Exam 2 Lectures 8-13 Flashcards
What is a biofilm?
Essentially matrix-enclosed bacterial populations adherent to each other and/or to surfaces or interfaces another def. is multicellular, multispecies complexes held together by linking polymers
What are five roles of normal flora?
Competition, vitamin K synthsis, immune stimuli, source of opportunitsts, etiologic agents of caries and chronic imflammation They are in dynamic equilibrium and are not usually pathogenic at their normal site)
Whare are supplemental and transient flora?
Supplemental flora are found in a minority of the population, where they generally act like normal flora. Transient flora consist of microorganisms that are brought to the area from somewhere else. They almost always have a very difficult time colonizing and competing in the area and are generally cleared within a few hours or days.
What is the characteristic sequence of bacterial colonization?
Exposure to microbes at birth & additional microbes when kissed –>when teeth erupt four niches develop (fissures, approximal surfaces, smooth surfaces and gingival-tooth interfaces, biofilms form, dental plaques, etc.
Describe Loe’s model of the early changes in an ‘uncared for’ plaque ‘lawn’, and development of gingivitis
Dr. Loe developed a model to study the effects of poor oral hygiene and found that an increase in anaerobic bacteria as well as increased total bacterial mass correlates to the emergence of gingivitis. Gingivitis is reversible with brushing & oral maintenance.
Describe the concept of ‘plaque food chain’ and oral ecology
As plaque increases in complexity and density, a ‘food chain’ develops, where some bacterial end products provide the substrate or conditions beneficial for other bacteria. (ex. Veillonella can live off lactic acid produced by Strep. & Actinomyces).
What are the major niches for microbes to colonize in the oral cavity?
The primary niches for most bacteria are the tongue papilla & crypts. Additional niches include: fissures, approximal surfaces, smooth surfaces, and gingival-tooth interfaces
What are some of the protective features of the oral cavity that prevent bacteria from forming biofilms/plaque?
Saliva-flushing and epithelial shedding, immune protection, etc.
What are two examples of pioneer bacterial species that are able to bind to the pellicle proteins and provide further binding sites for secondary colonizers in growing plaque biofilm?
S. sanguinis (requires teeth to colonize) and S. mitis (there are others)
What is the source of the early microbial oral colonization of babies?
The infant’s mother (or primary care-giver) Additionally, the more Strep. Mutans mom has, the sooner her infant will be colonized
What is one of the major primary colonizers of oral soft tissues (generally occurring within hours/days of birth)?
Strep. salivarius is a primary colonizer of oral soft tissue and does not require teeth to be present
At what point in an infant’s life does Strep. Mutans generally first appear in large numbers?
Strep. Mutans reauire teeth hard surfaces to colonize and appear in large numbers when the pits & fissures of the 2nd molars emerge at around 19 months. (they do not compete well on smooth tooth surfaces)
Babies and edentulous adults are able to bypass which marjor cariogenic microbe because they have no teeth?
Strep. Mutans: this bacteria is dependent on the enamel surface for colonization whereas other Step. Species (e.g. salivarius) are not.
What are two major groups of bacteria associated with SUPRA-gingival plaque?
Streptococcus and Actinomyces (primarily streptococcus Gram-positive bactera–there are very few Gram-negative bactera.)
What are two major groups of bacteria associated with SUB-gingival plaque?
Gram-negative bacteria such as Treponema and Fusobacterium (with very few gram-positive bacteria).
What are the primary characteristics of bacteria that flourish SUPRAgingivally?
Mostly Gram-positive, cocci and branched rods, facultative & some anaerobes, carbohydrates (fermented), firmly adherent to plaque, Diseases caused include caries and gingivitis
What are the primary characteristics of bacteria that flourish SUBragingivally?
Mostly Gram-negative, mostly rods and spirochetes, mostly anaerobes, energy sources are proteins, many motile forms & adherences is less-pronouced, diseases caused include Gingivitis and periodontitis
How would you describe the pH associated with conditions surrounding SUPRAgingival plaque?
