"Other" Oral Inflammatory Conditions Flashcards
1
Q
What is a granuloma?
A
- Focus of chronic inflammation.
- Microscopic aggregation of activated epithelioid macrophages fused to form giant cells, surrounded by lymphocytes +/- plasma cells +/- a rim of fibroblasts and connective tissue
2
Q
What are orofacial granulomatosis?
A
- Unexplained granulomatous inflammatory lesions
* Non-specific diagnosis of exclusion
3
Q
Subtypes of orofacial granulomatosis…
A
• Cheilitis granulomatosis - Limited to lips • Melkersson-Rosenthal Syndrome - Swells of face, oral mucosa, etc - Fissured tongue - Unilateral facial nerve paralysis
4
Q
Clinical features of orofacial granulomatosis
A
- Lips affected more than other parts of face
- Swelling: nontender, persistent
- Rare lymphangioma-like vesicles
- Rare cervical lymphadenopathy
- Intraoral edema, ulcers, papules
- Gingival swelling, erythema, pain, erosions
- Buccal cobblestone
- Vestibular linear hyperplastic folds
5
Q
Histology of orofacial granulomatosis
A
- Non-necrotizing granulomas
- Edema, dilated lymphatics, scattered lymphocytes
- Negative for micro-organisms and foreign substances
6
Q
Diagnosis of orofacial granulomatosis
A
• Unexplained granulomatous inflammatory lesions
• OFG is diagnosis of exclusion - known causes of granulomatous lesions must be eliminated:
- Systemic:
• Chronic granulomatous disease
• Crohn's disease
• Sarcoidosis
• Infections (fungi, TB, etc)
- Local
• Chronic oral infection
• Foreign body reactions
• Allergy
7
Q
Management for orofacial granulomatosis include…
A
- Special stains (for microorganisms)
- Polarize microscopy (for foreign material)
- Eliminate chronic inflammatory bowel disease
- Eliminate sarcoidosis
- Look for antigen
- Topical or intralesional corticosteroids
- Clofazimine (antileprosy agent)
- Surgical recontouring (but often recur)
8
Q
Differential diagnosis for fissured tongue
A
- Normal variant
- Inherited condition
- Down syndrome
- Melkersson Rosenthal syndrome
- Erythema migrans-associated
- Plasma cell gingivitis
9
Q
Causes of foreign body granulomas…
A
• Endogenous substances - Keratin - Bony sequestra • Exogenous - Usually birefringent (seen under polarized light) - Sutures - Dental materials
10
Q
Clinical presentation of granulomatous gingivitis
A
- Solitary or multifocal lesions
- On interdental papilla or gingival margin
- Up to 2cm in diameter
- Red macules or enlargements
11
Q
Diagnosis of granulomatous gingivitis…
A
• Rule out:
- Histologically distinctive/specific granulomatous conditions
• Foreign substances
• Deep fungal infections
• Acid fast bacilli
- Systemic granulomatous diseases
• Crohn's
• Wegener
• Sarcoid
• Diagnosis of nonspecific granulomatous gingivitis is made after r/o other diagnoses
12
Q
Histology of granulomatous gingivitis
A
• Foreign particles identified associated with:
- Granulomas = foreign body granulomatous gingivitis
- Nonspecific mucositis
- Lichenoid reaction
• Particles less than 1um may be undetected
• When there are granulomas without particles, diagnosis of nonspecific granulomatous gingivitis can be made after r/o all other diagnoses
13
Q
Etiology of granulomatous gingivitis
A
- Trimming restorations near gingival margin
* Dental prophylaxis paste used too soon
14
Q
Clinical features of Wegener granulomatosis
A
- Probably immune dysfunction
- Starts in upper respiratory tract
- Initially, nasal discharge or sinus pain
- Nasal septum and/or palatal destruction
- May affect lungs and kidneys
- May involve paranasal sinuses, TMJ, or gingivae
- Untreated disseminated cases survive only a few months
15
Q
Treatment of Wegener’s granulomatosis
A
• Cytotoxic drugs
- Especially cyclophosphamide with prednisone
• can achieve long-term survival, even cure
16
Q
Histology of Wegener’s granulomatosis
A
- Necrotizing vasculitis associated with granulomas
- Leukocytoclastic vasculitis
- Diagnosis involves identification of c-ANCA (serum antibodies against cytoplasmic components of neutrophils)
