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159 Cards in this Set
- Front
- Back
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Oral Streptococci
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Gram + chains of cocci
Facultative anaerobes Part of Normal Flora Require elevated CO2 for growth Inhabit oral cavity and upper respiratory tract |
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S. mutans
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dental caries
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S. anginosus
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purulent infections/abscess
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S. sanguis
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gingivitis
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S. pneumoniae
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pneumonia
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viridans Streptococci
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bacteremia, endocarditis
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molecular methods can be used for species ID by isolating...
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16S ribosomal RNA sequences
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# of distinct oral species
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700+
Gram+, Gram-, cocci, rods, filaments, spirochetes, etc |
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Although consensus PCR is a powerful tool in variation analysis it often produces amplicons of ....
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identical size but with variations in sequence
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What can you know from DGGE?
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Community complexity. More bands = more complexity.
Identify community members by sequencing Distribution of microbial populations inhabiting different environments (e.g. temperatures) Monitor community changes |
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Fluorescent in situ hybridization (FISH)
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Can figure out what species are interacting, etc.
Probe = commercially available ssDNA with label (Cy3, Cy5, etc.) Complementary to specific nucleotides on Ribosomal RNA 100-1000 ribosomes/cells Probe + cells = specific cells that have ribosomal RNA complementary to the probe will light up upon excitation |
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Benefits of FISH
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Low relative microbial populations detected
Specific Culture-independent |
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Limitations of FISH
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Low volumes (10 - 50 μl)
Technically challenging Need to know the species first |
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454 Pyrosequencing
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Human genome completed by 3 technicians in 3 days.
1. Shear DNA and melt (single strand) 2. Add “A” and “B” Linkers 3. Connect strand to bead via “B” 4. Put each bead in a well. PCR amplify 5. Flood thousands of wells with TACG 6. Measure fluorescence of each well at each nucleotide addition |
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Primary colonizers of plaque (Gram+)
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Streptococci bind pellicle proteins from saliva
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Secondary colonizers of plaque (Gram-)
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Bridge species - F. nucleatum
Bind other bacteria |
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Tertiary colonizers of plaque (Gram -)
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Porphyromonas gingivalis
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Interspecies collaboration - O2
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Streptococcus cristatus
Facultative species Can live w/ or w/o O2 Uses up O2 when available Fusobacterium nucleatum Robust anaerobe Binding strep improves survival when O2 is present Porphyromonas gingivalis Sensitive anaerobe Coaggregation essential to survival when O2 is present |
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Inter-species competition Overlay experiment:
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Streptococcus sobrinus lawn
Spotted with : wild-type Streptococcus mutans strain producing mutacins I and IV Killed sobrinus |
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Streptococci ferment CHO and excrete...
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lactic acid
Veillonella uses lactate made by Strep for nutrition = biofilm buddies |
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Veillonella sends a chemical signal to activate transcription of Strep _____ gene
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amylase
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Streptococcus cristatus coaggregates with
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F. nucleatum
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considered a bridge species because it is a promiscuous coaggregator
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Fusobacterium nucleatum
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After coaggregation, S. cristatus is carried inside by...
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F. nucleatum
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High biomass sites in the mouth
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Non-shedding surfaces
- Supragingival tooth surfaces - Subgingival tooth surfaces Shedding surface - The tongue |
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Low biomass (reservoir) sites
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Shedding oral mucosal surfaces:
Buccal, palate, external gingiva, floor of mouth |
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Salivary transport of bacteria
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Quorum sensing tells bacteria when to grow, and when it’s time to go
Bacteria at the outer surface of mature biofilms are signaled to detach and become planktonic Saliva is the transport medium for planktonic oral bacteria Exfoliated epithelial cells in saliva can also transport bacteria |
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Host defenses in the mouth
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Epithelial cells
- Barrier function - Innate immunity - sensors (Toll-like receptors) - Inflammatory mediators, antimicrobial peptides Salivary antimicrobial factors - Histatin Mucosal antibodies (secretory IgA) Cell-mediated immunity (T-cells) |
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Are there true oral pathogens?
