au14_-_pediatric_dent_final_exam_20141210195054 Flashcards
1
Q
What are the 3 ways discussed to detect bacterial species? What are the limitations of each?
A
- MICROSCOPY: difficult to distinguish similar morphotypes- CULTIVATION: special nutrient requirements; inhibition of some species by others; minor species overgrown; slow growing species overgrown- 16S SEQUENCING: rDNA gene alignments construct phylogenetic trees (not really a limitation…)
2
Q
In the oral cavity, what proportion of the species have been cultivated?
A
over half (300+ species)
3
Q
How many organisms are present in the oral cavity by cultivation? By 16 S sequence diversity? How many species are in each person?
A
- by cultivation, 300+ species- by 16S sequence diversity, around 700 species- each person harbors 100-200 species
4
Q
The mouth is an open system. We have ___ species vs. ___ of the oral cavity that grow.
A
- transient species- true residents
5
Q
What factors lead to bacterial diversity in the species that are adapted to the oral cavity and those who are transient?
A
contact with:- water- soil- plants- animals- other humans- other body sites
6
Q
What are the 4 purposes/goals of the Human Microbiome Project?
A
- determining whether individuals share a core human microbiome- understanding whether changes in the human microbiome can be correlated with changes in human health- developing the new technological and bioinformatic tools needed to support these goals- addressing the ethical, legal, and social implications raised by human microbiome research
7
Q
True or false: Each of us includes more bacterial cells than human cells.
A
true (our microbiota includes many-fold more DNA variety than our human genome)
8
Q
What are the different body sites that have distinct microbial communities?
A
- oral cavity- gastrointestinal- urogenital- skin- nasal
9
Q
Describe how the human oral microbiome is acquired. (include the study that addressed this)
A
- study tested the hygiene hypothesis (“don’t kiss babies or share utensils to avoid transmission of S. mutans)- study looked at babies in the NICU vs. babies that were home-reared- after 1 day, the difference between the babies was significant, but after 3 months, the babies were very similar in bacterial load
10
Q
What is the definition of ecology? Of a niche?
A
- ECOLOGY: study of the interrelationships of organisms and their environment- NICHE: a specific combination of conditions that are necessary for the survival of a particular organism; parameters may be physical, chemical, and biological
11
Q
The mouth has multiple niches:- non-shedding hard surfaces of teeth are unique because microorganisms can form ___- microorganisms can invade soft tissues, as in ___ and ___.
A
- stable, thick biofilms called “dental plaque”- periapical and odontogenic infections
12
Q
How do oral structures change over time?
A
- teeth erupt and are lost- pockets form (caused by bacteria)- injuries occur
13
Q
Name the oral surfaces to which bacterial adhere.
A
SOFT-TISSUE SURFACES:- sulcus, tongue, mucosa, gingivaHARD SURFACES:- supragingival: fissures (*most common), proximal surfaces, buccal and lingual enamel surfaces, cementum, restorations, calculus- subgingival: enamel, cementum, restorations, calculus
14
Q
Some bacteria are ___, but most of the bacteria that cause dental problems and many medical problems are ___.
A
- planktonic (floating in water)- sessile (attached to surface of biofilm)
15
Q
Biofilms are made up of ___ and ___ in a ___ environment.
A
- adherent microorganisms- extracellular matrix- aqueous environment
16
Q
What is the extracellular matrix of a biofilm?
A
- bacteria adhere to surfaces in aqueous environments and excrete a slimy glue-like substance that can anchor them to surfaces such as tooth, metal, plastics, medical implant materials, and tissue- sticky material that hold the biofilm together is called the extracellular matrix!- water flows through channels in the matrix like a circulatory system
17
Q
What is the biofilm life cycle?
A
- attachment- growth to mature biofilm community- detachment of cells to seed a new biofilm formation
18
Q
Describe the composition of a biofilm.
A
- can be formed by a single bacterial species, but more often, includes many species of bacteria- may also include other microorganisms like fungi, algae, or protozoa
19
Q
What is quorum sensing?
A
used by bacteria to know when there is a group large enough to do a specific activity
20
Q
When are biofilm-adaptive genes turned on?
A
- bacteria detect surfaces- bacteria detect each other (quorum sensing)- signals pass between bacteria
21
Q
How do multiple species co-exist and cooperate in a biofilm?
A
- provide nutrients for each other (food chains)- remove toxins- inter- and intra-species signaling is important- “division of labor” within the same species and among species
22
Q
What are biofilms resistant to?
A
- antibiotics- host defense- mechanical disruption
23
Q
True or false: Antibiotic doses that kill biofilm cells need to be increased as much as 1000-fold to kill suspended cells.
A
FALSE. Antibiotic doses that kill suspended cells need to be increased as much as 1000-fold to kill biofilm cells.
24
Q
What are the primary mechanisms for biofilm antimicrobial resistance?
A
- slowing of diffusion- “persister cells” that are alive but metabolically inactive survive and repopulate- close proximity and exchange of resistance genes
25
Are most bacteria in the mouth planktonic or in a biofilm? Is saliva considered a "sink of media"?
- most are attached in biofilms- saliva is just a thin film a few microns thick on oral structures, not a sink of media
26
What oral problems can be caused by biofilms?
- caries- periodontitis- osteomyelitis- osteonecrosis secondary to bisphosphonate therapy (anti-osteoclastic drug)
27
True or false: Preventing oral biofilms would prevent some invasive diseases as well
true
28
What are the 6 factors that contribute to the environment in the oral cavity and create specific niches?
- bacterial adherence- oxygen tension- pH- bacterial food supply or substrate- host inhibitory factors- bacterial community interactions
29
What are the surface sites for bacterial adherence to make biofilms? What common measures are used to disrupt bacterial adherence in the mouth?
- host surfaces (receptor molecules)- direct bacterial interactions- extracellular matrix- tooth brushing and flossing
30
What is salivary binding? What molecules are involved?
- promotes bacterial adherence by providing binding sites or inhibits by agglutinating and clearing- antibodies (acquired immunity)- salivary agglutinins- proline-rich glycoproteins- alpha-amylase
31
What is the % of oxygen in the air? In the closed mouth? In the periodontal pocket? In the supragingival plaque?
- air: 21%- closed mouth: 12-14%- periodontal pocket: 1-2%- supragingival plaque: 1-20% depending on age of the plaque
32
What is the oxidation-reduction potential (Eh)? What does a positive Eh mean? A negative Eh?
- electrical potential or tendency to oxidize or reduce (oxygen level)- positive Eh = aerobes (high oxygen)- negative Eh = anaerobes (low oxygen)
33
What is the difference between obligate anaerobes, facultative anaerobes, microaerophilic, aerotolerant anaerobes, and obligate anaerobes?
- OBLIGATE ANAEROBES: require oxygen at atmospheric levels for growth- FACULTATIVE ANAEROBES: can switch between aerobic and anaerobic metabolism- MICROAEROPHILIC: require low levels of oxygen- AEROTOLERANT ANAEROBES: anaerobic metabolism but can tolerate the presence of oxygen (*mostly in oral cavity!)- OBLIGATE ANAEROBES (AEROPHOBES): do not use oxygen as a nutrient and oxygen is toxic (kills or inhibits growth)
34
What are the 2 mechanisms of oxygen toxicity?
- causes oxidation of membrane lipids and destruction of cell integrity- causes oxidation of sulfhydryl groups in enzymes resulting in cross-linking and inactivity
35
What enzymes cannot be made in anaerobes? In the absence of these enzymes, what is produced?
- superoxide dismutase, catalase, or various peroxidases- superoxide and peroxide that can damage the cell
36
Where are anaerobic species found in tooth biofilms? Facultative and microaerophilic species? What species scavanges oxygen to help provide an anaerobic environment?
- oxygen-protected sites like the sulcus or mature coronal plaque- supragingival plaques- Fusobacterium
37
What common therapy is designed to exploit the oxygen sensitivity of oral bacteria?
peroxide
38
What is the normal oral pH? What may affect that pH?