17
Q
Discuss ANCAs as seen in Wegener Granulomatosis
A
• Circulating autoantibodies against a component of granules in cytoplasm of neutrophils
- Serum from patients with vasculities reacts with cytoplasmic antigens in neutrophils - Due to antineutrophil cytoplasmic antibodies - Cause IF patterns in ethanol-fixed neutrophils - One shows cytoplasmic localization of stain (c-ANCA) - Group of autoantibodies against enzymes mainly in azurophilic or primary granules in neutrophils - The most common target antigen is proteinase-3 (PR3), a component of a neutrophil granule
18
Q
Autoantibodies present in Wegener granulomatosis…
A
- c-ANCA: autoantibodies against a component of granules in cytoplasm of neutrophils
- Titers correlate with disease activity
- May be important in pathogenesis
19
Q
Etiology of sarcoidosis
A
• Abnormal immune response to unknown antigen
- Infectious agent
- Environmental factors
• Genetic predisposition
20
Q
Clinical presentation of sarcoidosis
A
- Multisystem disease characterized by non-caseating granulomas in many organs
- Bilateral hilar lymphadenopathy or lung disease in 90% of cases
- Skin and mucous membranes (including nose and mouth)
- Eyes in 25% (blindness rare)
- Also lymph nodes, bone marrow, spleen, liver, kidneys, heart, CNS, parotid glands enlarged in 10-20% (cause of xerostomia)
21
Q
Demographics of sarcoidosis
A
- Incidence varies wildly in countries throughout the world
* In U.S. it affects blacks more than whites, with peak incidence in the fourth decade.
22
Q
Oral lesions in sarcoidosis…
A
• Soft tissue - Salivary gland enlargement --> xerostomia - Submucosal enlargements - Mucosal macules • Intraosseous - Radiolucencies
23
Q
Histology of sarcoidosis
A
• Non-caseating granulomas
- Schaumann bodies (laminated calcifications in giant cells)
- Asteroid bodies in giant cells
24
Q
Laboratory tests for Sarcoidosis…
A
• Elevated: - Angiotensin converting enzyme - Erythrocyte sedimentation rate - Serum calcium - Alkaline phosphatase - Vitamin D (Mnemonic: A SAVE) • Positive Kveim-Siltzbach skin test (but not often performed) • Transbronchial lung biopsy is often used
25
Pronosis for sarcoidosis
* Most patients recover
| * 10-20% succumb to progressive fibrosis and cor pulmonale
26
Treatment for sarcoidosis
* Corticosteroids
* Steroid-sparing agents
* Antimalarial agents
27
Area mostly affected in Crohn's disease
Mainly affects distal small intestine and proximal colon.
28
What is Crohn's disease?
• Inflammatory GI (mainly) disease:
- Non-necrotizing granulomas
- Probably immunologically-mediated
• Abdominal cramping, nausea, diarrhea, etc.
29
Demographics of Crohn's disease
Diagnosis in teens or in people over 60 years of age
30
Oral manifestations of Crohn's disease...
```
• Initial manifestation in some cases
• Diffuse or nodular swellings
• Cobblestone
• Deep linear ulcers in vestibule
- Denture hyperplasia
• Mucogingivitis: patchy red macules and plaques
• Recurrent aphthous ulcers
• Pyostomatitis vegetans
- Manifestation of CIBD
- Multiple pustules
- Intraepithelial abscesses
• Eosinophils +++
```
31
Reactions to physical & chemical agents include...
* Frictional keratosis
* Traumatic ulcers
* Eosinophilic ulcers
* Burns
* Submucosal hemorrhage
* Anticancer therapy
* Reactions to amalgam
* Tobacco
* Cervico-facial emphysema
* Hairy tongue
* Toxic metals
* Drug-related discolorations
32
What is frictional keratosis?
* Chronic mechanical irritation --> frictional keratosis
| * Reversible
33
Clinical types of frictional keratosis
* Linea alba
* Morsicatio
* Toothbrush gingival abrasion
* Irritation including broken teeth, prostheses, and restorations
* Mastication on edentulous alveolar ridge
34
What is linea alba?
* Clinical type of frictional keratosis
* Very common
* White line on buccal mucosa (often bilateral) at level of occlusal plane
* Friction or sucking trauma
35
What is chronic mucosal chewing?
