Retention / Stagnation Sites 

Where plaque is found

i.e.- interproximal spaces, gingival margin, fissures

material alba

Alba is latin for white:

Non- bacterial debris that forms film on top of plaque (white color)

dead host cells/ food

How biofilms increase survival of bacteria

1. gene up or down regulation

2. symbiotic relationships 

3. quorum sensing 

Quorum Sensing

Bacterial communication via signaling molecules

Way for bacteria to sense how many bacterial cells are around before a specific gene product (protein) is made

Need a lot of bacteria to make it worth synthesizing and realeasing proteins into ECM

These proteins can be enzymes or virulence factors

Trend in oxygen sources for bacteria that make biofilms 

Start out as facaultative (can grow in O2 and O2 free environments) -> obligate anaerobes because it gets so dense in there

Colonizers for non- pathogenic dental plaque

[Gram positive facaultative]

Early colonizers

Streptococcus sanguinis 

Streptococcus mitis 

Followed by..

Actinomyces

[Gram negative obligate anaerobes] 

Subsequent colonizers: 

Veillonella

Prevotella

Fusobacterium 

Campylobacter

Treponema

Pathogenic Plaque:

Indigenous residents

Opportunistic pathogens

Bacteria that are permenantly in the mouth

When they reach a critical level they become pathogenic

Potential for non-harmful resident bacteria to become harmful = opportunistic pathogens

carious lesion

subsurface demineralization with thin layer of enamel on top

cavitation

when the thin surface of the carious lesion breaks and exposes the deminearlized area

Initiator of dental caries 

Strep mutans

Strep mutans releases this acid 

lactic acid -> decrease in pH

Decrease in pH due to secretion of lactic acid by Strep mutans allows this family of bacteria to come in an dominate 

lactobacillus

property of lactobacillus

acidophillic 

second most common site for caries

interproximal space 

Strep mutans and lactobacillus are:

indigenous and opportunistic

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How is a cavity formed?

When strep mutans exceeds a critical level it creates a subsurface carious lesion by excreting lactic acid. Once the thin surface above the carious lesion is broken a cavity forms. Since buffer cannot reach the area the pH drops and acidophillic lactobacilli come to the area and take over. Lactobacilli then cause further damage to the tooth by degrading the enamel, dentin and then finally the pulp -> can lead to the loss of a tooth!

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Chronic Gingivitis - Clinical Manifestations 

1. enlarged papillae

2. color change

3. blunted gingival margins 

4. loss of stippling 

Chronic Gingivitis vs. Periodontitis 

In gingivitis there is 

1. NO Pain

2. No pocketing

Cause of gingivitis 

Gram negative anaerobic bacteria that release 

EXOTOXINS

Necrotizing Ulcerative Gingivitis 

Compared to chronic gingivitis this IS associated with pain (sharp)

pseudo- membrane- tissue covered with pus and necrotized epithelium

Treponema- causative spirochete 

Hormonal gingivitis 

Prevotella intermedia

increase in estrogen and progesterone increase indigenous populations of Pi -> opportunisitc 

Puberty gingivitis 

hormonal gingivitis, same etiology

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Chronic periodontitis 

periodontal pocket 

loss of attachment 

episodic- periods of active tissue breakdown and periods of no breakdown 

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Organisms that cause periodontitis 

Porphyromonas gingivalis

Treponema denticola 

Tanerlla forsythia

HIV Periodontitis causative agent

Candida 

Aggressive Periodontitis causative agent

Aggregatibacter actinomycetemcomitans

Types of Aggresive Peirodontitis 

Happens in young people (<30)

1) generalized aggressive periodontitis of primary dentition with generalized bone loss

2) localized agressive periodontitis (loss of localized bone in teenagers)