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Classic concept of a pathogen
Not normally present Produces “virulence factors” Damage host directly (e.g. toxins) Induce host to damage itself (immune responses) Presumed oral pathogens don’t quite fit that model Normally present throughout life Damage requires presence in large numbers |
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S. mutans is considered the major cause of...
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dental plaque and cavity formation
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Virulence Factors of S. mutans
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Specific adherence to tooth surface using antigen I/II adhesin and GTF
Production of extracellular polysaccharides (dextran) Accumulation of intracellular amylopectin-like polysaccharides (carbon/energy reserve) Lactic acid production from sugar metabolism High tolerance for acid IgA proteases -inactivate secretory IgA by detaching the Fc region of the immunoglobulin |
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Dental Caries – Cavity Formation
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Initial attachment of S. mutans to tooth pellicle is mediated by antigen I/II (adhesin) and Glycosyl transferase (GTF).
Sucrose is broken down into fructose and glucose by glucosyltransferases (GTFs). Fructose and glucose are both metabolized, resulting in lactic acid accumulation. Glucose is stored as a glucan polymer (dextran). S. mutans accumulates as glucosyltansferases (GTFs) adhere to glucans produced by other bacteria in plaque. |
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Gingiva Resistance to Disease
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(1) In the coronal part of the junctional epithelium quick cell exfoliation
(2) Rapid cell division (3) Laterally, the (external) basement membrane forms an effective barrier against invading microbes (4) Active antimicrobial substances are produced in junctional epithelial cells Epithelial cells activated by microbial substances secrete chemokines, e.g. IL-8 and cytokines, e.g. IL -1 and -6, and TNF-α that attract and activate professional defense cells, such as lymphocytes (LC) and polymorphonuclear leukocytes (PMN) (5)Their secreted product, in turn, cause further activation of the junctional epithelial cells |
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Bacterial species associated with periodontal health
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Streptococcus sanguis
Streptococcus mitis Veillonella parvula Actinomyeces naeslundii Actinomyces viscosus Rothia dentocariosa |
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Bacterial species associated with Gingivitis
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Actinomyces species
Streptococcus species Veillonella species Fusobacterium species Prevotella intermedia |
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Bacterial species associated with Periodontitis
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Porphyromonas gingivalis
Bacteroides forsythus Treponema denticola Actinobacillus actinomycetemcomitans |
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Secondary invaders in gingivitis include...
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S. sanguis and lactobacilli.
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Attachment and Invasion of P. gingivalis
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adhere to the epithelial cell membranes and microvilli and this is followed by internalization of the bacteria into the epithelial cell cytoplasm
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Attachment and Invasion of Fusobacteria
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can attach to and invade epithelial cells, replicate intracellularly, and translocate to the extracellular space where they are able to survive under aerobic conditions.
Develop a form of intracellular biofilm communities |
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Bacterial factors associated with periodontitis
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- Sufficient numbers of bacteria are present to exceed disease threshold (ie 108 bacteria/pocket)
- Periopathogens are of a virulent clonal type - Invasion: P. gingivalis can invade epithelial cells and gain access to the connective tissue of the periodontium - Toxins: A.a. produces a leukotoxin that kills neutrophils strong correlation go disease. - Enzymes: P. gingivalis produces a protease that degrades host tissues including antibodies and other host defense proteins - Toxic products: gram negative bacteria release LPS that can induce bone resorption |
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Purulent oral infections
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Following plaque formation by S. mutans, colonization by S. anginosus (S. milleri) can lead to painful dento-alveolar abscesses.
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Endodontic Infection
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Once treatment via root canal is accomplished, if the infection is not cleared (i.e. hypochlorite), you have a moist environment and an attachment surface = Biofilm
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Infectious Implantitis
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Fransson et al. (2005) studied 662 subjects with a total of 3413 implants found progressive bone loss in 28% of the patients (5 year follow).