* "Morsicatio buccarum, linguarum, labiorum"
* White plaques with surface shedding
* +/- focal red erosions or ulcers
* Often bilateral
36
Histology of frictional keratosis
• Benign hyperkeratosis +/- other features:
- Ragged surface projections
- Bacterial colonies may coat surface
- Vacuolated spinous cells
37
Clinical features of traumatic ulcers
```
• Cause usually readily identified
• Symmetrical or irregular
• Shallow or deep
• Base usually firm
• Onset abrupt or gradual
• Persist until cause is removed
• Acute ulcers painful but chronic may be non-painful
• Often exhibit a white or yellow surface
- Removable, fibrinopurulent membrane
```
38
Describe an acute traumatic ulcer...
* Pain
* Yellow base, red halo
* History of trauma
* Heals in 7 to 10 days if cause eliminated
39
Describe a chronic traumatic ulcer...
* Little or no pain
* Yellow base, elevated margins (scar)
* History of trauma, if remembered
* Delayed healing if irritated, especially tongue lesions
* Clinical appearance mimics carcinoma and infectious ulcers
40
What are traumatic eosinophilic ulcer or ganuloma?
• Deep ulcer with indurated elevated border
• Clinical resemblance to SCC (or pyogenic granuloma)
• Pain and source of trauma may be lacking
• Most on tongue; may be multiple
• Traumatic eosinophilic granuloma is variant
- Discolored nodule, resembling pyogenic granuloma
41
Histology of traumatic eosinophilic ulcer or granuloma
* Ulcer bed: fibrin and inflamed granulation tissue
* Inflammation extends into underlying tissue
* Deeper inflammatory infiltrate eosinophils and histiocytes (some atypical)
* Inflammatory tissue replaces skeletal muscle
42
What is Riga-Fede disease?
* Variant of traumatic eosinophilic ulcer on anterior ventral tongue of infants
* Chronic mucosal trauma due to lower anterior teeth (natal or neonatal)
43
Types of burns
* Electric burns
* Thermal burns
* Chemical burns
44
Electric burns
• Most electric burns in oral cavity are arc type
- Saliva acts as conducting medium
- Electric arc flows between source and oral mucosa
• Heat up to 3000°C possible with resulting tissue damage
45
Examples of electrical burns
* Chewing on female end of extension cord or biting through live wire
* Biting through live wire
46
Thermal burns
* Most thermal burns in mouth are from hot food/drinks
* Zones of erythema and ulceration +/- necrotic epithelium at periphery
* If swallowed, upper airway swelling --> dyspnea
47
Chemical burns
• Caustic chemicals and medications
- Aspirin, phenol, H2O2, bisphosphonates
- Gasoline, turpentine, rubbing alcohol
• Brief exposure --> superficial white wrinkled appearance
• Longer exposure --> necrosis increases
- Epithelium desquamates --> bleeding connective tissue surface
- Sometimes coated by fibrinopurulent membrane
48
What is "Cotton roll stomatitis"?
* Caustic mat leaks into roll and damages mucosa
| * When dry roll is pulled away, it strips epithelium
49
Histology of burns
* White slough: coagulative necrosis of stratified squamous epithelium
* Level of necrosis depends on duration of contact and concentration of agent
* Connective tissue: acute and chronic inflammatory cells
50
Submucosal hemorrhage
```
• Blood entrapped in connective tissue
• Non-blanching, flat or raised
- Petechiae: minute hemorrhage into mucosa
- Purpura: slightly larger
- Ecchymosis: more than 2 cm diameter
- Hematoma: if it's a mass
• Red to blue to black to green to yellow
• Initial pain
• R/o systemic disease
```
51
Reactions to amalgam includes...
1) Frictional keratosis
2) Pigmented macule (inert)
3) Foreign body reaction
4) Contact hypersensitivity reaction
52
Clinical features of amalgam tattoo
* Black, blue, or grey macules more often than papules
* Shape varies
* Local spread after implantation
* Some visible on radiograph
53
Histology of amalgam tattoo
```
• Dark-brown or black fragments
• Varied tissue reaction
- Inert
- Stained reticular fibers
- Dense fibrous connective tissue
- Chronic inflammatory cells
- Foreign body granulomas
```
54
Reactions to tobacco include...
