs in lichen planus, warts and vitiligo

Picture

4. Oral submucous fibrosis

• Etiology: Areca nut chewing, genetic trait

• Clinical:
  • Stiffnes in oral mucosa – limits mouth opening
  • Epithelial atrophy
  • Fibrosis of subepithelial connective tissue

• Histology:
  • Severe epithelial atrophy and dysplasia
  • Hyperkeratosis, no retepegs

• Management: Can transform to malignancy, long term follow up

Picture

5. Lupus erythematosus

• Etiology: Autoimmune disease, affects humoral and cell mediated immunity

• Subtypes:
  • Acute/ Systemic (SLE)
  • Subacute (intermediate features)
  • Chronic/ Discoid

• Histology:
  • Keratosis
  • Epithelial atrophy
  • Basal cell loss
  • Subepithelial + perivascular lymphocyte infiltrate

• Direct immunofluorescence (DIF): Granular/ linear basal membrane deposits of IgG, IgM, IgA, C3 and fibrinogen

	Discoid/ Chronic	Systemic/ Acute
Organs affected	Skin Oral lesions	Skin Oral Heart Kidney Joints
Symptoms	Local only	Fever Malaise Weight loss
Serology	No detectable antibodies	+ve antinuclear antigen (ANA) Anti DNA antibodies
Management	NSAIDS Topical cortiosteroids	NSAIDS Systemic corticosteroids

Picture

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Infective

1. Candidiasis

• Etiology: Normal flora C. albicans turns pathogenic

• Pathology:
  • Adhesion using molecules – lectins, integrins, mannose containing proteins – bind to lectin like molecules on epithelial cells
  • Produce toxins – aspartyl proteases
  • Enhance survival by transitioning between: Yeast blastospore form ↔ Hyphae form

• Diagnosis:
  • Histology: Basic PAS (Periodic acid–Schiff) – shows candidal hyphae/ blastospores
  • Germ test tube – Culture at 37°C in serum for 3 hours – hyphae growth

• Management:
  • Topical: Nystatin, clotrimazole
  • Systemic – Fluconazole, ketoconazole

• Predisposing factors:

1. Systemic antibiotics
2. Immunodeficiency – infancy/ acquired
3. Xerostomia
4. Poor oral hygiene
5. Endocrine disturbance – DM, pregnancy, hypoadrenalism, hypoparathyroidism
6. Corticosteroids

Mnemonic: SIXPEC

• Types:

1. Acute: Pseudomembranous (yellow/white) or erythematous lesion (red and painful)

• Extreme age
• Immunosuppressed
• Cancer therapy

2. Chronic: Erythematous or hyperplastic lesions

• Denture sore mouth in 65% geriatric denture wearers

3. Mucocutaneous: Underlying systemic disease

• 1. Localized
• 2. Familial
• 3. Syndrome associated

4. HIV associated

5. Others:

• Angular chelitis
• Median rhomboid glossitis Picture

Picture

2. Hairy leukoplakia

3. Koplik spots

• Etiology: Complication of measles (paramyxoviridae)

• Clinical:
  • White spot < 1cm in diameter in children
  • Precedes maculopapular rash of measles

• Histology: Superficial necrosis + neutrophilic inflammatory infiltrate

• Management: Supportive, antipyretics

Picture

4. Syphilis

• Etiology: 2ry syphilis can turn malignant

• Clinical:
  • Atrophic epithelium
  • Glossitis

• Histology: Atrophic epithelium

More notes

Picture

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Others

1. Ectopic lymphoid tissue/ fordyce granules

• Etiology: Ectopic sebaceous glands

• Clinical:
  • Yellow white elevations on:
    • Post-lat aspect of tongue
    • Buccal mucosa
    • Upper lip vermillion

Picture

2. Geographic tongue

AKA Migratory glossitis, erythema migrans

• Etiology:
  • Aggravated by stress
  • Irritated by spicy food

• Clinical: Keratosis on dorsum of tongue ± fissuring

• Histology:
  • Atrophic filiform papillae
  • Hyperkeratosis
  • Dense inflammatory infiltrate
  • Acanthosis

Picture

3. Hairy tongue

• Etiology:
  • Chronic smoking
  • Broad spectrum antibiotics

• Clinical:
  • Overgrowth of filiform papillae on tongue
  • Colonization by chromogenic bacteria – change in colour of papillae