21 studies showed 38.7% of the patients with implant had complications after 5 years (Pjetursson et al. 2004) |
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Ludwig’s Angina
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80% have had recent dental work
Involvement submandibular spaces bilaterally and submental space in midline Rapid spread to lateral pharyngeal/retropharyngeal space The most serious early complication of Ludwig’s angina is asphyxia due to expanding edema of the soft tissues of the neck. Impending respiratory obstruction may be heralded by increasing anxiety, tachypnea, stridor, and the assumption of a “sniffing” position. |
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Bacteria involved in Ludwig’s Angina
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Dominant isolates are anaerobic bacteria (75% of isolates). Peptostreptococci, Bacteroides organisms (frequently beta lactamase positive), and Fusobacterium nucleatum.
Aerobes (25%) - Alpha-hemolytic streptococci are most common but MRSA is on the rise. |
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Endocarditis
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Bacteremia following infection via the oral cavity by viridans streptococci can lead to infective endocarditis
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A thick cell wall and beta-glucan molecules are present in fungal cells
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A thick cell wall and beta-glucan molecules are present in fungal cells
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There are around 200,000 species of fungi but only about ___ are presently known to be Pathogenic for man.
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300
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Pathogenic fungi can exist as _____ or _____
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yeasts or as hyphae
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Yeasts
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unicellular organisms which reproduce by budding. This is the form usually seen in tissue.
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Hyphae (mycelia)
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multicellular filamentous structures and this form is observed in nature.
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Some fungi may occur in both the yeast and mycelial forms. These are called...
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dimorphic fungi
Conversion to the yeast form is essential for pathogenicity. |
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three genera of dermatophytes:
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1. Trichophyton sp
Infect skin, hair and nails. Take 2-3 weeks to grow in culture. The conidia are large (macroconidia), Identification requires special biochemical and morphological techniques. 2. Microsporum sp. May infect skin and hair, rarely nails. Microsporum canis is one of the most common dermatophyte species infecting humans. 3. Epidermophyton floccosum Infect skin and nails and rarely hair. |
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Tinea corporis
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small fungal lesions occurring anywhere on the body.
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The 3 most common Aspergillus species
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1. Aspergillus fumigatus
2. Aspergillus niger 3. Aspergillus flavus |
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There are three clinical types of pulmonary aspergillosis:
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1. Allergic. Hypersensitivity to the organism. Symptoms may
vary from mild respiratory distress to alveolar fibrosis. 2. Fungus ball. Characteristically seen in the old cavities of tuberculosis patients. The patients may cough up the fungus elements because the organism frequently invades the bronchus. 3. Aggressive tissue invasion. Primarily a pulmonary disease, but the aspergilli may disseminate to any organ. They may cause endocarditis, osteomyelitis, otomycosis and cutaneous. |
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Penicillium pathogenicity
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Are occasional causes of infection in humans, particularly in the immunocompromised and have been isolated from patients with keratitis, esophagitis, pneumonia, endocarditis, peritonitis and urinary tract infections.
Infection is acquired via inhalation of spores and results in initial pulmonary infection, followed by fungemia and dissemination of the infection. |
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Penicillium marneffei
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Discovered in 1956 and is endemic in Southeast Asia
Unlike other Penicillium species, it is the only dimorphic species that can cause lethal systemic infections. Specifically infects AIDS patients but have also been reported in patients with hematological malignancies and those receiving immunosuppressive therapy. The portal of entry is the lung and the infection spreads rapidly and often cutaneous lesions are seen. |
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BLASTOMYCOSIS (Blastomyces dermatitidis)
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Blastomycosis is a rare chronic infection that develops when people inhale the fungus.