1) Melanosis
2) Nicotine stomatitis
• Reverse smokers' palate --> SCC: epithelial dysplasia
3) Hyperkeratosis
4) Epithelial dysplasia
5) Invasive SCC
55
Demographics of Smoker's melanosis
* Seen more often in whites than in blacks
| * More often in women than in men
56
What is smoker's melanosis?
* Oral pigmentation (melanosis) is protective reaction against components of tobacco smoke.
* Cigarette smoking: anterior gingivae is most common site
* Pipe smoking: commissures and buccal mucosa
* Reverse smokers: hard palate
57
Etiology of cervicofacial emphysema
```
• Air forced into tissues
• Most linked to surgery
- Difficult extractions
- Sneezing after oral surgery
• Compressed air
- Air-driven hand pieces
```
58
Clinical features of cervicofacial emphysema
* Soft tissue enlargement
* Little pain
* Crepitus (crackling/grating sound)
* Swelling increases if there is 2nd inflammation and edema
* +/- pain, facial erythema, dysphagia, vision defect, mild fever
59
Prognosis and treatment for cervicofacial emphysema
• Usually subsides 2-5 days
- Rarely respiratory distress
• Broad-spectrum antibiotics in some cases
60
Appearance of hairy tongue due to...
Appearance is due to keratin accumulation on filiform papillae and/or increased keratin production or decreased keratin desquamation.
61
Etiology of hairy tongue
```
• Uncertain
• Many affected people are heavy smokers
• Basic problem may be altered oral flora resulting in:
- Proliferation of fungi and chromogenic bacteria
- Papillae overgrowth
• Systemic medications
- Broad-spectrum antibiotics
- Corticosteroids
```
62
Clinical features of hairy tongue
```
• Starts on dorsal midline
• Color due to:
- Pigment-producing bacteria
- Food
- Tobacco
• Asymptomatic (occasional gagging)
```
63
Treatment for hairy tongue
* Identify and eliminate initiating factor
* Brush/scrape tongue with baking soda
* Treat underlying disease
* Little significance, other than annoying to patient, cosmesis
* Bx (biopsy?) rare
64
Predisposing factors of hairy tongue
* Systemic or topical meds
* Heavy smoking
* Debilitation
* Poor oral hygiene
* Radiotherapy
65
Toxic metals include...
* Bismuth
* Lead
* Arsenic
* Cis-platinum
* Silver
66
Lead as a toxic metal...
• Lead solder (plumbing), paint, gas (all now banned)
• Industrial use
• Systemic effects
- Acute: abdominal colic, anemia, fatigue, etc.
- Chronic: affects nervous system, kidneys, bone marrow, bone, teeth
• 90% of lead deposits in bone
67
Clinical presentation of lead in oral cavity...
• Ulcerative stomatitis
• Burton's line: gingival lead line
- Bluish line along gingival margin due to bacterial H2S acting on lead in sulcus --> precipitation of lead sulfide
68
Medicinal heavy metals that are toxic metals include...
Silver was the most common heavy metal employed historically. Others included arsenic, bismuth, cis-platinum.
69
Clinical manifestation of medicinal heavy metals (toxic metals)
```
• Acute and chronic manifestations
• Systemic
• Skin and oral mucosa
• Gingivae:
- Gray to black
- Linear along gingival margin
- Staining proportional to inflammation
- Metal reacts with H2S produced by bacteria
```
70
SYSTEMIC clinical manifestations of silver as a toxic metal
• Systemic:
- Acute: coma, pleural edema, bone marrow failure
- Chronic = argyria
• Subepithelial deposits in skin
• Diffuse gray discoloration especially in sun-exposed sites, nails, sclerae
71
ORAL clinical manifestations of silver
• Oral (may be first sign)
- Slate-blue silver line along gingival margins
• This is 2nd to deposits of Ag and Ag2S (silver sulfide)
- Diffuse blue-black mucosa
72
Drug-related discolorations can be caused by...
```
• Phenolphthalein
• Minocycline
• Tranquilizers
- Chlorpromazine
• Anti-malarials
• Estrogen
• Chemotherapeutic agents
- Cyclophosphamide
• AIDS medications
- AZT
```
73
Mechanisms involved in drug-related discolorations
* Metabolite deposition
| * Melanocyte stimulation
74
Affects of drug-related discolorations
```
(For minocycline?)