- pH 7.0 (usually ranges from 5 (sugar fermentation) to 7.5 - direct affect: carbonated soft drink (pH 3)- indirect affect: bacterial fermentation of sugars to lactate (pH 5)
39
A low pH inhibits most oral species except ___.
acid tolerant strep and lactobacilli
40
What are the 2 major nutrient niches in the oral cavity?
- supragingival environment: saliva (endogenous) and ingested food (exogenous)- subgingival environment: crevicular fluid and cells (endogenous)
41
How are different types of exogenous nutrients ingested by bacteria in the oral cavity?
- low MW soluble carbohydrates and amino acids are readily taken up by bacteria- starches and proteins must be retained (sticky foods) for bacterial digestion
42
What are the endogenous nutrient sources? What does each contain?
- SALIVA: contains glycoproteins, inorganic salts, amino acids, glucose, vitamins- SHED HOST CELLS- GINGIVAL CREVICULAR FLUID: contains tissue and serum proteins, amino acids, glucose, vitamins, hemin (especially in gingivitis), hormones (estradiol, progesterone); degree of inflammation influences flow and composition- BREAKDOWN PRODUCTS FROM PERIODONTAL TISSUES (from bacterial proteases and host inflammatory degradation)
43
True or false:1. Endogenous nutrients are sufficient for plaque.2. Endogenous nutrients are sufficient for caries.
1. true (tube-fed patients have abundance of both supra- and subgingival plaque)2. FALSE. (need exogenous carbohydrate for caries)
44
What antibody is present in the saliva? In the crevicular fluid? Where are they produced? What do they do?
- sIgA (secretory immunoglobulin A) in saliva; prevents adhesion- IgG in crevicular fluid directly against peridontally important organisms- both systemically and locally produced- inhibit colonization, act as opsonins, and activate complement system
45
What are the 5 modes of innate immunity in the oral cavity?
- epithelial barrer and desquamation (soft tissues)- saliva flow- neutrophils (95% of leukocytes in crevicular fluid)- complement proteins from crevicular fluid- antimicrobial peptides produced in salivary glands, epithelium, and immune cells (defensins, histatins, cathelicidins)
46
What are the major salivary proteins? What are the mechanisms of saliva for maintaining the integrity of the tooth?
- alpha-amylase (digests starch and binds bacteria) and mucins (lubricants)- pellicle proteins/salivary minerals; salivary buffering
47
What are the 5 minor salivary proteins/defenses? What does each do?
- SALIVARY LYSOZYME: digests peptidoglycan in bacterial cell wall leading to osmotic disruption and cell death- SALIVARY LACTOFERRIN AND SERUM TRANSFERRIN: proteins that bind iron so that it is not bioavailable to bacteria- SIALOPEROXIDASE SYSTEM: generates superoxide radicals which inactivate bacterial enzymes leading to bacterial death- ANTIMICROBIAL PEPTIDES: have activity against bacteria and yeast- ACIDIC PROLINE-RICH PROTEINS AND STATHERIN: modulate salivary calcium and phosphate chemistry
48
Describe the food chain of lactic acid
- Strep produces lactic acid by metabolism of sugars- Veillonella requires lactate and converts it to propionate etc. and raises the pH for acid-sensitive Strep
49
Describe the food chain of vitamin K3 (menadione).
- Veillonella parvula synthesizes vitamin K3- used by P. gingivalis and P. intermedia
50
Who generates carbon dioxide in the biofilm? Whose growth is enhanced?
- generated by a number of organisms including peptostreptococci and Eubacteria- enhances growth of Capnocytophaga and A. actinomycetemcomitans
51
What bacteria removes oxygen from the biofilm and what bacteria survives because of it?
- Fusobacterium nucleatum/periodonticum- Tanerella forsythia
52
What are the 3 bacterial community interactions?
- bacterial products as nutrients (complex food chains)- bacterial products altering environment (oxygen/carbon dioxide availability)- microbial inhibitory factors
53
What are the major oral niches/ecosystems for bacteria?
- supragingival tooth surface and dorsum of tongue- gingival crevice (subgingival tooth and crevicular epithelial surface)
54
Saliva contains bacteria shed from all ecosystems - what are the implications for collecting samples for clinical diagnostic tests?
limitations because there are things being diluted, etc.; if you want to know what is going on in the tooth, look at the tooth
55
What are 3 ways microbes can be beneficial?
- resistance against pathogens- metabolic functions- immune activation
56
Describe the paradigm shift in microbiology.
- germs (bacteria = pathogenic invaders) --> microbes are essential- goal is sterile environment --> preserve native microbes- Koch's postulates & single-species acute diseases --> chronic diseases caused by microbial community disruptions (rather than invasive pathogen)- therapies focused on broad eradication (antibiotics/antiseptic) --> therapies to encourage healthy communities (probiotics/prebiotics/targeted antimicrobials)
57
The oral microbiome includes approximately ___ species of bacteria.
1000
58
What phyla of bacteria is most common in the oral cavity? What genera?
- firmicutes- streptococcus
59
What is the Theory of Focal Infection?
idea that removing oral "focus of infection" could cure systemic disease; goes back to ancient times (Hippocrates reported the cure of arthritis after removal of a tooth)(theory was challenged and discredited by 1930)
60
What do all of these diseases have in common?- cardiovascular disease- type 1 diabetes- infective endocarditis- cardiovascular implantable electronic devices (CIED)- prosthetic joints- bone pins, plates, and screws- intravascular access devices- cerebrospinal fluid (CSF) shunts- vascular grafts- pneumonia- immunosuppression- preterm birth- systemic lupus erythematosus
diseases that may have oral-systemic connections
61
How can causality be established to link oral-systemic effects?
- trials showing treatment effect (ex. remove periodtonal disease to see if heart disease reduces)- metastatic presence of bacteria- model systems
62
What are the 3 mechanisms for oral-systemic connections? Describe each.
- distant site infection seeded by oral bacteria (oral bacteria gain entry to circulatory system (bacteremia) or airway (aspiration))- distant site injury from toxin produced by bacteria in oral cavity (oral bacterial produces (such as endotoxin) gain access to circulatory system)- host genetic hyper-susceptibility to inflammation is common pathway to disease (ex. a genetic hyper-reactive host innate immune response may be a common predisposing factor for periodontitis, cardiovascular disease, obesity, etc.)
63
How can bacteremia be prevented?
- antibiotic prophylaxis- improved oral health
64
Describe the progression of Infective Endocarditis.
- platelets and fibrin adhere to exposed connective tissues producing "vegetation" or nonbacterial thrombotic endocarditis (NBTE)- bacteria from distant site (oral cavity!) enter blood stream (bacteremia) and adhere to NBTE- bacteria multiply and infiltrate heart tissues causing cardiac and valvular injury- discharged into circulation producing emobli and stroke
65
What bacteria are usually associated with Infective Endocarditis?
- Streptococci (sanguis, mitis group, mutans) (60+%)- Aggregatibacter actinomycetemcomitans- Gemella- Staphylococci (skin bacteria) (25+%)
66
What is antibiotic prophylaxis used for? What risks are associated with it? Is it successful?
- in theory, AP prevents hematogenous spread of bacteria (bacteremia)- risks: allergy, resistance- in practice, AP does not prevent bacteremia and is unlikely to prevent many cases of infective endocarditis
67
True or false: No evidence is available that dental procedures are associated with Infective Endocarditits.
true (random bacteremia from routine daily activities like chewing food or brushing are more likely to cause IE)
68
What is the most successful way to reduce risk of Infective Endocarditis?
more important to optimize regular oral hygiene measures to keep bacterial load low than to give antibiotic prophylaxis
69
Indications for antibiotics prophylaxis are based on what 2 factors? What antibiotic is usually used?
- invasiveness of procedure- high risk of infective endocarditis- single high dose of amoxicillin
70
Who is most susceptible to pneumonia caused by oral bacteria? What is the best way to prevent lung infections?
- those with poor airway protective reflexes (physically handicapped, elderly)- improved oral hygiene measures prevent lung infection (reduce nosocomial pneumonia by 40% and prevent 1/10 deaths in elderly in nursing homes)
71
Do randomized clinical trials show periodontal treatment reduces the risk of preterm birth or low birth weight? How are preterm birth and oral bacteria related? Is the evidence for causal relationship strong or weak?