In general terms, the pH is slightly acidic (aroud 6.5) considering the end-products of carbohydrate fermentation are alcohols, ketones and acids
How would you describe the pH associated with conditions surrounding SUBgingival plaque?
Slightly basic: pH around 7.5 considering the end-products of protein fermentation include sulfur and nitrogen-end products.
What features (esp. WRT exclusive activities) make biofilms/plaques so pathogenic?
Various bacterial species adhere to one another, bacteria products and salivary proteins. As the plaque matures it begins to exclude saliva, oxygen and some food sources. This causes pathologies to increase.
What are two additional names for glucose polymers?
Dextrans and Glucans
What does the term “climax community” refer to?
Climax community refers to how bad bacteria can permanently take over and prevent good bacteria from providing any protection–>truly gram-negative BAD bacteria. This is a slippery slope down to oral health destruction.
What is something to know about menadione?
It is a precursor to vitamin K and serves like a fertilizer utilized by subgingival bacteria
Why is gingivitis a reversible host inflammatory response to microbial products?
Both degree of toxicity and concentration of toxins play major roles. Fluctuations in the host defense capabilities brought on by stress, drugs, disease, etc. contribute heavily to disease outcome.
Why do most chronic gingivitis sites (stable) not progress to periodontitis, even when not treated?
Gingival health demands an inflammatory response to ensure plaque bacteria don’t invade the tissues. Most have chronic gingivitis but many factors (temporary, long-term or permanent immune dysfunction) can cause this balance to tip towards progressive disease (periodontitis)
What is the role of anaerobic flora in the progression leading to bleeding gingivitis?
Bleeding induced by the inflammatory reaction provides RBCs needed for Bacteroides organisms. These organisms in turn produce LPS that is highly inflammatory.
What are some of the factors that contribute to increased susceptibility to sulcular disease?
Hormones, drugs, predisposing diseases, stress and oral habits
What is the relationship (and differences) between gingivitis and periodontitis?
Gingivitis can progress to periodontitis, but the differentiation lies in the fact that gingivitis does not cause destruction of the periodontal ligament, bone loss or apical migration of the junctional epithelium.
What role do reduced host defenses play in the development of NUG?
Patients with NUG are usually debilitated by some other disease or very stressed (leading to elevated corticosteroid levels and suppressed immunity (they also have been shown to have decreased PMN numbers.
What roles do spirochetes and selective gram-negative pathogenic rods play in NUG development?
NUG is a true tissue infection (typically superficial). Invasive Gram-negative spirochetes (Treponema spp-30%) and rods (Prevotella intermedia -24% which produce noxious sulfur products have been found in necrotic tissues of patients with NUG.
What is the ‘classic’ case of NUG and what are other factors that influence the development of this disease?
The classic case is trench mouth for soldiers in combat. Othes who suffer from this disease are usually debilitate by some other disease or very stressed (often exaggerated by poor sleep, poor eating habits, smoking (which constricts blood flow) and poor plaque control.
What is gingivitis?
Gingivitis is an inflammation of gingival tisues, due to plaque build-up and is characterized by redness, swelling, and bleeding of gingival tissues.
What are some of the features associated with pseudopockets?
+Junctional epithelium, + capillary flow, + junctional fluid, margination and migration of PMNS, and perivascular infiltrate mainly lymphocytes.
What are some key features between chronic (adult) and aggressive (juvenile/adult) periodontitis and periodontitis associated with systemic disease WRT PMN defects?
Chronic (adult) periodontitis can be localized or general and PMN defects are RARE. Aggressive juvenille/adult periodontitis can also be localized and general and has SOME to MANY PMN defects. WRT systemic disease, PMN defects are COMMON.
What is the key to the induction of exudate and bleeding in gingivitis (as well as periodontitis)?
The progression of the plaque community to one with more anaerobic, gram-negative bacteria
How would you describe the progression of the plaque community in gingivitis? (w/some specific examples)
Strep. & Actinomyces species–>plaque load grows a more anaerobic environment (+ in microaerophilic G+ Actino. Species) and emergence of Gram-Negative anaerobic rods and Spriochetes–>bleeding provides heme necessary for Bacteroides–>LPS produces inflammatory response.