It occurs in people living in the south-central and midwestern United States and Canada. Pulmonary and skin involvement is the most common. The disease usually affects people immunocompromised individuals and men are more likely to be affected than women. |
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SPOROTRICHOSIS (Sporothrix schenckii)
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A chronic infection of the cutaneous or subcutaneous tissue which tends to ulcerate and drain. The fungus is found in vegetation and infection commonly occurs when the skin is broken while handling plants and therefore can be an occupational disease for farmers and gardeners.
Symptoms include a small, painless, red lump at the site of infection (usually hands and arms) and eventually turns into an ulcer. These lesions do not heal unless treated and may remain ulcerated for years. Widespread (disseminated) sporotrichosis can develop in immunocompromised people when they inhale spore-laden dust. |
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HISTOPLASMOSIS (Histoplasma capsulatum)
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It occurs throughout the world. In the United States, it is most common in the southeastern, mid-Atlantic and central states.
Fungus grows as a mold in the soil and infection results from breathing in spores. Soil contaminated with bird or bat droppings may have a higher concentration of histoplasma. The lungs are the portal of entry and therefore, infection commonly appears as a pulmonary disease. There may be a short period of active infection or it can become chronic and spread throughout the body. Systemic disease manifests itself in the bone marrow, lungs, liver and the spleen. If untreated, the disseminated form of disease is usually fatal. Those who have a weakened immune system are the most vulnerable. About 10% of people with histoplasmosis will develop inflammation in response to the initial infection which can affect the skin, bones, joints heart lining |
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COCCIDIOIDOMYCOSIS (Coccidioides immitis)
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Endemic in the wilderness areas of the southwest of the United States.
Primarily a pulmonary disease and about 60% of the infections in the endemic area are asymptomatic and about 25% suffer a “flu-like” illness. However, CNS infection is common and there is a much greater mortality rate in dark-skinned people. |
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PARACOCCIDIOIDOMYCOSIS (Paracoccidioides brasiliensis)
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Exists in the soil as a mold present in North to Central and South America.
Infections happen through the inhalation spores causing a chronic granulomatous disease of mucous membranes, skin, and lungs where the spores convert into yeasts and spread to other sites haematogeneously. Most primary infections are self-limiting, however the organism has the ability to remain dormant in the human host for long periods Overt infection results in a progressive mycosis with lesions of the skin, mucous membranes and internal organs. |
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Cryptococcosis
(Cryptococcus neoformans) |
Initial cryptococcal infections occur through inhalation of the yeast from the environment (pigeon droppings).
The inflammatory reaction to the inhaled organisms produces a primary pulmonary–lymph node complex and the upper respiratory tract infection is frequently followed by cutaneous infection. The yeast spreads from the lung to circulate in the blood, especially if the host is immunocompromised. The most commonly involved site is the central nervous system (CNS). Most patients with C neoformans CNS infection present with subacute or chronic illness; altered mental state; behavioral changes; headache and fever. Mortality: Without treatment 100%. |
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virulence factors of Cryptococcus neoformans
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capsules and melanin production
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Baker’s yeast
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S. cerevisiae
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Saccharomyces cerevisiae
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converts sugar into alcohol by means of enzymes.
The yeasts used to ferment sugars in the manufacture of baked goods, beers, wines |
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Erythematous candidiasis
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presents as a red, flat, subtle lesion. Tends to be symptomatic with patients complaining of oral burning, most frequently while eating salty or spicy foods or drinking acidic beverages.
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Pseudomembranous candidiasis (thrush)
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white curd-like plaques on the buccal mucosa, tongue and other oral mucosal surfaces that will wipe away, leaving a red or bleeding underlying surface.