- do NOT show periodontal treatment reduces risk- bacteria in amniotic fluid (some common oral species) associated with preterm birth- evidence for causal relationship NOT strong
72
Immunosuppressed individuals have a higher risk for what types of infections?
disseminated Strep or Candida of oral origin
73
Are dental treatment or antibiotics successful for prevention of oral-systemic infections in immunosuppressed individuals? What else can be used?
- lack of evidence for relationship to dental treatment or efficacy of antibiotics- focus on achieving/maintaining good oral health; consider invasiveness of procedure, bacterial load, and degree of immunosuppression
74
What are the thoughts on Cardiovascular Implantable Electronic Device infections as a result of oral species?
- CIED infections caused by bacteria from skin of patients or from hands of hospital workers or environment (Staph, etc.), not oral species- AHA guidelines: Nonvalvular Cardiovascular Device Related Infections 2003 recommend NO antibiotic prophylaxis for dental treatment
75
What are the thoughts on vascular grafts/stents infection as a result of oral species?
- most infections (90%) caused by bacteria native to skin or bowel- oral organisms rarely infective agent, but mortality rates are high- AHA guidelines: Nonvalvular Cardiovascular Device Related Infections 2003 recommend NO antibiotic prophylaxis for dental treatment
76
What are the thoughts on intravascular access device infections as a result of oral species?
- infections usually caused by Staph or other skin or environmental bacteria- CDC Guidelines for Prevention of Intravascular Catheter-Related Infections 2011 recommend NO antibiotic prophylaxis for any reason (good infection control practices and monitoring are key)
77
What are the thoughts on joint prostheses infections as the result of oral species?
- 1-2% become infected; mobidity high- most often Staphylococci, but 5% by bacteria found in oral cavity- dental procedures unrelated to implant infection; evidence for protection by antibiotic prophylaxis prior to dental treatment lacking- American Academy of Orthopaedic Surgeons/ADA Guidelines 2012: consider discontinuing the practice of routine prophylactic antibiotics when undergoing dental procedures; patient preference should be considered; maintain appropriate oral hygiene (emphasis!)
78
What is the difference between primary and secondary prophylaxis? What are the thoughts on each?
- PRIMARY ANTIBIOTIC PROPHYLAXIS: at the time of device placement; evidence-supported- SECONDARY ANTIBIOTIC PROPHYLAXIS: before dental procedure, etc.; lack of evidence to reduce procedure-related bacteremia and distant site infection
79
What are the thoughts on bone pins, plates, and screw infections as the result of oral species?
- orthopedic hardware not within synovial joint not at increased risk for hematogenous seeding by microorganisms- caused by staph or other skin bacteria- external fixation especially prone to infection- guidelines consistent: no indication for antibiotic prophylaxis to prevent oral bacterial source for patient with pins, plates, and screws
80
What are the two types of Cerebrospinal fluid shunts? What are the thoughts on cerebrospinal fluid shunt infections as the result of oral species in each?
- VENTRICULO-PERITONEAL (VP): does not involve vascular structures so low bacteremia; high rate of infection with skin bacteria; prophylaxis not recommended- VENTRICULO-ATRIAL (VA): AHA 2003 said no evidence that microorganisms associated wth dental procedures cause infection of nonvalvular cardiac devices
81
Describe the relationship between periodontitis and diabetes.
- increased prevalence of periodontitis in diabetics- treatment of periodontitis improves glycemic control- hyperactive innate immune response antecedent of both diseases- diseases have synergistic effect on inflammation- may promote dyslipidemia leading to CVD
82
Describe the relationship between cardiovascular disease and oral bacteria and the evidence for causality.
- coronary heart disease, stroke, and peripheral vascular disease are all associated with periodontitis; association is modest; link but no causative relationship established- may have a common cause (inflammation) or bacterial toxins or seeding of bacteriaEVIDENCE:- perio treatment trials have shown favorable responses but have not shown reduction in CVD- P. gingivalis exacerbates CVD in animal models- P. gingivalis and other perio pathogens found in atherosclerotic lesions
83
Describe the relationship between periodontitis and pancreatic cancer.
- studies show increased risk of pancreatic cancer in patients with periodontitis- pancreatic cancer is also linked to smoking, obesity, type 2 diabetes, insulin resistance
84
What should be of concern if you have a patient with systemic lupus erythematosus?
half of SLE patients have cardiac involvement (mitral valve insufficiency); prophylaxis is indicated with valve replacement only!
85
What precautions should be taken to prevent direct transfer of infective agents (infective endocarditis, pneumonia in compromised airway, immunosuppression, preterm birth)?
- improve oral health- reduce bacterial load- antibiotic prophylaxis only in high risk situations
86
What precautions should be taken when there is a possible transfer of an agent, but a common pathway is most likely (type 2 diabetes, cardiovascular disease, pancreatic cancer)?
primary preventive strategy is to treat periodontal disease to improve microbial profile and improve overall health by addressing risk factors
87
What precautions should be taken to prevent oral effects on systemic disease with the following conditions?- cardiovascular implantable electronic devices (CIED)- vascular grafts/stents- intravascular access devices- prosthetic joints- bone pins, plates, and screws- renal dialysis shunts- cerebrospinal fluid (CSF) shunts- systemic lupus erythematosus
NO SPECIAL ORAL PRECAUTIONS! (not oral bacteria)
88
Describe the dynamic balance of demineralization and remineralization.
- lactic acid produced by bacteria dissolves mineral from enamel- salivary minerals are deposited in enamel- no net change occurs
89
Describe the pathophysiology of caries progression.
- bacteria produces lactic acid from glycolysis of sugars- lactic acid drops pH and mineral matrix of tooth dissolves- tooth surface is stabilized by pellicle proteins so initial demineralization is subsurface (thin shell of enamel overlying body of lesion)- cavitation when subsurface demineralization becomes too severe or extraordinary force applied- remineralization possible as long as surface is retained
90
Is remineralized tooth structure or virgin enamel stronger? Why?
- remineralized tooth structure- incorporation of fluoride into hydroxyapatite crystal structure
91
What bacteria are involved in caries initiation?
- Streptococcus mutans- other Strep., S. sobrinus, S. salivarius- Veillonella metabolizes lactic acid- Actinomyces?
92
What bacteria are involved in caries progression?
- S. mutans- Lactobacillus casei, rhamnosus, gasseri, fermentum- Bifidobacterium & Scardovia
93
What type of bacteria is the most common supragingival organisms? Name each of them.
StreptococcusS. mutans (mutans streptococci)S. sobrinus (mutans streptococci)S. sanguinis (mitis group, including those below)S. parasanguinisS. mitisS. pneumoniaeS. gordoniiS. salivarius
94
Is S. mutans gram positive or negative? What shape? What type of respiration? What is its nutrition?
- gram-positive- cocci- facultative- ferments carbohydrate (only nutrient source)
95
Describe S. mutans biofilm behavior. Explain how it adapts for feast or famine.
- biofilm behavior: attaches to S. sanguinis; elaboration of extracellular polysaccharide matrix- feast: active transport ans self-protection by excretion of lactate- famine: good scavenger; good storage mechanisms; can maintain energy source (and low pH) over a long period of time
96
How can the environment affect S. mutans? What is the advantage of S. mutans to the host?
- fluoride interferes with transport and intracellular processes; pH dependent (activated at low pH)- advantage to host: protective against beta-hemolytic or other pathogenic strep (lactate and bacterocins)
97
What are the similarities and differences between S. mutans and S. sobrinus?
- similarities: closely related to S. mutans (collectively termed "mutans streptococci"); strongly associated with caries- differences: usually found in lower numbers than S. mutans
98
Describe S. mitis.
- ubiquitous- earliest acquired oral bacteria- bound by salivary amylase- not cariogenic
99
Where is S. sanguinis found? Gram positive or negative? What shape? What type of respiration?
- found in healthy (noncariogenic) plaque- gram-positive- cocci- facultative
100
How does S. sanguinis colonize? Describe its metabolism.