• Management:
  • OHI
  • Sodium bicarbonate

Picture

Exogenous pigmentation

1. Accidental:

• Foreign substance – Pencil graphite

2. Iatrogenic:

• Amalgam tattoo:
  • Condensation of mercury in abraded gingiva/breakage of filling
  • Histology: Dark granules along collagen bundle + multinucleated cells

• Chlorhexidine mouthwash:
  • Yellow brown on surface of oral tissues and surface of teeth (cervical + interproximal)

3. Drugs and heavy metals:

• Lead & bismuth – blue black deposits along gingival margin

4. Localized:

• Hairy tongue – green brown on dorsum, overgrowth of filiform papilla by chromogenic bacteria
• More under white lesions
• Click here for picture

5. Superficial staining of oral mucosa:

• Topical medications
• Smoking
• Tobacco
• Foods/drinks

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Endogenous pigmentation (melanotic lesions)

1. Developmental causes:

• Racial pigmentations
• Naevi/mole
• Peutz-Jeghers syndrome
• Polyostotic fibrous dysplasia
• Neurofibromatosis

2. Acquired causes:

• Systemic disease – Addison, HIV
• Smoking
• Hyperkeratosis and chronic inflammation/trauma
• Drugs (minocycline)
• Idiopathic oral melanotic macules
• Lentigo simplex

3. Malignant causes:

• Malignant melanoma
• Melanotic neuroectodermal tumor of infancy

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Other endogenous pigmentation

• Blood breakdown products and other disturbances of iron metabolism

1. Hemoglobin: Blue, red, purple

• Kaposi’s sarcoma
• Varix/hemangioma
• Hereditary hemorrhagic telangiectasia (HHT)

2.Hemosiderin/bilirubin: Brown

• Ecchymosis
• Petechia
• Hemochromatosis
• Varix/hemangioma

3. Melanin: Brown, black, grey

• Melanotic macule
• Basilar melanoma
• Naevus
• Melanoma

Oral pigmentations:

• Exogenous
• Endogenous
• Other

White lesions:

• 1. Hereditary:
  • Leukoedema
  • White sponge naevus
• 2. Reactive:
  • Frictional keratosis*
  • Nicotine stomatitis*
  • Hairy leukoplakia
  • Burns
• 3. Preneoplastic & neoplastic:
  • Actinic chelitis
  • Leukoplakia
  • Lichen planus
  • Oral submucosus fibrosis
  • Lupus erythematous
• 4. Infective:
  • Candidiasis
  • Hairy leukoplakia
  • Koplik’s spots
  • Syphilis
• 5. Other:
  • Ectopic lymphoid tissue/ fordyce granules
  • Geographic tongue
  • Hairy tongue

* Observe for neoplastic changes

Red-blue lesions:

1. Extravascular:

• Petechia (1-2mm) – reduced platelet/clotting factors
• Ecchymoses (1-2cm) – reduced platelet/clotting factors
• Gingival enlargement – leukemic infiltrates
• Gingival inflammation/hyperplasia – poor oral hygiene
• Excessive gingival bleeding – reduced platelet/clotting factors
• Refractory gingivitis – leukemic infiltrate + reduced platelet/clotting factors

2. Intravascular:

• 1. Congenital vascular anomalies:
  • Hemangioma
  • Vascular malformation
  • Sturge-Weber syndrome
  • Rendu-Osler-Weber syndrome
• 2. Reactive lesions:
  • Acquired vascular malformations e. varices – focal dilation of single vein
  • Pyogenic granuloma
  • Peripheral giant cell granuloma
• 3. Neoplasms:
  • Erythroplakia
  • Kaposi’s Sarcoma
• 4. Metabolic endocrine conditions:
  • Vitamin B deficiency
  • Iron deficiency anemia
  • Pernicious anemia
  • Burning mouth syndrome
• 5. Immunological abnormalities:
  • Plasma cell gingivitis
  • Drug reaction and contact allergies
• 6. Infectious conditions:
  • Scarlet fever

Brown melanotic lesions:

1. HIV oral melanosis
2. Drug induced melanosis
3. Physiological pigmentation
4. Oral melanotic macule
5. Melanoma
6. Pituitary hyperfunction
7. Other hormonal imbalance
8. Naevus
9. Smokers melanosis