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Angular Cheilitis (a form of Oral Candidiasis)
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Angular cheilitis is erythema and/or fissuring of the corners of the mouth. Treatment involves the use of a topical antifungal cream directly applied to the affected areas four times a day for the two-week treatment period
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Denture Stomatitis
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Candida-associated denture stomatitis is prevalent in up to 70% of denture wearers, mostly the upper denture, this condition tends to be persistent and recurrent as it is a consequence of the abiliy of C. albicans to form biofilms on surfaces, where candidal cells adhere to the denture material and colonizes the denture surfaces leading to inflammation of the denture-exposed palatal mucosa
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C. albicans is a dimorphic species capable of switching its morphology between and yeast and hypahl forms, a property involved in pathogenesis. The ____ form is involved in tissue invasion whereas the _____ form in bloodstream and systemic infections.
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hyphal; yeast
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The two main antifungal classes available for the treatment of systemic fungal infections are:
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1. Azoles (fluconazole or Diflucan)
2. Polyenes (amphotericin B) |
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Fluconazole (Diflucan):
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Considered the drug of choice for the treatment of oral, vaginal and systemic candidiasis.
Well tolerated with very low incidence of side effects. Commonly used as prophylaxis for fungal infections in neutropenic patients and for preventing oropharyngeal candidiasis in HIV+ individuals. |
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Azoles - Mechanism of Action
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The azoles are fungistatic
They target the gene coding for the enzyme responsible for the biosynthesis of ergosterol, the main sterol in the fungal cell membrane. Depletion of ergosterol compromises the integrity of the cell membrane causing cell growth arrest *Amphotericin B has serious side effects such as nephrotoxicity. |
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Polyenes - Mechanism of Action
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The polyenes are fungicidal.
They kill the fungal cell by intercalating into cell membranes where they form channels leading to cell death due to leakage of cytoplasmic contents. |
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Primary Resistance:
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an organism is resistant to the drug prior to exposure.
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Secondary Resistance:
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resistance is developed in response to exposure to the drug. This accounts for the emergence of resistance to azoles seen over the last few years.
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Mechanisms of Antifungal Drug Resistance
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1. Over-expression of the ERG11 gene which codes for a key enzyme in the synthesis of ergosterol
2. Over-expression of genes encoding multi-drug efflux proteins that actively pump the drug from the cells |
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Histatin-5
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Hst-5 is a small protein produced and secreted by human parotid and submandibular-sublingual glands into the saliva.
Hst-5 exhibits potent activity against C. albicans and therefore, has been proposed to play an important role in protecting the mucosa from C. albicans |
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ETIOLOGY OF Chronic Periodontitis
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1. Susceptiblity of host
2. Sufficient periopathogens 3. Absense of beneficial species |
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RED COMPLEX
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1. P.gingivalis
2. T. forsythia 3. T. denticola |
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Gingipain
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a cysteine protease secreted by Porphyromonas gingivalis.
1.ADHESION - gingipains expose binding sites on the epithelia and allow invasion. 2. ACQUISITION OF IRON - giniginapains lyse RBCs once they have been hemagglutinated by P.g. 3. BREAKDOWN OF COLLAGEN - gingipains stimulate certain WBCs that induce bone loss. |
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Major bone loss and collagen loss in periodontitis is caused by...
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the host immune response
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DENTILISIN
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T. denticola chymotyrpsin-like protease. It has roles in hemagglutination, penetration of epithelium and attachment
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T. DENTICOLA
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Anaerobe.
Motile. Frequently attached to surfaces. Td attaches to Tf, Pg, other bacteria, teeth and epithelium via dentilisim and Msp Motility of Td allows invasion of dentinal tubules or cemental voids by itself, or with attached bacterial aggregates |
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T. FORSYTHIA
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Gram -
Most pathogenic features are in the S layer. A surface protein on the S layer called Bacteroides surface protein A (BspA) mediates attachment Tf produces a gingipain-like proteolytic enzyme, called prtH from the prtH gene, and other histolytic enzymes and maintains them on the cell surface. |
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Bacteroides surface protein A
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mediates attachment of T. FORSYTHIA
Also, triggers the release of bone-resorbing pro-inflammatory cytokines from monocytes. |
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prtH
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a gingipain-like proteolytic enzyme, produced by Tf, that allows invasion of epithelium.