- good initial colonizer of pellicle-coated tooth surface; attaches via adhesins; adheres well- ferments carbohydrate and proteins; produces lactic acid well at high pH; can survive without sugar (ariginine hydrolase pathway raises pH (arginine -> urea -> NH3))
101
What bacteria is often a cause of infective endocarditis?
S. sanguis
102
Where can S. salivarius be found? Is it associated with caries? Is it found in saliva? What can it do?
- tongue and tooth are both niches- has been associated with caries- detected in saliva but doesn't grow there- excludes S. pyogenes
103
What effects does fluoride have on S. mutans?
- blocks active transport- blocks enolase (used to release lactic acid)
104
What type of caries can Actinomyces contribute to? Gram positive or negative? What shape? Respiration? Metabolism?
- root caries or early stages of enamel caries- gram-positive- filamentous- anaerobic or facultative- saccharolytic; acidogenic
105
Describe the metabolism of Veillonella. What is its contribution to the biofilm? Gram positive or negative? Respiration?
- does NOT ferment carbohydrates; ferments lactate -> propionate, etc -> raises pH!- protects against acid or helps acidogenic community members survive and contributes to caries- gram-negative- anaerobic
106
What are the different species of Lactobacilli? Where are Lactobacilli important? Gram positive or negative? Shape? Respiration? Metabolism?
- casei, rhamnosus, gasseri, fermentum- important in established or deep lesions- gram-positive- rod- anaerobic- saccharolytic; acidogenic; extremely acid tolerant
107
Where are Bifidobacterium and Scardovia important? Gram positive or negative? Shape? Respiration? Metabolism?
- may be important in deep caries- gram-positive- pleomorphic rods- anaerobic- saccharolytic and acidogenic and acid tolerant
108
Describe the attachment of S. sanguinis and S. mutans and development of biofilm.
- S. sanguinis binds to pellicle via specific adhesins- S. mutans binds to S. sanguinis via specific adhesins- S. mutans elaborates extracellular matrix from available sucrose (cross-linked insoluble polysaccharide = glucan)- S. mutans attaches glucan via glucan-binding proteins- both organisms can divide and stick, plus provide sites for attachment of other species
109
Describe the mechanism through which extracellular matrix is made.
sugar binds to glycosyl transferase site; monosaccharide is sent into the cell while the rest is bound to a glucan binding site on the cell surface
110
What is the difference between aciduric and acidogenic?
- aciduric: acid tolerant (can survive low pH)- acidogenic: can drive down pH (acid producing)
111
What is the difference between S. sanguinis and S. mutans at high/low pH?
S. sanguinis beats S. mutans in fermenting sugars at high pH, but S. mutans does better at low pH
112
Describe the acid tolerance response in S. mutans in response to environmental exposure (change in gene expression).
- resistance to acid increases- resistance to UV and oxygen increases- enhanced glycolysis- increased acid tolerance- increased acid production
113
What is different about the lactic acid production of S. mutans at different pHs compared to that of S. sanguis and other bacteria? Compared to L. casei?
- S. mutans has the highest lactic acid production at pH 5.0- other bacteria steadily decrease in lactic acid production from pH 6.5 to 4.0- L. casei increases in lactic acid production as the pH decreases
114
What is the short term effect of sugar consumption? The long term effects?
SHORT TERM:- drop in pHLONG TERM:- selection of S. mutans in plaque (acid-tolerant, acid-producing, even at low pH)- de-selection for alkali-generating organisms like S. sanguinis- removal of protective check on S. mutans- resting plaque pH may be 1 pH unit lower- net demineralization greatly enhanced- vicious cycle by further deselecting healthy bacteria
115
How does the response to glucose differ in a person with caries and a person without caries?
the pH of someone with caries will drop more after glucose exposure than someone without active caries
116
How does the plaque mass compare between a person who eats only meals (no snacks) and someone who eats meals with snacks between?
the plaque mass of someone who snacks between meals is higher than someone who only eats meals
117
When do children usually acquire S. mutans? From where?
- "window of infectivity" around 26 months based on cultivation, but often acquired very early; DNA-based studies show all children have S. mutans, perhaps in low levels in some- strains are acquired from mother (or other primary caregiver) and may be stable
118
What does the caries vaccine (to S. mutans) target? What 2 approaches are currently under investigation?
- targets glucosyl transferase (GTF) and binding proteins- mucosal vaccination for ACTIVE IMMUNITY (nasal and injected); adjuvants required to elicit much response- PASSIVE IMMUNITY from antibodies raised in tobacco plants or antibodies in immunized cow's milk; show effects when repeated doses are combined with removal of biofilm
119
What is replacement therapy? What are STAMPs?
- REPLACEMENT THERAPY: replacement of wild-type strain with genetically engineered strain of S. mutans that does not produce lactate- STAMP: Specificially Targeted AntiMicrobial Peptides; pheromone or antibody-guided antimicrobials that kill only target species
120
What is the ideal concentration of fluoride for maximum caries benefit and minimal fluorosis?
1 ppm
121
True or false: The benefits of fluoride are systemically incorporated into developing teeth.
FALSE. There is no benefit of fluoridated water before tooth eruption. The effects of fluoride are TOPICAL.
122
Which of these statements are true/false?1. In order to continue benefits, fluoridation must continue throughout life.2. People moving into a fluoridated area do not benefit after teeth erupt.
1. true2. FALSE. (they do benefit)
123
True or false: Fluoride should be delivered topically, rather than systemically.
true (risk of fluorosis increases by ingestion)
124
Describe what occurs during fluorosis during the secretory and maturation stages.
- during secretory stage of ameloblasts, very high levels of F can cause pitting and disturbances in form (not common)- during maturation stage, chronic moderately high level of F causes disruption in crystal formation that appear as chalky whiteness and weakness of enamel on the surface; after eruption, weakened enamel may fracture/stain
125
Where does fluorapatite form during fluorsis?
- pre-eruptively on the surface of enamel (surrounded by follicular fluid)- dentin-pulp interface
126
What is the composition of enamel? What is pure hydroxyapatite?
87% mineral (HA)11% water2% organic matrixCa10(PO4)6(OH)2
127
What is post-eruptive enamel maturation? How does this change the enamel?
- after eruption, when bathed in saliva (with calcium and phosphate) and exposed to fluoride, enamel crystals tend to perfect itself- phosphate replaces carbonatecalcium replaces sodiumfluoride replaces hydroxyl- makes HA less soluble and therefore stronger
128
Describe how acid dissolves enamel. At what pH does HA dissolve?
- pH 5.5- after dissolving some HA crystals, acid continues to dissolve HA crystals because the surrounding solution remains unsaturated due to the removal of component ions from solution under acidic conditions (H+ combines with (PO4)-3 and OH- to make (HPO4)-2 and H2O)
129
How does the presence of fluoride change the acidic dissolution of enamel?
- if the pH remains above 4.5 and F is available, fluorhydroxyapatite forms on the surface when HA dissolves- when the pH rises above 5.5, F ions enhance remineralization of enamel and dentin- presence of F at low levels in solution is more beneficial than high concentrations incorporated into enamel
130
True or false: Presence of F at low levels in solution is more beneficial than high concentrations incorporated into enamel.
true
131
Where is fluoride most present within the enamel? What type of lesion does this create when lactic acid is present?
- surface has more fluoride and less carbonate so the outer enamel is less soluble than the interior- whitespot lesions form when there is a hard stable surface layer (with very high fluoride concentrations) and a demineralized subsurface zone (since fluoride cannot penetrate to that area)
132
Are each of these true or false?1. Areas covered by plaque have high F levels2. Worn areas (abrasion, erosion) contain high levels of F3. Hard surface prevents or slows subsurface remineralization and demineralization.
1. true2. FALSE (low levels of F)3. true
133
What happens in the topical fluoride application of 50 ppm or lower? In an application of 100 ppm or higher?