Syndromes with orofacial pigmentations

1. Addison’s disease
   • Chronic adrenal insufficiency
   • Clinical:
     • Bronzing of skin
     • Pigmentation of mucosa
     • Decreased cardiac activity
     • Malaise
     • Sever anemia
2. Peutz-Jegher syndrome
3. Neurofibromatosis
4. Albright syndrome

Etiology:

• Immunologic disease – Lymphocyte mediated destruction of exocrine glands – Xerostomia and keratoconjunctivitis sicca
• Lymphocytic infiltration and acinar destruction of lacrimal and salivary glands
• Autoimmune destruction in patients with the following HLA types:
  • Primary: HLA-B8, HLA-DR3
  • Secondary: HLA-DR4

(HLA – Human leukocyte antigen)

• This induces production of numerous autoantibodies:
  • Rheumatoid factor
  • Antinuclear antibodies (ANA)
  • Anti-Sjogren syndrome A (SS-A)
  • Anti-Sjogren syndrome B(SS-B)

Epidemiology:

• 90% women
• Swedish women
• Onset at 50 years

Classification:

• Primary:
  • Keratoconjunctivitis sicca (dry eyes)
  • Xerostomia (dry mouth)
• Exocrine glands only
• 80% unilateral/ bilateral salivary gland swelling

• Secondary:
  • Keratoconjunctivitis sicca (dry eyes)
  • Xerostomia (dry mouth)
  • Autoimmune condition, eg.:
    • Rheumatoid arthritis
    • SLE
    • Systemic sclerosis
    • 1ry biliary cirrhosis
• Exocrine glands + systemic/autoimmune disease
• 30-40% unilateral/ bilateral salivary gland swelling
• Rule out lymphoma

Clinical presentation:

Extreme tiredness due to multisystem effects

1. Glandular manifestations:

• Salivary – Xerostomia
• Lacrimal – Xerophthalmia
• Skin – Xeroderma
• Respiratory tract – Nasal dryness, sinusitis, tracheitis
• Pharynx and GIT – Dysphagia, atrophic gastritis, pancreatitis
• Oral cavity – Salivary gland enlargement, glossitis, mucositis
• Reproductive – Mucosal dryness

2. Extraglandular manifestation:

• Joints – Arthritis
• Skin – Purpura, Raynaud’s phenomenon
• Liver – 1ry biliary cirrhosis
• Renal – Renal tubular defects
• Endocrine – Thyroiditis
• Neurological – Neuropathy
• Hematological – Decreased RBC, WBC, Platelets
• Immunological – Autoantibodies,

Complications:

1. Candidiasis
2. Ascending sialadenitis
3. Pseudolymphoma, B-cell lymphoma
4. Dental caries

Diagnosis:

1. Schirmer’s test:

• 5 x 35mm strips of red litmus paper – place inside lower eyelid in inferior fornix
• Leave for 5 minutes – assess how far the tears have travelled
• +ve = lacrimation of ≤ 5mm
• 85% specific and sensitive

2. Sjogren’s lip biopsy:

• Shallow horizontal incisions made of 1.5 to 2cm on either side of inner lip (numb with LA)
• Approx 5-7 glands removed with sterile tweezers
• Close incisions with resorbable suture
• Assess number of foci of lymphocytes/4mm²/gland

3. Sialography:

• Snow storm or cherry blossom appearance

4. Scintiscanning:

• Technetium-99m pertechnetate

5. Serology:

• SS-A
• SS-B
• ANA
• Anti-dsDNA

6. FBC:

• Anemia
• Leukoplakia
• Eosinophilia

Histology:

• Replacement of gland parenchyma by inflammatory infiltrate with remnants of epimyoepithelial cells
• Therefore there is:
  • Lymphocytic infiltration
  • Acinar atrophy
  • Proliferation of duct epithelium
  • Epimyoepithelial islands

Management:

• Salivary substitutes/ sprays
• Sugar free gum
• Sialagogue eg. pilocarpine
• No alcohol/ tobacco
• Avoid xerostomic meds
• Palliative care + artificial saliva/tears

NB: Normal saliva flow 1-2 ml per min. Sjogren’s: 0.5 ml/min or less

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