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CHARACTERISTICS OF AGGRESSIVE PERIODONTITIS
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Pocket formation does not correspond with amount of plaque present.
Familial associations Predilection for females 3:1 Rapid attachment loss and bone loss Association with Aggregatibacter actinomycetemcomitans (Aa) High incidence among North Africans and Indonesians (7.6%) |
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LOCALIZED AGGRESSIVE PERIODONTITIS (LAP)
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AFFECTS ADOLESCENTS FROM 12 TO 16
LOCALIZED POCKETING AROUND MOLARS AND INCISORS LOW DENTAL CARIES RATES LOW PLAQUE LEVELS HEALTHY APPEARING GINGIVAL TISSUE PMN CHEMOTACTIC DEFECTS FAMILIAL ASSOCIATION HIGH COLONIZATION BY AA PREDILECTION FOR FEMALES 3:1 |
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AGGREGATIBACTER ACTINOMYCETEMCOMITANS (Aa)
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Fimbriated Gm neg. rod, non-motile and faculative
In LAP serotype B is predominant. Aa strains of this serotype are the most virulent. Virulent strains:Y4 and JP2. JP2 is the most virulent and has prediliction for North African decendents. Attachment: Fimbria, cell attachment. Fibronectin adhesin, used for cell penetration Extracellular leukotoxin (LT) kills PMN, monocytes and some lymphocytes Cytolethal distending toxin (CDT) induces apoptosis in target cells |
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cytolethal distending toxin
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Toxin secreted by Aa that induces apoptosis in target cells
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Viruses destroy ____ ______ on macrophages allowing red complex to proliferate.
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LPS receptors
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SUGGESTIVE EVIDENCE for herpes involvement in NUG:
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Time course like viral
Self-limiting like viral Low recurrence rate like viral Prediliction for young individuals like CMV infections Common in HIV |
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Stage 1 Gingivitis
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- Initial Lesion
- Time: 2-4 days - Blood vessels: Vascular dilation - Junc. and Sulc. Epithelium: Infiltration by PMNs. - Predominant Immune Cell: PMNs - Collagen: Perivascular loss - Clinical Findings: gingival fluid flow |
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Stage 2 Gingivitis
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Early Lesion
- Time: 4-7 days - Blood vessels: Vascular proliferation - Junc. and Sulc. Epithelium: Infilt by PMNs, rete pegs - Predominant Immune Cell: Lymphocytes - Collagen: Increased loss around infiltrate Clinical Findings: Erythema, BOP |
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Stage 3 Gingivitis
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Established Lesion
- Time: 14-21 days - Blood vessels: Vascular proliferation, blood stasis - Junc. and Sulc. Epithelium: Infilt by PMNs, rete pegs - Predominant Immune Cell: Plasma cells - Collagen:Continued loss Clinical Findings: Changes in color, size, etc |
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3 major vascular events of inflammation
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1. Increase in vascular diameter
2. Leukocyte emigration and accumulation 3. Increase in vascular permeability |
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The host components involved in the immediate phase of inflammation
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- Complement
- Resident WBCs - Mast cells |
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PMN transendothelial migration
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1. Rolling adhesion
2. Binding 3. Diapedesis 4. Migration |
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Outcomes of acute inflammation
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1. Resolution
2. Scar 3. Abscess Formation 4. Chronic inflammation |
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Bacteria induced phagocytosis of P. gingivalis occurs due to adherence of FimA to...
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Beta-1 integrin
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Bacteria induced phagocytosis of A.a. occurs due to binding of A.a. to host integrins and
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platelet activating factor receptor.
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Periodontal pathogens that have been reported to invade the coronary artery endothelial cells:
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E. corrodens
P. gingivalis Prevotella intermedia |
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Of the periodontal pathogens found in coronary vessels, which were most common?