- LOW F: fluorhydroxyapatite is formed on the outermost layers of enamel; this is stable and only lost if enamel wears away- HIGH F: calcium fluoride precipitates (CaF2); acid helps because it makes Ca available; spherical globules precipitate on surface, in crevices, and in plaque; cariostatic effect from deposition in micropores of initial lesions, but is gradually dissolved (stays better in protected spots)
134
What factors increase CaF2 deposition?
- increasing concentration of F- increasing exposure time- lowering pH- protecting (limit rinsing or cover with varnish)
135
How does saliva play a role in the stability of the tooth surface?
- saliva is saturated with calcium and phosphate so teeth don't dissolve- crystal growth does not occur because of salivary pellicle proteins that coat the enamel surface (tyrosine-rich peptides, statherin, proline-rich proteins)- proteins also prevent spontaneous precipitation in salivary ducts
136
True or false: In a plaque biofilm, interbacterial fluid can have even higher concentration of calcium and phosphate.
true (it helps with remineralization but can lead to calculus formation)
137
True or false: The body has a mechanism that controls the F levels.
FALSE. There is no homeostatic mechanism to control F concentration anywhere in the body so levels depend on daily intake and bone stores.
138
Do the pits, bands, and loss of areas of enamel due to fluorosis occur pre- or post-eruptively? The brown discoloration?
- post-eruptively- post-eruptively (due to staining of exposed protein)
139
True or false: Flurosis severity and incidence is correlated with the amount of exposure.
true (mild white mottling to severe brown stain)
140
True or false: A low-level exposure of fluoride will create no fluorosis.
FALSE: Even with a low-level exposure, a certain level of fluorsis occurs; there is no threshold below which no effect will be seen
141
Is mild fluorosis cosmetically objectionable? What concentration is considered cosmetically objectionable?
- mild fluorosis is perceived as attractive to most people- 0.1 mg/kg is high risk
142
What teeth and at what age is the fluorosis risk highest?
- upper central incisors- 15-30 months old
143
What are the antimicrobial effects of fluoride?
- F binds to sites that would normally bind OH and inhibits enzymes and regulatory proteins- fluoride is highly concentrated in plaque and bacteria do not develop a resistance to F- F inhibits enolase (enzyme in glycolytic pathway to lactate production); binding is enhanced by acidification so it is most effective against glycolysis at low pH- affects ecology of biofilms by reducing enrichment of acid-tolerant species
144
True or false: Fluoride inhibits the growth of bacteria at a normal pH.
FALSE. The inhibitory effects of F occur best at a low pH
145
What are the 3 methods of fluoride delivery?
- community-based water- self-applied- professionally-applied
146
What % of the US population has fluoridated water? What % of reduction in caries is seen? What is one perk of this method of fluoride delivery?
- 50%- 50%- highly cost-effective
147
What ppm F is in toothpaste in the US over the counter? By prescription? What % of caries reduction is seen?
- 1000 ppm F; 5000 ppm by prescription- 25% reduction over 2-3 years
148
In what forms is F included in toothpaste? Which of these are compatible with chalk-based formula or silica-based formula?
- NaF2: not compatible with chalk-based (precipitates out as CaF2); requires silica-based- MFP: compatible with chalk-based- SnF2
149
True or false:1. Using more toothpaste = less caries.2. Using toothpaste 2x/day is better than 1x3. Less rinsing is better.
1. FALSE (no relationship between amount of toothpaste and caries)2. true3. true (smaller amounts of water and less vigorous = better)
150
What ppm of F is present in OTC Fluoride rinses? What % reduction of caries is seen?
- 200 ppm (0.02% F)- 25% reduction (surprising benefit considering low concentration; probably because no rinsing)
151
What % of F is in professional foam gels and rinses? What % of reduction in caries is seen?
- 1.23% acidulated phosphate fluoride; 0.9% fluoride as NaF2- 30% reduction in caries
152
What % of F is in fluoride varnish? What % of reduction in caries is seen?
- 2.2% F as NaF- 40% reduction in caries
153
Describe how the deposition of CaF2 on the surface of the tooth affects the tooth.
- topical products deposit CaF2 on the surface of the tooth; this is a temporary reservoir that will be lost over time by dissolution and wear- during an acid attack, CaF2 will dissolve and increase remineralization and become incorporated into fluorapatite
154
True or false:1. Water fluoridation does not deposit CaF2 on the surface of the tooth.2. Incorporation of fluoride into enamel during development provides significant anti-caries benefit.
1. true2. FALSE: does NOT provide
155
True or false: There is no evidence that nutrition in post-developmental period has any effect on caries.
true (however, poorly mineralized teeth are more susceptible to demineralization but they will not decay if the local substrate for bacterial acid production is not present)
156
True or false: Smooth surface caries are primarily a disease of industrialized societies. In pre-industrialized societies, caries rates are low and primarily confined to root surfaces and fissures.
true (as diet of refined foods are adopted, caries rates climb)
157
Describe the relationship between sugar utilization and DMF teeth (decayed, missing, filled).
direct correlation (countries with more sugar utilization have more DMF teeth)
158
What happens to the number of DMF teeth as sugar consumption increases in a NON-INDUSTRIALIZED country? In an INDUSTRIALIZED? Why?
- NON-INDUSTRIALIZED: number of DMF teeth increases as sugar consumption increases- INDUSTRIALIZED: number of DMF teeth is constant as sugar consumption increases- this is because of confounding factors (fluoride, oral hygiene, frequency of sugar consumption, and nutritional/general health factors)
159
What did the study of wartime sugar restrictions in England during WWII show?
- caries rates in children declined dramatically 1-3 years after reduction in sugar intake- caries rate increased sharply 1-2 years after postwar changes in diet
160
What were the results of the control group of the Vipeholm study? The sucrose group? The sweetened bread group?
CONTROL GROUP:- no sugar for 3 years = almost no caries- small amount of sugar then added at meal time = small caries incrementSUCROSE GROUP:- 300 gm of sucrose in solution at meal time = small caries incrementSWEETENED BREAD GROUP:- addition of afternoon sweet bread snack = no increase in caries- addition of afternoon snack plus sweet bread with all meals = significant increase in caries
161
What were the results of the chocolate group of the Vipeholm study? The toffee group (8 toffees/day)? The caramel group (22 caramels/day)?
CHOCOLATE GROUP:- sucrose solution with meals plus chocolate between meals = 4x increase in cariesTOFFEE GROUP (8 toffees/day):- 8 toffees between meals = extreme rise in caries- 24 toffees between meals = very extreme rise in cariesCARAMEL GROUP (22 caramels/day):- year 1, vitamins = no effect on caries rates- year 2, sticky carbs with meals = minimal effect on caries rates- year 3, 2 caramel snacks = rise in caries rate- year 4, 4 caramel snacks = further rise in caries- year 5, no caramel snacks = back to baseline
162
What did the Vipeholm study conclude that caries rates were based upon?
- amount of sugar- between meals- sticky form
163
What was the Hopewood study and what did it show?
- 80 children in Austrailian orphanage were fed natural food, vegetarian diet that was low in refined carbs; between meal eating was controlled; hygiene was poor; fluoride was deficient- after 10 years, the number of DMF teeth was 1.3 compared to 10.4 in the general population- after age 13, the children were relocated and their caries rates soared, although still not as high as those in general population
164
True or false: Sweet preference is genetic and not environmentally affected.
FALSE: Sweet preference changes with exposure to sugar. A higher threshold for sweetness and greater sugar consumption correlates with caries.
165
In the study that tested children's sensitivity to 6-n-proplthiouracil (PROP), how did their sensitivity correlate with the number of DMF teeth?
children who were more sensitive to the sweetness had lower caries rates (probably because they didn't need to add as much sugar to taste it)
166
What was the result when dental students had no oral hygiene and had 9 daily rinses with 50% sucrose?
white-spot lesion after 2 weeks
167
What did the Turku study find between a diet of sucrose, fructose, or xylitol?