• Bones and developing teeth
• Skin and eyes
• Oral mucosa:
- Linear band cervical to facial attached gingiva
- Broad zone on palate
- Lips, tongue
```
75
What happens in immunologic reactions to local agents (stomatitis venenata)?
• Antigens presented to T-cells by Langerhans cell
• 2nd exposure:
- Lymphocytes --> cytokines --> clinical and histologic changes
• Agents: toothpaste, mouthwash, candy, chewing gum, cinnamon, amalgam
76
Clinical features of immunologic reactions to local agents
* Changes occur adjacent to causative agent
* Acute or chronic
* Localized -- isolated allergen
* Widespread -- food, drink, etc
77
Acute contact stomatitis
* Burning
* Red (mild to brilliant)
* +/- edema
* Superficial ulcers (like RAU)
* Vesicles rare
78
Chronic contact stomatitis
* Red or white-adherent
* Focal erosions within these areas
* Some allergens (in toothpastes) --> widespread erythema with desquamation of superficial epithelium
79
What is cinnamon contact stomatitis?
* Cinnamic aldehyde has a hyacinth odor and is often used as a fragrance in perfumes, cosmetics, detergents, and as flavoring in chewing gums, confectionary, ice cream, oral hygiene products and soft drinks.
* Concentration up to 100x normal spice.
* Reactions linked to contact time and frequency
80
Organic compound that gives cinnamon its flavor and odor
Cinnamaldehyde
81
Cinnamaldehyde
* Organic compound that gives cinnamon its flavor and odor
* Pale yelow, viscous liquid that occurs naturally in the bark of cinnamon trees and other species of the genus Cinnamomum
* The essential oil of cinnamon bark is about 90% cinnamaldehyde
82
Clinical features of cinnamon contact stomatitis...
```
• Pain and burning
• Pattern linked to mode of delivery
- Toothpaste: diffuse
• Plasma cell gingivitis
• Erythematous mucositis
- Gum and candy: localized
• White due to hyperkeratosis with ragged surface
- Like morsicatio
• Bilateral buccal mucosa
- Oblong patch
- White on red base +/- ulcer
• Lateral tongue
- Vertically corrugated
```
83
Histology of cinnamon contact stomatitis
Lichenoid and perivascular mucositis
84
What is plasma cell gingivitis?
• 1970s chew gum --> "plasma cell gingivostomatitis"
- Entire gingivae bright red & enlarged
- Cinnamon possible allergen
- Lips dry, atrophic, fissured
- Angular cheilitis
- Tongue red, loss of papillae, enlarged, furrowed
• Recently
- Much less common
- Allergy to specific toothpaste, food, etc (not chew gum)
- Many cases idiopathic
- Lesions often limited to gingivae
85
Epithelium histology of plasma cell gingivitis as caused by 1970s chew gum
* Psoriaform hyperplasia & spongiosis
| * Intense exocytosis with neutrophil microabscesses
86
Lamina propria histology of plasma cell gingivitis as caused by 1970s chew gum
* Dilated capillaries
| * Dense chronic inflammatory cell infiltrate, mainly plasma cells
87
Current histology of plasma cell gingivitis
* Less involvement of epithelium
| * Less dense plasma cells
88
Mucosal allergic reaction to amalgam
* Must rule out toxic reaction, frictionless keratosis, etc.
* True lichenoid hypersensitivity reaction to amalgam (Hg) rare
* Localized
* Clinical and histology like lichen planus: "Lichenoid contact stomatitis"
* Disappears when restoration removed (as does frictional keratosis)
89
Drug induced gingival fibrous hyperplasia
* Numerous medications have been reported to cause this condition
* Those with the strongest association are cyclosporine, phenytoin, and nifedipine
* These agents may interfere with normal intracellular degradation of collagen
90
Nonimmunologic mucosal reactions to systemic medications include...
* Drug-induced gingival fibrous hyperplasia
| * Anticancer therapy
91
Etiology of immunologic mucosal reactions to systemic medications (Stomatitis medicamentosa)
• Triggered by antigenic component (hapten) on drug molecule
• Reaction depends on:
- Immunogenecity of drug
- Frequency of use
- Route of administration
• Mechanisms
- IgE-mediated (type I)
- Cytotoxic (antibody binds to drug already on cell surface) [type II]
- Circulating antigen-antibody complexes (type III)
- CD8 cytotixic T cells and CD4 helper T cells recognize antigens (type IV)
92
Drug-induced allergic changes resemble the following oral mucosal diseases clinically, histologically, and immunologically...