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P. gingivalis
T. denticola |
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Calprotectin
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Cytosolic calcium-binding protein
May inhibit or kill P. gingivalis Elevated in GCF in perio patients |
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Beta defensins
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Associated with epithelial surfaces
May restrict intracellular replication and destruction of the cell' P. gingivalis and A.a. increase epithelial cell expression |
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Adults with extensive PD had __% higher mean C-reactive protein levels
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30%
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Plasma levels of this interleukin were significantly higher with adults with PD
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IL-6
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Perio pathogens associated with elevated CRP
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P. gingivalis, T. forsythia and T. denticola
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Activation of endothelial cells due to gingivitis results in expression of...
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selectins that are important for transendothelial migration of leukocytes.
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What % of neutrophils migrate across the junctional epithelium every day?
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1-2% of neutrophils
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P gingivalis impedes neutrophil migration by blocking epithelial secretion of this interleukin
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IL-8
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Membrane bound PRRs
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1. Receptor Kinases
2. TLRs |
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Cytoplasmic PRRs
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NLR receptors
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Secreted PRRs
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Mannan-binding lectin
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NF-kB
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Transcriptional regulator plays a central part in responses to inflammatory signaling through TLRs, TNF receptors and the IL receptor
Induces expression of cytokines, chemokines, effector molecules of immunity and pro-survival factors |
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Primary inflammatory cytokines
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- IL-1
- IL-6 -TNF |
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IL-1 and TNF-alpha activity
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Stimulate endothelial cells to express selectins, facilitating recruitment of leukocytes.
Activation of IL-1 production, achieving amplification Induction of prostaglandin E2 by macrophages and fibroblasts. |
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IL-1, TNF and LPS upregulate...
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COX-2
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________ and _______ are primary sources of prostaglandins in the periodontium.
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Macrophages; fibroblasts
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PGE2 actions
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Vasodilator and increases vascular permeability
Down regulates ICAM expression in gingival fibroblasts Stimulator of bone resorption via enhancement of osteoclast formation |
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Matrix metalloproteases
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Produced by Neutrophils, macrophages, fibroblasts, etc
Family of zinc-dependent endopeptidases They degrade ECM molecules (collagen, gelatin, elastin) MMP-8 is most prevalent MMP in periodontitis |
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Periostat
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Systemically delivered collagenase inhibitor
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Bisphosphonates
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- Analogues of inorganic pyrophosphates are incorporated into the skeleton
- Nitrogen-containing bisphosphonates are most potent. - DECREASE BONE TURNOVER |
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P. Gingivalis FimA adhesion binds the host ____ intergrin
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Beta-1 integrin
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Top 3 cytokines for inflammation
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1. IL-1
2. IL-6 3. TNF-alpha |
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Host epithelial cells produce what cytokine in response to F. Nucleatum
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IL-8
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3 main avenues for communication between the periodontium and pulpal tissues:
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1. Apical Foramen
2. Lateral and Accessory Canals 3. Dentinal Tubules |
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Possible channels between the pulp and periodontium
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- Neural pathways
- Lateral canals - Dentinal tubules - Palatogingival grooves (developmental anomalies of the maxillary incisor teeth, lateral more than central) - Periodontal ligament - Alveolar bone - Apical foramen - Common vasculolymphatic drainage pathways - Developmental malformations – such as palatogingival grooves of maxillary incisors. - Perforations – these may result from extensive carious lesions, resorption, or from operator error direct communication between the root canal system and periodontal ligament. - Vertical root fractures – these can produce deep periodontal pocketing and localized destruction of alveolar bone. The fracture site provides a portal of entry for irritants from the root canal to the PDL |
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the principal and the most direct route of communication between the pulp and periodontium
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APICAL FORAMEN
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% of all teeth that have lateral or accessory canals
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30-40%
the majority of them are found in the apical third of the root |
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Typically, ______ lesions resorb bone apically and laterally and destroy the attachment apparatus adjacent to a nonvital tooth
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Typically, endodontic lesions resorb bone apically and laterally and destroy the attachment apparatus adjacent to a nonvital tooth
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dentinal tubules range in size
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1 to 3 microns in diameter
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Typically, ______ lesions resorb bone apically and laterally and destroy the attachment apparatus adjacent to a nonvital tooth
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Typically, endodontic lesions resorb bone apically and laterally and destroy the attachment apparatus adjacent to a nonvital tooth
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dentinal tubules range in size
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1 to 3 microns in diameter
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some studies suggest that the effect of perio disease on the pulp is degenerative in nature including an increase in....