- ordinary sucrose-containing diet: caries- sucrose replaced with fructose: lowered white-spot increment- sucrose replaced with xylitol: lowest white-spot increment
168
True or false: British children consume more sucrose than US children and have higher proportion of smooth surface caries.
true
169
Why is sucrose more important for smooth surface caries than fissure caries?
surface molecule takes up sucrose and helps bacteria make copious amounts of ECM to hang on
170
Currently, what type of sugar is more common in consumption in the USA: cane/beet sugar or corn sweeteners?
corn sweeteners (because of carbonated soft drinks)
171
What is the current leading source of added sugars in the daily diet of young Americans?
soft drinks (rapid rate of increase of carbonated beverages begins at age 8; in 1985, pop consumption became greater than tap water consumption)
172
What dietary guidelines for children should be followed to decrease caries?
- limit intake of 100% juice to 4-6 oz daily- restrict other sugared beverages to occasional use- consume 2 or more servings of dairy food
173
What is the long term effect of a high sugar diet on the pH in the mouth?
in someone who typically has a high sucrose diet, when sugar is introduced, the pH drops lower than someone who has a normal diet
174
Between sorbitol, mannitol, xylitol, and erythritol, which is as sweet as sucrose? Which is the most effective decay preventive sweetener? Which have a laxative effect?
- xylitol is as sweet as sucrose- xylitol is the most effective decay preventive sweetener- sorbitol and mannitol have a laxative effect
175
True or false: Xylitol gum may be more effective than sorbitol gum or combinations of xylitol and sorbitol.
true, but the superiority of xylitol is not confirmed in 2 out of 4 clinical trials; chewing sugar free gum 3 or more times daily for prolonged periods of time may reduce caries regardless of the type of sugar sub
176
How do polyol-containing gums and candies (sugar substitute) prevent caries?
probably based on stimulation of salivary flow, and maybe an antimicrobial effect
177
What no-calorie sweetener is described below?- dipeptide of phenylalanine and aspartic acid- not safe in phenylketonuria- approx 200x sweeter than sugar- clean sweet taste- digested but in such small amounts that it can be considered calorie free- used as table top sweetener and in soft drink (not heat stable so not in baked goods)
aspartame (Equal or Nutrasweet)
178
What no-calorie sweetener is described below?- used for over a century- until 1970s, was only low-calorie sweetener in USA- some bitter after taste- not metabolized so noncaloric and noncariogenic- used in wide variety of low-calorie and sugar-free foods, beverages, and pharmaceutical applications- temperature stable- causes bladder cancer in rodents, but appears to be safe in humans
saccharin (Sweet N' Low)
179
What no-calorie sweetener is described below?- high-intensity, non-caloric sweetener approximately 200x sweeter than sucrose- clean, sweet taste with no aftertaste- not metabolized and is excreted unchanged so no calories and does not contribute to caries- temperature stable
acesulfame-potassium (Sunette or Sweet One)
180
What no-calorie sweetener is described below?- chlorinated sucrose derivative with 3 atoms of chlorine substituted for 3 hydroxyl groups on the sugar molecule- 600x sweeter than sucrose- not metabolized so noncaloric and noncariogenic- tastes like sugar- stable and can be used anywhere sugar is used- sold as table top sweetener and many food/drinks
sucralose (Splenda)
181
What is the critical pH for cariogenicity?
pH 5.5
182
How does adhesion of food play a role in caries? Is cooked starch or unprocessed starch retained longer?
- more adhesion to teeth = more acid production; addition of water to diet reduces caries (probably because it can wash teeth off)- cooked starch is more soluble and may be retained longer
183
What types of foods inhibit caries?
- xylitol- calcium- phosphates (like phytate) (buffer and crystal stabilization by protecting Ca)- fat- casein phosphopeptide (may inhibit demineralization and promote remineralization)- sodium bicarbonate (baking soda) (raises plaque pH)- carbamide (raises plaque pH)
184
What are the sites where caries most commonly occurs?
- fissures- proximal surfaces- facial and lingual surfaces- margins of restorations
185
True or false: Toothbrushing without fluoridated toothpaste does not reduce caries rate.
true
186
What are the main reasons for the lack of efficacy of brushing teeth for caries reduction without fluoride toothpaste?
- bristles do not reach the caries prone sites (fissures and proximal surfaces)- usually not carried out sufficiently thoroughly
187
What is the recommended frequency of brushing? For when to brush?
- FREQUENCY: 2x per day (plaque removal every other day appears to be sufficient to prevent gingivitis)- WHEN: before meals reduces acid production; before bed gives long-term fluoride benefits
188
What is the recommended amount of toothpaste to use? Rinsing behavior? Age to begin brushing?
- AMOUNT: amount doesn't matter, but higher concentrations of fluoride are more effective- RINSING: volume of water and vigor both affect caries; should rinse minimally- AGE: earlier (before age 1) seems better
189
What is the ideal manual toothbrush?
filaments arranged at different heights and angles; good for plaque removal and reducing gingivitis, but no data on caries reduction
190
Which is better: a manual or powered toothbrush?
powered toothbrush with rotation oscillation action reduce plaque and gingivitis more than a manual toothbrush
191
Which is better: oscillating/rotating/pulsating toothbrush vs. high frequency toothbrush?
studies have found each more effective than the other; vague
192
What is the best way to deliver oral hygiene instruction?
modify patient's existing method, emphasizing the need to reach all surfaces
193
What has evidence shown about the effectiveness of professional prophylaxis (AKA professional mechanical removal of plaque)?
- semi-annual cleanings have no effect on caries; every 2 weeks prevented caries- professional mechanical plaque removal with OHI in adults is more effective for the prevention of periodontal disease than no treatment, but not necessarily better than OHI alone
194
What is the most effective agent for chemical plaque control?
fluoride
195
True or false: Rinses are effective against periodontitis.
FALSE. Rinses cannot enter the sulcus so they are not effective against subgingival problems like periodontits.
196
What are the side effects of chlorhexidine rinse? Does it add to the effects of fluoride? Does it reduce caries?
- staining, calculus, taste alterations, tissue irritation- adds little to the effects of fluoride- no good evidence for reduction of caries
197
How does casein phophopeptide work as chemical plaque control? Quaternary ammonium compounds like cetyl pyridinium chloride?
- CASEIN PHOSPHOPEPTIDE: milk protein bound to amorphous calcium phosphate; binds to plaque; supplies calicum and phosphate during acid attack- QUATERNARY AMMONIUM COMPOUNDS (Scope, Cepacol, Viadent): may reduce plaque; not proven to prevent caries
198
How does triclosan work as chemical plaque control? Essential oils? Oxygenating mouthrinses?
- TRICLOSAN (Colgate Total toothpaste): slightly more effective than fluoride alone; effective against gingivitis- ESSENTIAL OILS (thymol, eucalyptol, methyl salicylate, menthol (Listerine)): effective against gingivitis; some evidence for protection from caries- OXYGENATING MOUTHRINSES (orajel): carbamide peroxide-containing rinses release oxygen on contact with tissue; effective against anaerobic bacteria; may be anti-inflammatory? not tested on caries
199
How do prebrushing rinses work as chemical plaque control? Sanguinarine?
- PREBRUSHING RINSES (Plax): not any more effective than placebo- SANGUINARINE (herbal remedy): may reduce plaque; not safe (precancerous lesions)
200
True or false: Caries is NOT dichotomous.
true (it is a continuum from incipient to advanced)
201
What are the advantages of using the explorer stick method to diagnose caries? What are the disadvantages?
ADVANTAGES:- can feel for soft areas in enamel with poor light on a wet uncleaned toothDISADVANTAGES:- can produce irreversible traumatic defects in demineralized areas in occlusion fissures which could prevent repair of lesion by remineralization and contribute to lesion progression
202
What is an alternate to the "explorer stick" method to diagnose caries? Describe.
- visual exam and gentle exploration with probe- needs optimal conditions (clean, dry tooth; good light; sharp probe (light touch, stroke across surface); magnification)- observe for: frank cavitation, decalcification (white-spot; refractive index of air > water > tooth), opalescence (deep caries), discontinuities in surface* black/brown staining is NOT a reliable indicator of caries* use the probe lightly or not at all!
203
What is the spectrum on how early lesions should be managed?
