Quiz 5 Flashcards
Risk factor
any attribute, characteristic, or exposure associated with increased likelihood of developing disease/injury
Etiological factor
any attribute, characteristic, or exposure known to CAUSE disease
Modifiable risk factors
either acquired or anatomical (ex/restorations, biofilm, malposition teeth, smoking, diet)
Nonmodifiable risk factors
socioeconomic status, genetics, adolescence, pregnancy, age, leukemia
Aquired local risk factors
calculus, overhanging restorations, poorly contoured restorations
Anatomic risk factors
malpositioned teeth, root grooves, concavities, furcations
Systemic risk factors
uncontrolled diabetes, stress, hormonal changes, systemic bone disorders, neutrophilic disorders (perio as manifestation of systemic disorder)
Tobacco use
most significant known risk factor for perio
Medications
can cause gingival enlargement
calcium channel blockers, anticonvulsants, immunosuppressants
Biological equilibrium
physiological mechanism that functions to maintain balance in body
aka homeostasis
microbes
all types of microscopic organisms
bacteria, fungi, protozoa, viruses
not all are pathogenic
Gram staining
classified bacteria based on cell envelop structure, either gram-positive or gram-negative
Gram-positive
thick single cell wall, stains purple
Gram-negative
double cell wall (2 membranes with single wall between) containing LPS (endotoxin), pink or red
Biofilm
dynamic microbial community embedded into matrix adhered to living or nonliving surface, may be responsible for 65% of diseases
Biofilm formation timeline
within minutes: free floating attach to surface
2-4 hours: strongly attached microcolonies
6-12 hours: produce initial extracellular matrix
Biofilm evolves into fully mature biofilm in…
2-4 days, extremely resistant to antibiotics and antimicrobial agents
What is the best way to control biofilm?
physical removal to break up dental biofilm
Commensal bacteria
part of normal floral in mouth, prevent colonization of opportunistic pathogenic bacteria
Transmissible (direct or indirect)
transfer of bacteria that may or may not produce infection in an individual
periodontal pathogens are transmissible, but it is NOT an infectious disease
Vertical tranmission
most common, sharing salsa between caregiver and child, occurs between different generations
Horizontal transmission
less common, individuals of same generation kissing
Gram negative species
Neisseria, Veillonella, Aggregatibacter, Campylobacter, Prevotella, Spirochetes of ANUG
Gram positive spices
streptococcus, peptostreptococcus, actinomyces, rothia, eubacterium, mycoplasm
Stage 1: Initial attachment
dynamic and reversible, pellicle of tooth, within hours
Stage 2: permanent attachment
….
Stage 3: Maturation Phase I
self protective extracellular matrix
Stage 4: Maturation Phase II
micro colony formation, microbial blooms (specific species growing at accelerated rates
Quorum sensing
bacterial signaling; communicate by releasing small proteins
Fluid channels
facilitate movement of nutrients and O2 to bacteria, carry away waste products
Stage 5: Dispersion
escape from the matrix, enables bacteria to spread and colonize new tooth surfaces
*essential stage of lifecycle
Non specific plaque hypothesis (historical)
over accumulation of plaque biofilm and overabundance of bacteria in biofilm lead to gingival inflammation
Socransky’s microbial complexes (historical)
microbial composition of biofilm, rather than the amount, is deciding factor in development of periodontal disease
Orange and red complexes
periodontal disease
Red: P. gingival, T. forsythia, T. denticola
Yellow, green, blue, purple complexes
gingival health
Ecological plaque hypothesis (current)
accumulation of nonspecific bacteria triggers host inflammatory response, environment in sulcus becomes more conductive to growth of pathogenic bacteria
*shift in local environment driving disease
Microbial homeostasis-host response hypothesis (current)
shift from beneficial to pathogenic bacteria triggers uncontrolled host inflammatory response, causes tissue destruction
Keystone pathogen host-response hypothesis
SPECIFIC species of pathogenic bacteria trigger uncontrolled host immune response