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48 Cards in this Set
- Front
- Back
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What disease are early colonizers associated with? What about when the plaque biofilm matures? What are late colonizers associated with?
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Early - gingivitis, reversible
Late - periodontitis, more severe inflammation. Extension of inflammation of gingiva to attachment apparatus. Any spread to attachment apparatus is irreversible. |
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How do bacteria cause disease? What is the sequence of events that occurs?
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-Acquisition
-Adherence or Retention -Initial Survival -Prosperity and Long-term Survival -Avoidance of Elimination -Multiplication -Elaboration of “Virulence Factors” |
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How does acquisition occur?
Endogenous vs. exogenous organisms |
-Occurs at birth via vertical transmission.
-Endogenous organisms: those organisms already present within the host when the disease is developed -Exogenous organisms: those acquired from other individuals or the environment which may initiate the disease process or enable its progression. Mostly dealing with endogenous infections. |
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Within 4-12 hrs of birth, what 2 types of bacteria appear?
When teeth appear? Puberty? What kind of sugar does Strept mutans break down? What is produced as a result? |
Within 4-12 hrs: lactobacilli, streptococci
Strep salivarius, staph, Neisseriae, Moraxella catarrhalis When switching to solid food, the microflora becomes similar to parents. Teeth appear: get Strep mutans and Strep parasanguis Gingival cervice: anaerobic, yeasts Puberty: bacteroides, spirochetes Sucrose. Lactic acid produced which lowers pH and aids in growth of lactobacilli. |
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What types of microbes are found in the gingival space or pocket?
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Anaerobic. Pockets tend to have low O2 or absence of O2.
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What types of microbes are in the normal oral flora?
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Blue/purple complex mostly aerobic, Gram positive bacteria. May find some periodontal pathogens as well in low numbers.
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What was Pasteur's hypothesis? What did Lister do?
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Normal bact is healthy and essential to life. Only foreign bacteria are responsible for causing disease. He proposed preventing entry of microorganisms into human body.
Lister then developed an antiseptic method in surgery. |
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When the oral cavity is sterile in utero, how long does it take for bacteria to develop?
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4-12 hours lactobacilli.
Usually from the first feeding: Streptococcus salivarius, staphylococci, Neisseriae, Moraxella catarrhalis -Switch to solid food: Microflora similar to parents |
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What bacteria do you have when teeth appear? Wat's in gingival crevice? How about during puberity?
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Teeth appear=
nondesquamating surface Streptococcus mutans, Streptococcus parasanguis - Gingival crevice area: Anaerobic species, yeasts - Puberty: Bacteroides, spirochetes |
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What is a sign of acute necrotizing ulcerative gingival disease?
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Punched out papilla.
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What 3 physiological factors that effect where microbes can be found?
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Temperature
Moisture Presence of nutrients |
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What are the benefits of normal flora to the host?
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1. The normal flora occupy available colonization sites
which makes it more difficult for other microorganisms (nonindigenous species) to become established. 2. Also, the oral flora contribute to host nutrition through the synthesis of vitamins, and they contribute to immunity by inducing low levels of circulating and secretory antibodies that may cross react with pathogens. 3. Finally, the oral bacteria exert microbial antagonism against nonindigenous species by production of inhibitory substances such as fatty acids, peroxides and bacteriocins. |
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What is adherence/retention?
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-Ability of organism to attach to surface. Gram posit. bacteria produce EPS which has polysacch, proteins, NAs, etc. this is the major compound in biofilm.
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What is initial adhersion mediated by? Later adhesion?
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Initial adhesion between bacteria and non-living surfaces is
usually mediated by non-specific (e.g. hydrophobic) interactions, whereas adhesion to living surfaces is usually accomplished through specific molecular docking mechanisms. |
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Wht is cell to cell adhesion mediated by? What is coaggregation?
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Later on, during the biofilm growth, cell-to-cell adhesion can be
mediated by specific adhesins or cell surface modifications such as pili or fimbriae. - Coaggregation of genetically distinct bacteria via specific molecules has been shown common in the development of oral mixed-species biofilms. |
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What is essential to the initial survival of bacteria?
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-Bacteria requires not only a
stable surface, it also needs a source of nutrients. -Gingival crevicular fluid is a rich source of nutrients such as essential energy sources like glucose and iron. But it also contains host-derived elements which can decrease bacterial survival such as antibodies and complement. |
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Describe avoidance of elimination..
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-Key survival strategy.
Bacterial capsules faciitate this; -some bacteria go through drift and shift to mutate their antigens so that host can't regonize it. Uses sIgA protease, iron acquisition, intracellular residence in vacuole or free in cytoplasm, survive phagocytosis, prevent migration of phagocytes. Bacteria can migrate into dentinal tubules and make a pool for recolonization of periodontal pockets once therapy has been provided to patient. |
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Why don't we use antibiotics to treat chonric periodontitis?
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-counter productive since by the time the agents has penetrated the biofilm, its concentration is too low to be effective and resistant strains can emerge.