- HIGHLY AGGRESSIVE: "exploratory" excavation and enameloplasty, seal/restore- seal deep fissures and excavate & seal/restore chalky or soft enamel- HIGHLY CONSERVATIVE: seal incipient decay and intact fissures
204
What is the definition of reliability? Validity? What is the "gold standard" for validity for detection of caries?
- RELIABILITY: the reproducibility of measurements- VALIDITY: degree to which a measurement expresses the true value- histologic exam is the "gold standard" (but can't be used in vivo!)
205
What is the definition of sensitivity? Of specificity?
- SENSITIVITY: proportion of people/teeth with caries who have a positive test result- SPECIFICITY: proportion of healthy people who have a negative test result
206
How is reliability determined statistically? Describe the scoring.
kappa statistical test1 = perfect agreement> 0.75 = excellent> 0.40 = good< 0.40 = poor
207
For a routine clinical examination, what are the best methods for diagnosing fissure caries?
visual inspection augmented with appropriate radiographs
208
For diagnosis of fissure caries, is sensitivity high or low? Specificity?
sensitivity is lowspecificity is high
209
Describe the evidence of the effectiveness of conservative treatment options for fissure caries.
- there is a decrease in viable microorganisms in lesions under intact sealants and caries progression is negligible; result from blocking nutrients- simply sealing cavitated lesions was 84% sucessful after 9 years while sealed conservative amalgams were 97.5% and conventional amalgams were 83%
210
True or false: Hidden sealed caries will progress.
FALSE (myth not supported by science)*however, restorations must be mechanically supported and margins must be sealed
211
What are the 2 major (and balancing) concepts in management of small lesions?
- diagnostic tests are not very sensitive (incipient lesions are hard to detect)- minimal treatment is effective for incipient and moderate lesions (early detection may not change treatment strategy)
212
What are the scores for the International Caries Detection and Assessment Score System?
0 = sound tooth surface1 = first visual change in enamel2 = distinct visual change in enamel3 = microcavitation4 = underlying dark shadow from dentin with or without cavitation5 = distinct cavity with visible dentin6 = extensive distinct cavity with viable dentin
213
Does an explorer exam have a high or low sensitivity? Specificity? What is a disadvantage?
- low sensitivity- high specificity- may cause damage
214
What's the difference between a visual inspection for caries and an explorer exam?
- both have low sensitivity and high specificity- there is no damage from visual inspection!
215
What do you do if there is severe caries hidden due to constricted fissure anatomy? Probe won't stick and nothing is visible!
- this is not found in nature, silly- you do not need to buy new equipment to find these- you could seal them; intact sealants block substrate and halt decay
216
How do caries detection dyes work? How specific are they?
- non-specific protein dyes stain organic matrix of less mineralized dentin- false positives at the DEJ and circumpulpal (may lead to over-preparation!)
217
What is a KaVo DIAGNOdent laser? How does it work? Does it have high or low sensitivity? Specificity?
- 655 nm diode laser- detects fluorescence from demineralized enamel- low specificity (false positives)- high sensitivity
218
What does the DIAGNOdent respond to? What are the reading related to?
tooth needs to be clean and dry...- decalcified enamel (caries)- hypocalcified enamel- high natural fluorescence of the tooth- plaque and organic plug- composite and stained margins- calculus- prophy paste (particularly green)- food (particularly green)- readings related to degree and intensity of demineralization NOT depth of lesion (penetrates 2-3 mm)
219
True or false: All fissures should be scanned with DIAGNOdent before placing fissure sealants. This will alert you to the presence of damaged enamel that could prevent successful resin bonding which can lead to failure of the sealant
FALSE: if the damaged enamel isn't on the surface, how would it interfere with bonding
220
True or false: Air abrasion improves the success rate of sealants.
FALSE (not proven)
221
What is the Midwest Caries ID Detection Handpiece? How does it work?
- has a green LED light, red LED light, and receiving fiber- when green light is deflected by demineralized enamel, red light and audible signal is activated
222
What is the INSPEKTOR PRO Caries Detection System (QLF)? How does it work?
- research instrument that monitors caries PROGRESSION; expensive and time-consuming- early caries detection = fluorescence of tooth tissue- bacterial activity detection = red fluorescence from bacterial metabolites*fluorescent bacteria = veillonella, prevotella, and other species
223
Does the QLF have a high or low sensitivity? Specificity? Advantages? Disadvatages?
- high sensitivity (finds "hidden caries"; reliable for determining absence of disease)- low specificity (false positives)- advantage: tracks lesions over time to locate active caries and remineralization- disadvantage: expensive and time consuming for clinical practice; research tool
224
For a Caries Scan Pro, does it have a high or low sensitivity? Specificity? What confounding factors play a role?
- high sensitivity- low specificity (less mineralized tissue contains more fluid and has greater electrical conductivity)- confounding factors: young teeth are more porous, enamel hydration, enamel thickness, area of contact
225
How does transillumination technology work? What are the advantages?
- visible light illumination is captured by computer imaging- advantages: research suggests that it is more sensitive than radiography and there is no risk
226
How does DEXIS CariVu work?
utilizes near infra-red light and the images captured are transmitted to the DEXIS system
227
How does the Canary System work? How does its sensitivity/specificity compare to radiology?
- laser system measures luminescence and heat- creates a Canary Number to reflect the state of mineraliztion and crystalization- detects up to 5 mm from the tooth surface and as small as 50 microns- in vitro studies show performance > radiography for detection of proximal lesions- better sensitivity and equal specificity
228
What are the 3 microbiologic tests for risk assessment?
- saliva-check mutans- CariScreen susceptibility test- CRT (caries risk test)
229
How does the Saliva-Check Mutans test work? How effective is it?
- immunochromatography quick test contains moncolonal antibodies (mabs!) that selectively detect Strep mutans- results in 15 min- values above the red line mean salivary levels of S mutans is equal to or above 500,000 cfu/mL- tests have not been shown to be good risk predictors on an individual basis
230
How does the CRT (caries risk test) work? How effective is it?
- CRT bacteria cultivation test for S. mutans and lactobacilli; results in 2 days- CRT buffer also checked via dipstick for salivary buffering capacity; results in 5 min- evidence is limited
231
What is a CariScreen caries susceptibility test? How effective is it? Sensitivity? Specificity?
- 1-minute chair-side bacterial test that measures ATP bioluminescence; claims to detect levels of acid-producing, decay-causing bacteria residing in an individual's plaque and assesses patient's caries risk- evidence is limited; not diagnostically useful predictor of caries risk- low sensitivity- good specificity
232
True or false: The new technologies to diagnosis/detect caries (KaVo DIAGNOdent, Inspector Pro, etc.) can replace probe/visual exams.
FALSE. The new technologies are adjunctive tools (expensive, time consuming, false positives, impress your patients, generate income, and reduce radiographs (?))
233
Describe chronic periodontitis.
- slowly progressing, cumulative disease- usually first diagnosed in adulthood but may begin early- sporadic, unpredictable disease activity- detectable only by observing residual damage from previous disease- most patients have mild to moderate disease- not all sites equally affected
234
Describe aggressive periodontitis.
- begins early- rapidly progressing- shows site-specific patterns of destruction in young patients (localized aggressive periodontitis)
235
What is the primary defense against bacteria in the sulcus?
neurtrophils
236
If tissue damage does not include bone, it is ___ and is called ___.If tissue damage includes bone, it is ___ and is called ___.
- reversible- gingivitis- irreversible- periodontitis
237
What are the 3 zones of subgingival plaque biofilm?
- tooth attached plaque- epithelium attached plaque- unattached plaque
238
What occurs if tissue invasive bacteria invades deeply (close to the bone)?
- prolong osteoclastic activity- block osteoblastic activity- net result is bone loss
239
True or false: The bacterial species in the periodontal pocket are only gram negative.
FALSE: both gram negative and gram positive
240
What type of molecule is the food source for supragingival bacteria? For subgingival?
- saccharolytic (carbs)- proteolytic (proteins)
241
The bacteria in the periodontal pocket that cause disease, are they true pathogens or commensal species?
very recent studies suggest pathogens and commensals work together to cause disease
242
What species are part of the Red Complex?