3) generalized aggressive periodontitis - young adults 

Pulpitis - types

reversible - excavation and restoration 

irrreversible- root canal therapy

Prevotella intermedia 

Porphymonas gingivalis 

Porphyromnas endodontalis 

Enterococcus faecalis

Fungi are 

eukaryotes

saprobes

feed on decaying matter

don't rely on host cell for nutrients

Instead of cholesterol, fungi have this compound in thier plasmalemma

ergosterol

hypae

filamentous extensions from bacteria 

collectively known as mycelium

allow existance of mold

yeast

unicellular and round

mycoses

fungal infections

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Classifcations of mycoses

1. superficial - outermost layer of skin and hair 

2. cutaneous- deeper into epidermis, also skin and nails

3. subcutaneous- via traumatic implantation, dermis, subcutaneous tissues, fasia, muscles 

4. systemic- involves inhilation of spore, initial infection in lungs with then spreads

5. opportunistic- in immunecompromised patients

Two types of infectios bodies

conida- on tips of stalk- like projections

anthrospores or anthroconidia- septal fragments of hyphae

Cutaneous Mycoses causative agent

dermatophyte

Describes lesions found in cutaneous mycoses

tinea - latin for "worm"

Types of tinea found in cutaneous mycoses

1. tinea capitis- scalp

2. tinea pedis- feet

3. tinea manus- hands

4. tinia- unguium- nails

5. tinea corporis- body

6. tinia cruris- penis 

Subcutaneous mycoses

lymphocutaneous sporotrichosis 

chromoblastomycosis 

Systemic mycosis

Histoplasma capsulatum

Blastomyces dermatitidis

Paracoccidioides brasiliensis 

Coccidioides immitis 

Cryptococcus neoformans 

Histoplasmosis

Histoplasma capsulatum

- aka cave disease or spelunkers disease

- in soil rich in shit from bats and birds

- Mississippi Valley region

- symptoms: flu, pneumonia -> calcificaitons in the lung (chest X- ray)

- becomes systemic via marophages

Blastomycosis

Blastomyces dermatitidis

- aka chicago disease or Gilchrist's disease

- Mississippi and Ohio Valley Region

-systemic infection -> macrophages

-disseminated skin and bone loss when becomes systemic

- compared to Histoplasmosis NO CALCIFICATIONS

Coccidioidomycosis 

Coccidioides immitis

- desert rheumatism and San Joaquin Valley fever 

- American South west, dust storms

- primary infection in LUNGS: inhalation of arthroconidia or arthrospores 

- can spread to skin in immunecompromised people

Cryptococcosis

Cryptococcus neoforman

disemmination in both immune compromised and immune competant cause cryptococcus meningitis

droppings of pigeons 

yeast form

Cryptococcosis 

-Cryptococcus neofroman

- dropping of pigeons

- only in yeast form

-chest X- ray : lung nodules

- dissemination causes cryptococcus meningitis in both immunecompromised and healthy individuals

Paracoccidioidomycosis 

Paracoccidioides brasiliensis 

- south america (hence, brasil)

-affects men more- inhibition of estrogen in hyphae -> yeast infection 

- becomes systemic in immunecompromised people

-systemic -> ulcers in oral, nasal and GI mucosa 

Opportunistic mycosis

mainly affect immunecompromised 

also applies to indiginous populations - Candida in HIV patients

Aspergillosis causative agent

aspergillus fumigatus 

Aspergillosis clinical manifestations

mycetomas or "fungal balls"

they are tubercular growths

due to inhalation of conida that cause localized infections in the lung

Pneumocystis jirveci penumonia causative agent

Pneumocystis jirveci

Pneumocystis jirveci pneumonia 

- who it's found in 

transmission

- pulmonary signs

-treatment

- late stage HIV patients 

- droplet inhalation and close contact

- sporocyst ruptures, leaves holes in lungs -> decrease pulmonary exchange 

- death by asphyxiation 

- treat with trimethoprim and sulfa drugs + oxygen

Drugs to treat fungal infections target this compound in the cell membrane 

Ergosterols

Polyenes 

Nystatin and Amphotericin B 

(NAP)

Mechanism of nystatin and amphoteracin B

 bind to ergosterol in cell membrane -> large pores that allow leakage

last resort because affects membranes in humans

Azoles

impair biosynthesis of sterols (membrane)

imidazoles 

triazoles

Nucleoside analog

5- flurocytosine

inhibit RNA and DNA function

Griseofluvin

treatment for dermatophytes