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Describe multiplication...
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Need this for long term survival.
-Critical mass with certain microbes needed, and after which mutliplication beyond a threshold is neeed for disease to occur. Potential theories for the shift: -transient immunosuppression from stress -meds -concurrent infection -response to signal, bact, env, or host derived |
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3 categories of virulence factors
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-Enzymes
-Metabolic waste products -Toxins |
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The ability of bacteria to cause disease is describe in general terms of the following 4..
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- the number of infecting
bacteria, -the route of entry into the body, -the effects of host defense mechanisms -intrinsic characteristics of the bacteria called “virulence factors”. |
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What are virulent bacteria?
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The factors are usually proteins or molecules made by enzymes of bacterial origin.
-Usually proteins are coded for by genes in chromosomal DNA, bacteriophage DNA, or plasmids |
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Describe host mediated pathogenesis
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Host-mediated pathogenesis is often important
because the host can respond aggressively to infection with the result that host defense mechanisms do damage to host tissues while the infection is being countered. |
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Describe expression of virulence factors
Constitutive? Under Specific environmental signals? Only in vivo? |
-Constitutive: “all the time”
-Under Specific Environmental Signals -can be identified by mimicking environmental conditions in a laboratory -many virulence-associated genes are coordinately regulated by environmental triggers -Only in vivo -Cannot be identified in a laboratory setting |
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Describe the toxins made by bacteria
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Inhibition of PMNs
Poison PMNs. This allows bacteria extra time to invade into teh body. Can produce chemotaxis inhibitors -Decrease phagocytosis and intracellular killing -resistance to complement mediated killing |
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Collagenase
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-Damages CT esp gingiva and PDL. Destroying PDL takes longer but it can happen
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What are some of the metabolic products of bacteria?
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-Hydrogen sulfide
-Ammonia -Indole -Acids |
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Exotoxins
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-A soluble protein excreted by a
pathogen. -Causes damage to the host by destroying cells or disrupting normal cellular metabolism. -Both gram negative and gram positive bacteria produce exotoxins. They are highly potent and can cause major damage to the host. -Exotoxins may be secreted, or may be released during lysis of the cell. -Usually made by living bacteria but some of them store it in vacuoles. When bacteria is killed off, vacuoules burst and exotoxins still spread. Theorectically, we dont just need living bacteria to cause problems. |
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Endotoxins
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- Potentially toxic, natural compounds found inside
pathogens. -An "endotoxin" is a toxin which, unlike an "exotoxin", is not secreted in soluble form by live bacteria, but is a structural component in the bacteria which is released mainly when bacteria are lysed. -In periodontal disease, endotoxins: -Cause tissue damage -Amplify the inflammatory response |
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LPS
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FOund in Gram neg bacteria.
-Endotoxin that elicits strong immune response. -Large molecules consisting of a lipid and a polysaccharide joined by a covalent bond -Found in the outer membrane of Gram-negative bacteria, act as endotoxins and elicit strong immune responses in animals. -Contributes to the structural integrity of the bacteria, and protects the membrane from certain kinds of chemical attack. |
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Describe the 3 parts of LPS
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1.) Polysaccharide (O) side chains: Also referred to as the
O-antigen. A polysaccharide chain that extends from the core polysaccharide. The composition of the O side chain varies between different gram-negative bacterial strains. O side chains are easily recognized by the antibodies of the host, but, can easily be modified by Gram-negative bacteria to avoid detection. 2.) Core : Core oligosaccharide contains unusual sugars. The core oligosaccharide is attached to lipid A. Partly responsible for the toxicity of gram-negative bacteria. 3.) Lipid A: contains unusual fatty acids and is embedded into the outer membrane while the rest of the LPS projects from the surface. This is the key in the toxicity. side chains can vary, leading to varying degrees of toxicity with LPS of some bacteria being more potent than others. |
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What if we cleave LPS from bacteria?
What are some other properties of LPS |
Death results if its mutated or removed.
-Loose association with cementum -Activate host clotting factors (Hageman Factor) causing intravascular coagulation, thrombosis and ischemic necrosis of the gingiva -Complement activation a subsequent inflammation -Priming of phagocytes for “activation” and release of enzymes and oxygen radicals -Activation of the immune response (antigenicity) -Macrophage toxicity -Bone resorption -Fibroblast toxicity -Inhibition of connective tissue attachment (collagen) |
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Why are pockets form in periodontal disease?
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The toxins stimulate a chronic
inflammatory response in which the body in essence turns on itself, and the attachment apparatus that supports the teeth is broken down and destroyed. The epithelial attachment migrates apically, forming pockets that become further colonized by bacteria. As the disease progresses, the pockets deepen and more of the periodontium is destroyed. -Often, this destructive process has very mild symptoms however eventually, teeth can become mobile and may exfoliate. |
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What are the big 3 of AAP?
What's another one worth remembering? |
1.Porphyromonas
gingivalis (red) 2.Tannerella forsythia (Bacteroides forsythus) (red) 3.Aggregatibacter actinomycetemcomitans (green) -Treponema denticola |
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Characteristics of porphyromonas gingivalis..