- Porphyromonas gingivalis- Tanerella forsythia- Treponema denticola* these are species found consistently in chronic disease
243
What are some other species (not Red Complex) that under suspicion in chronic disease?
- Prevotella intermedia- Campylobacter rectus- Selenomonas noxia- Aggregatibacter actinomycetemcomitans
244
What species is associated with localized aggressiver periodontitis?
Aggregatibacter actinomycetemcomitans
245
What species are under suspicion in chronic disease based on DNA-based studies?
- Fillifactor alocis- Desulfobulbus sp.- Synergistetes sp.- Treponema sp.
246
True or false: Transmission of periodontal pathogens can occur between spouses AND from parents to children.
true
247
What is the most common cause of pulpal inflammation and necrosis? How can this occur?
- bacterial infection- direct pulpal exposure- bacterial penetration though dentinal tubules from caries- direct access due to traumatic fracture of tooth- travel from bloodstream (anachoresis)
248
How can physical trauma cause pulpal necrosis and subsequent infection?
- during injury, blood supply may be damaged or severed at the apex -> tissue death- once pulp is non-vital, the positive fluid pressure in dentinal tubules may be disrupted which makes teeth more vulnerable to invasion by microbes- tissue death is follwed by infection more or less quickly depending on bacterial access- since the pulp is non-vital, the immune system does not work and the bacteria can grow
249
True or false: Bacteria are necessary for pulpal and periapical disease to occur.
true (good seal is critical for success of pulpal therapy)
250
Of the bacteria involved with periapical and pulpal disease, are they anaerobic or aerobic? Gram positive or negative?
- anaerobic- gram-negative
251
What genus of bacteria have been associated with periapical abscesses especially?
- Prevotella- Porphyromonas* both are responsible for foul odor
252
True or false:1. Endodontic infections are usually the result of just one species.2. Both proteolytic and saccharolytic bacteria can be found in the pulpal canal.
1. FALSE: usually due to mixed bacterial infections2. true (saccharolytic more coronal, proteolytic more apical)
253
What is pulpitis? Can it be reversed? What are the symptoms?
- early stage endodontic infection; pulp compromised by inflammation; extent of bacterial growth unclear- can be reversed if treated early- early stage symptoms are lowered threshold and prolonged pain response to cold or other stimulus; onset of spontaneous pain signals shift to irreversible status and eventual pulpal necrosis (pain can be severe, sharp, throbbing)
254
Describe periapical lesions (apical periodontitis). (how do they occur, clinical signs, etc.)
- as pulp becomes necrotic, inflammatory cells can't enter pulp b/c lack of blood supply so they go to the periapical tissues- bone resorption takes place to allow space for barrier of inflammatory cells to accumulate and prevent spread of infection (bacteria are most numerous in the root canal)- inflammatory response is usually effective and bacteria are confined to periapical tissues- infections are asymptommatic and only detected on radiographs
255
Most periapical lesions are ___. ___-dominated, but there are other inflammatory cells present.
- granulomas- macrophage
256
Describe acute dentoalveolar (periapical) abscess.
- acute exacerbation of periapical lesion- purulent bacterial infection is confined to bone at apex; bacteria and PMNs are seen in the apical tissues- very painful; tooth sensitive to pressure; aching, throbbing, pain- drainage of pus brings relief; may be accomplished by endodontic access or tooth extraction
257
Where may an acute dentoalveolar abscess drain?
- draining may occur spontaneously through fistula to surface or into tissue spaces- draining to surface brings relief- drainage into tissue spaces is serious since it leads to orofacial involvement
258
What is pallative treatment of pulpal and periapical diseases?
- treatment aimed at relieving patient symptoms- pharmacologic treatment with analgesics and/or long-acting local anesthetic agents- antibiotics are not effective against infections confined to pulp or apical periodontitis or abscesses because they cannot get to the pulp during pulpitis
259
What is definitive treatment of pulpal and periapical diseases?
- treatment aimed at ridding the patient of cause of infection- should be attempted whenever possible- extraction of tooth- root canal treatment (thorough cleaning and good coronal seal is critical to success)
260
What are the possible reasons for persistant apical lesions?
- biofilm may be present on the surface of the tooth apex- debris may remain within inaccessible regions of the apical canals- foreign body such as infected dentin fragments may have been displaced by over-instrumentation
261
What is the treatment for persistant periapical lesions?
- external biofilm cannot be removed by conventional endodontic therapy- irregularly shaped apical foramen may be difficult or impossible to instrument from a coronal approach- apical debris cannot be reached by nonsurgical access- surgical therapy "endodontic microsurgery" also called "apicoectomy" effective- endodontic microsurgery/apicoectomy cleans the apex of bacteria and necrotic tissue; apex is accessed surgically and the tip of apex is removed to clean the apical foramen; foramen is then sealed with biocompatible agent like mineral trioxide aggregate
262
What is cellulitis? What can you tell about its origin from its location?
- infection spreads through soft tissue via vascular channels or direct autolysis of tissues; produces edema termed "cellulitis"- tissues are hard (indurated) to palpation and not fluctuant (no pus)- lower facial cellulitis almost always dental- upper facial cellulitis dental in origin about half the time
263
What may cellulitis progress to?
- cellulitis may proceed to 2nd phase: abscess formation- foci in badly infected tissues may be walled off and local acute inflammatory process stimulated with migration of PMNs and pus production- avascular sequestrum of cellular debris and bacteria (oxygen levels are low)- fluctuant, erythematous
264
How may an abscess from cellulitis drain?
natural drainage:- external: intra-oral or extra-oral fistula- internal: into tissue spaces leading to potentially serious infections* will NOT resolve without drainage!
265
Are cellulitis and abscesses due to one or many species? Aerobic or anaerobic? What species are common?
- polymicrobial (4-6 species)- cellulitis may have facultative, but abscess has anaerobes- streptococcus, peptostreptococcus, prevotella, fusobacterium
266
How is cellulitis treated? Abscess treated?
- cellulitis: temporarily managed with antibiotics but will resolve more quickly if source of infection removed- abscess: drainage via tooth extraction, root canal, surgical incision, etc.
267
What are the 2 first line antibiotic choices in treating cellulitis?
- penicillin- clindamycin (alternative)
268
What is alveolar osteitis (dry socket)? How is it treated?
- delayed healing of extraction site; premature breakdown of fibrin clot exposing bone; biofilm formation on bone surface; swelling, redness, exposed bone; painful, throbbing, aching; mal-odor, bad taste, oozing- treatment: systemic antibiotics not effective; gentle debridement, medicated dressing; time limited
269
What is ostomyelitis of the jaw? How is it treated?
- spread of odontogenic or peridontal infection to jaw bone- radiolucent area of bone; may be surrounded by involucrum (radio-opaque)- swelling, pain, erythema, maybe fever- may show pus and sequestra of nonvital bone- mixed species biofilms, resorption pits with biofilms- treatment: surgical debridement, longterm antibiotic therapy
270
What is Antiresorptive Agent-Induced Osteonecrosis of the Jaw (ARONJ)?
- occurs in patients who have taken bone antiresorptive agents (bisphosphonates, denosumab, cathepsin K inhibitors)- antiresorptive agents inhibit osteoclasts and bone remodeling- post-extraction swelling, pain, erythema, ulcer, pus, bone sequestra, failure to heal- rare in healthy adults; not reported in children- usually in immunocompromised
271
Describe the etiology of ARONJ.
- without osteoclasts, exposed bone becomes a non-shedding surface much like tooth- bone surface is also compromised by reduced vascularity- biofilms form on exposed bone surface after dental extraction or surgery- mixed species bacterial and yeast biofilms, resorption pits with biofilms
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What is the treatment of ARONJ?
- systemic antibiotics are ineffective!- remove biofilm by debridement- drug holiday (don't do drugs for a bit)
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How can ARONJ be prevented?
- avoid dental extractions in immunocompromised patients with history of bisphosphonate treatment- maintain good oral health in at-risk patients- conservative surgical approaches- avoid exposure of bone; cover if possible- antimicrobial mouth rinses after surgery