• These drug reactions patterns resemble several oral mucosal diseases:
- Angioedema
- Erythema multiforme
- Anaphylactic stomatitis
- Pemphigus-like
- Intraoral fixed drug reaction
- Lichenoid reaction
- LE-like drug reaction
- Nonspecific vesiculo-bullous or aphthous-like lesions
• These drug reactions are often bilateral
93
Immunology of drug-induced allergic changes
• I.F. studies in most cases do not separate drug reactions from primary vesiculo-ulcerative diseases, with some exceptions:
- In some lichenoid cases, I.I.F. for IgG shows a "string of pearls" due to circulating basal cell cytoplasmic antibody
- LE-like reasons are dsDNA negative with most (not all) drugs [SLE itself is dsDNA positive]
94
Pemphigus like drug reactions
* A variety of drugs have been implicated in the onset of drug-induced pemphigus
* Some of these drugs induce antibody formation, which results in acantholysis via a mechanism identical to that found in idiopathic pemphigus
* Other drugs are postulated to induce acantholysis directly in the absence of antibody formation
95
Lichenoid mucositis
* Lesions with clinical and/or histological resemblance to classical lichen planus
* May exhibit some variation from classical features
* These cases are often drug-related
96
Histology of lichenoid mucositis
* Classical lichen planus +/- other features
* Eosinophils
* Plasma cells
* Deep and perivascular lymphocytic infiltrate
97
What is acquired angioedema?
* IgE-mediated allergic reaction precipitated by drugs or foods
* These antigens --> IgE production
* 2nd antigenic challenge: mast cells bound with IgE release contents
98
Etiology of angioedema
```
• IgE-mediated allergic reaction
- Drugs, foods (nuts, shell fish), plants, dust
• Contact allergies
- Cosmetics, rubber dam, etc
• AD hereditary activated complement
- Type I
- Type II
• Acquired activated complement
• ACE inhibition --> elevated bradykinin
• Other
```
99
Clinical presentation of acquired angioedema
* Rapid onset of diffuse edematous connective tissue swelling
* Painless swelling of lips, face, neck
* Effect on GI or respiratory tracts rare but may be fatal
* Usually subsides in 1 to 2 days
100
Transient lingual papillitis etiology
* Some cases are food allergies
| * Some cases due to friction
101
Clinical features of transient lingual papillitis
```
• Affects fungiform papillae
• Solitary or multiple papules
- Red papules with yellow (ulcerated) cap
• Sensitive or pain (symptomatic)
• +/- fever
• Resolve in days, but may recur
```
102
What is oral reactive lymphoid hyperplasia?
* Discrete nontender submucosal swellings
* < 1cm diameter
* Color normal or yellowish
103
What sites are affected in oral reactive lymphoid hyperplasia?
```
• Foliate papillae lymphoid tissue
• Buccal lymph node
- Freely movable nodule
• Lymphoid tissue aggregates
- Floor of mouth
- Posterior soft palate
• Palatal follicular lymphoid hyperplasia
• Waldeyer's ring lymphoid tissue
```
104
Acute graft v host disease
* Within first 100 days of transplant
* Affects 50% of bone marrow recipients
* Skin mild to severe like "TEN"
* Severe GI symptoms and liver dysfunction
105
Chronic graft v host disease
* Continuation of acute GVHD or starts later than 100 days
* In up to 60% of bone marrow recipients
* Mimics A-I diseases (SLE, Sjogren, etc)
* Skin changes resemble lichen planus or systemic sclerosis
106
Oral changes in graft v host disease occurs in how many cases?
* In 33-75% of acute GVHD
| * In ~80% of chronic GVHD
107
Appearance and histology of oral changes in graft v host disease...
• Lichenoid appearance:
- Histology resembles lichen planus, but inflammatory response is not as intense
- With advanced cases, collagen deposition resembles systemic sclerosis
108
Clinical features of graft v host disease
• Lichenoid appearance
• Burning
• 2nd candidiasis
• Ulcers
• Xerostomia (immune destruction of salivary glands)
- Minor glands show periductal inflammation in early stages with gradual acinar destruction and periductal fibrosis later