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-Black-pigmented
asacchrolytic rodcarbohydrates are not used as an energy source -Non-fermentative -Anaerobic -Gram-negative -Major site of colonization is the gingival sulcus. -Overwhelming evidence for its role in the pathogenesis of chronic periodontitis. |
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How does porphyromonas gingivalis cause disease?
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-Cell surface adhesion molecules on the surface of
Porphyromonas interact with other bacteria, epithelial cells, and extracellular matrix proteins; they are currently being studied for their pathogenic potential. -P. gingivalis is thought to spread through tissue, destroy tissue, and evade host defenses by the use of secreted cellbound proteases, immunoactive cellular compounds, and toxins. -P. gingivalis cytotoxic metabolic end products, which include butyrate, propionate, have low molecular weights which allows them to easily penetrate periodontal tissue and disrupt the host cell activity. -P. gingivalis is associated with perio lesions, infection, and periodontitis |
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Virulence factors of Pg
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Involved in colonization and attachment:
fimbriae, hemagglutins, OMPs, and vesicles -Involved in evading (modulating) host responses: Ig and complement proteases, LPS, capsule, other antiphagocytic products -Involved in multiplying: proteinases, hemolysins -Involved in damaging host tissue and spreading: Proteinases “gingipains”, collagenase, trypsin-like activity, fibrinolytic, keratinolytic, and other hydrolytic activities |
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Characteristics of Tannerella forsythia
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-Formerly Bacteroides forsythus
-A Gram (-), filament-shaped, non-motile, non-pigmented oral bacterium -Difficult to culture -Not well characterized -Colonization may characterize the conversion of periodontally healthy sites into diseased sites and associated with “refractory” periodontitis. |
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Virulence factors of Tf
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-Pathogenicity is virtually unknown!
-Proteolytic enzymes, trypsin-like enzymes -Sialidase (Neuraminidase) -Leucin-rich surface protein (BspA) -Others to be identified |
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Characteristics of Aggregatibacter actinomycetemcomitans
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Formerly Actinobacillus actinomycetemcomitans.
-The genus name refers to the “star”- shaped internal structure. -Short, straight or curved Gram (-) rod with rounded ends -Ferments most sugars -Growth is enhanced by the presence of CO2 - Primary suspect in the etiology of localized aggressive periodontitis (localized juvenile periodontitis) -Releases leuokotoxin that kills host white blood cells. -Most of LAP pts have high antibody titiers vs. Aa. -Elevated in active lesions, and associated with refractory periodontitis in adult patients. |
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What is unique about Aa compared to the othr big 3?
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Only serotype b is found in localized aggressive periodontitis, strong leukotoxin expression.
-serotypes d and e also exist. |
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Spirochetes
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-Responsible for necrotizing periodontal disease
-Gram -, anaerobic, spiral, highly motile -Increased numbers in deep periodontal pockets -Difficult to distinguish individual species: 15 subgingival spirochetes have been described; classified small, medium, or large -T. denticola: common in diseased, subgingiva sites |
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Name some disease causing spriochetes
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Prevotella intermedia, nigrescens
Fusobacterium nucleatum Campylobacter rectus Eikenella corrodens Streptococcus micro Selemonas |
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Microbial invasion?
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-Once micro-ulceration occurs
within the sulcular epithelium, bacterial will colonize the underlying sites. However, whether they directly cause the ulceration through release of enzymes, or whether it results from the host’s inflammatory response, or a combination of both is unclear. -In vitro invasion has been demonstrated for a number of pathogens including Pg and Tf, in vivo invasion is more difficult to study. -Exception is necrotizing periodontal disease - tissue invasion of spirochetes leads ti NUG and NUP. |
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Tranmission of oral pathogens?
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-Can be transmitted between individuals within families
-Can go from animal to human too. -Repeated failure of perio therapy may be due to re infection from chornic contact with partner |
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What viruses are cause of gingivitis?
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Herpes simplex and varicella zoster. CMG and EBV may play role in onset also.
Do so via reliase of cytokines, overgrowth of periodontal bacteria, suppress immune system. Herpes associated periodontitis has higher levels of periodontopathic bacteria. -Lack of herpes virus infection or viral infetion may explian why some people carry periodontopathic bacteria while still mainting perio health |
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Germ Balanced
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-Beneficial and pathologic bacteria
are balanced in health -Beneficial species can cause a lowlevel gingival inflammation -All bacteria are constantly evolving and competing with dominance -Subsequent bacterial species become more virulent and have increased capacity to cause disease. -Pathogenic bacteria cannot colonize the biofilm until the beneficial bacteria are in place. |
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Probiotics
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Although you don't need probiotics to be healthy,
these microorganisms may provide some of the same health benefits that the bacteria already existing in your body do — such as assisting with digestion and helping protect against harmful bacteria. -However, studies have also shown that in some users these products have lead to serious and potentially lethal side-effects |
