best slides for UG seminar

1. Pathogenesis of PemphigusPathogenesis of Pemphigus
and Candidiasisand Candidiasis
Presented by
Nakul Bista
BDS Final
Year

2. PemphigusPemphigus
group of auto immune blistering disease of the skin and mucous membrane
characterised histologically by intra-epidermal blisters and immunologically by
finding circulating immunoglobulin G(IgG) autoantibody directed against the
cell surface of keratinocytes.
Pemphigus derived from greek word, ‘Pemphix’ - meaning bubble or blister.

3. Pathogenesis
Auto antibodies bind to Desmoglein 3 and Desmoglein 1
Inhibits molecular interaction responsible for adherence of
keratinocytes
Split develops in the epithelium
Blister formation
Proteolytic cleavage of desmosomal cadherins (Desmogleins and Desmocollins) by the
Auto-antibodies productions.
Desmoglein Compensation Hypothesis:This theory states that one Desmoglein
can compensate for the loss of function of another Desmoglein, induced by
Desmoglein specific auto-antibodies.

4. Basal cell layer
Hemidesmosomes
Desmosomes
Anchoring Fibrils
Basement Membrane
Connective Tissue
Desmosomes
Lamina densa
Lamina lucida
Epithelial Attachment Apparatus

6. antibodies directly interfere with
desmoglein trans-interaction
antibody binding triggers intracellular signalling pathways,
which indirectly results in loss of desmoglein-mediated
binding
Proteolytic cleavage of Desmogleins

7. Desmoglein compensation HypothesisDesmoglein compensation Hypothesis

8. Skin Oral mucosa
superficial split

9. Oral mucosaSkin
Supra-basilar split

10. Oral mucosaSkin

12. Direct Immunofluorescent
Stained with fluorescein-conjugated anti-human Immunoglobulin antibodies

13. CandidiasisCandidiasis
Infection of the skin, mucosa, and rarely of the internal organs caused by
yeast like fungal organism- Candida albicans.
Other species- C.tropicalis, C.krusei, C. glabarata, C. dubliniensis

14. NomenclaturesNomenclatures
Yeast: Round to oval unicellular fungi which reproduce by budding or
fission
Yeast like fungi: yeast which grow partly as yeast and partly as chains of
elongated budding cells joined end to end forming pseudo-mycelium.
Hypha: elongation of yeast producing a tubular thread like structure.
Mycelia: tangled mass of hyphae
Mould: Fungi which form mycelia

15. Yeast
Yeast like
Pseudo-hyphae
Hypha
Mycelia

16. Candida albicansCandida albicans
Candida albicans is a unicellular, oval-shaped diploid fungus that lives on
various mucosal surfaces of the body, including the oral cavity,
gastrointestinal tract, and vaginal mucosa.
the organism is dimorphic and changes from one morphological form to the
next in different environmental conditions.
Normal room temperatures or even anaerobic conditions favour the yeast
form of the organism.
Under physiological conditions (body temperature, pH, and the presence of
serum) it may develop into a hyphal form called pseudohyphae
an overgrowth of the invasive, multicellular filamentous pseudohyphae form
results in the fungal infection.

17. Periodic- acid Schiff Stain showing tubular hyphae of Candida albicans

18. PathogenicityPathogenicity
One of the virulence factor of Candida albicans is its use of cell wall adhesins.
Adhesin proteins promote the binding of the organism to host cells via hydrophobic
interactions.
This reduces the level of yeast clearance from the body under normal immune
regulation.
Following morphogenesis into invasive filaments, C. albicans penetrates host mucosal
surfaces.
The polymorphic growing pattern helps the yeast invade host tissue by secreting
various degradative enzymes, including various proteinases, aspartyl proteases, and
phospholipases.
Phenotypic switching also plays a role in altering the yeast's adherence properties,
antigen expression, and tissue affinity.

19. Early events in the pathogenesis of candidiasis

20. Pathogenesis of Candidiasis
Candida is an opportunistic organism.
It coexists in our bodies with many species of bacteria in a competitive balance.
Other bacteria act in part to keep candida growth in check in our body ecology . . .
unless that balance is upset.
When health is present, the immune system keeps candida proliferation under
control; but when immune response is weakened, candida growth can proceed
unhindered.
• Candida is not the problem, the problem is a compromised immune system
that fails to control the candida.

21. Predisposing factorsPredisposing factors
Acute and chronic diseases like Diabetes mellitus and Anemia
Immunodeficiency like AIDS
Nutritional deficiency like Fe, selenium, etc
Prolonged used of Antibiotics, corticosteroids and cytotoxic drugs.
Radiation therapy
Old age, infancy and in pregnancy
Prolonged hospitalisation for chronic illness.

22. Oral candidiasis

23. SummarySummary

24. antibodies directly interfere with
desmoglein trans-interaction
antibody binding triggers intracellular signalling pathways,
which indirectly results in loss of desmoglein-mediated
binding
Proteolytic cleavage of Desmogleins
Pemphigus

25. Desmoglein Compensation Hypothesis

26. CandidiasisCandidiasis
Stages Events
Stage I
(Colonisation)
Epithelial Adhesion
Nutrient Acquisition
Stage II
(Superficial infection)
Epithelial Penetration
Degradation of host proteins
Stage III
(Deep Seated infection)
Tissue penetration
Stages IV
( Disseminated
infection)
Endothelial Adhesion

27. Candida albicans - ability to bind to host
Production of Specific enzymes
Phenotype switching(yeast to hypha morphogenesis)
Immune modulating effects
Candida albicans binding to host cell

28. References:
Neville, Damm, Allen, Bouquot; Oral and Maxillofacial Pathology;3rd
Edition;
Saunders
Shafer, Hine,Levy; Shafer’s Textbook of Oral Pathology; 6th
edition; Elsevier
www.ppdictionary.com
www.becomehealthynow.com
www.ncbi.nlm.nih.gov