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On the other hand, some studies suggest that the effect of perio disease on the pulp is degenerative in nature including an increase in calcifications, fibrosis and collagen resorption
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PRIMARY ENDO WITH SECONDARY PERIO
The pathway of inflammation into the periodontium is through... |
PRIMARY ENDO WITH SECONDARY PERIO
The pathway of inflammation into the periodontium is through the apical foramen, accessory and lateral canals |
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PRIMARY PERIO WITH SECONDARY ENDO
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In this case, the apical progression of a periodontal pocket continues until the apical tissues are involved
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Polymicrobial nature of primary endodontic infection
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Predominant anaerobic bacteria
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Common isolated bacterial species in teeth with acute periapical lesions –endo
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P.anaerobius/P.micra
F.nucleatum/F.necrophorum P.intermedia/P.nigesecens P.endodontalis P.gingivalis Treponema spp./T.denticola |
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Periodontal microflora in disease are mainly ______ and ______
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Periodontal microflora in disease are mainly facultative and saccharolytic
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Endodontic Microflora vs. Periodontal microflora
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Access to nutrients in the periodontal pocket = higher bacterial activity and much higher numbers
Open Comunication between the periodontal pocket and the oral cavity = higher numbers of species and a more complex flora |
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Highly frequent species or groups in endo infections:
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Prevotella spp.
Fusobacterium spp. Prevotella intermedia Eubacterium spp. Propionbacterium spp. |
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the primary etiologic agent of the different forms of periradicular inflammation.
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Infection of the root canal
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the most common pathway for the root canal system for microbes
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Dental caries
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The number of microorganisms detected in endodontic infections increased to ____ organisms per infected root canal associated with an apical lesion.
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3-12
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Highly frequent species in infected root canals
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Prevotella spp.
Fusobacterium spp. Prevotella intermedia Eubacterium spp. Propionbacterium spp. T.forsythensis T.denticola E. faecalis |
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This important periodontal pathogen had never been detected in infected rot canals by culture, and was discovered through molecular methods
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T.forsythia
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the predominant microbe in root canals undergoing RETREATMENT
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Enterococcus facealis
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E.faecalis was found in ___ of root canal re-infection cases
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E.faecalis was found in 77% of root canal re-infection cases
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viruses associated with endo infections
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herpes viruses
Human cytomegalovirus Epstein-Barr virus |
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ENDODONTIC MICROBIOTA
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Gram negative bacteria most common:
Genera: Treponema, Fusobacterium, Porphyromonas, Prevotella and Tannerella Gram-positive bacteria: Genera: Pseudoamibacter, Micromoas, Peptostreptococcus, Actinomyces, Streptococcus, Olsenella, Propionibacterium |
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Bacteria implicated in endo re-infections
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Gram-positive facultative or anaerobic bacteria are predominant
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Symptomatic apical periodontitis
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Inflammation, usually of the apical periodontium, producing clinical symptoms including painful response to biting and percussion. It may or may not be associated with an apical radiolucent area.
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Asymptomatic apical periodontitis
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Inflammation and destruction of apical periodontium that is of pulpal origin, appears as an apical radiolucent area and does not produce clinical symptoms.
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presence of a sinus tract
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Chronic apical abscess
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the main example of extraradicular infection independent of the intraradicular infection
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Apical actinomycosis caused by some Actinomyces species and P. propionicum
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