periodontitis Flashcards
statistics According to the CDC:
___% of adults aged 30 years and older have some form of periodontal disease.
Periodontal disease increases with age, 70.1% of adults 65 years and older have periodontal disease.
Do not separate out the early stages, e.g. gingivitis
47.2% of adults aged 30 years and older have some form of periodontal disease.
Periodontal disease increases with AGE, 70.1% of adults 65 years and older have periodontal disease.
Do not separate out the early stages, e.g. gingivitis
what are the 3 hypothesis of how periodontal disease develops
- non-specific plaque
- specific plaque
- dysbiosis microbial imbalance (current)
nonspecific plaque hypothesis
old hypothesis that stated the accumulation of bacterial _______ leads to periodontal disease
Abundance of biofilm = ________
Issues with this hypothesis:
- Too ______
- Does not explain how some cases of _______ never progress to _________
- Does not explain why some sites can have a lot of ______ and others not as much, with the same oral hygiene ______ and about of biofilm
- ______ relationship
old hypothesis that stated the accumulation of bacterial BIOFILMS leads to periodontal disease
Abundance of biofilm = PERIO DISEASE
Issues with this hypothesis:
- Too SIMPLISTIC
- Does not explain how some cases of GINGIVITIS never progress to PERIODONTITIS
- Does not explain why some sites can have a lot of DESTRUCTION and others not as much, with the same oral hygiene HABITS and about of biofilm
- LINEAR relationship, more bacteria in gingivitis = periodontitis. NOT TRUE, depends on host response
specific plaque hypothesis
____ hypothesis that stated the specific pathogenic bacteria in biofilm leads to ______ disease
Microbiome shifts from _____, beneficial microbes to ________ pathogenic microbes
believes the _______ of biofilm is important
Issues with this hypothesis:
- Still too _______, but does give us a better understanding
- says ___ complex bacteria is the only factor
- Some studies contradict concepts of this theory
OLD hypothesis that stated the specific pathogenic bacteria in biofilm leads to PERIODONTAL disease
Microbiome shifts from GRAM POSITIVE, beneficial microbes to GRAM NEGATIVE pathogenic microbes
believes the COMPOSITION of biofilm is important
Issues with this hypothesis:
- Still too SIMPLISTIC, but does give us a better understanding
- says RED complex bacteria is the only factor
- Some studies contradict concepts of this theory
why is histopathology important
histo = microscopic
pathology = study of cause/effect of disease
important for understand the prognosis of disease
prognosis: guess on how the patient will respond to treatment
how much bacterial species are in the oral cavity
define microbe
what two groups are microbes put it depending on the staining process
650-1K
encompasses bacteria, fungi, protozoa, and viruses
gram positive or negative
staining depends on _______
gram negative has __ membranes
gram positive has __ membranes
which type has LPS
staining depends on PERMEABILITY
gram negative has 2 membranes
gram postiive has 1 membrane
gram negative has lipopolysaccharides that result in the direct breakdown of some tissues
MICROBIAL COMMUNITIES
social creatures
- many species ______ together
- _____ communities that live on ___ surfaces
- share ______ with each other through _____
biofilm
- complex and ______ microbial community
- ________ = several species
- contains a self protective matrix: ________
diseases
- estimates that ___% of ALL diseases are ________
-EX: (4)
social creatures
- many species CONGREGATE together
- COMPLEX communities that live on ALL surfaces
- share NUTRIENTS with each other through FLUID CHANNELS
biofilm
- complex and DYNAMIC microbial community
- POLYMICROBIAL = several species
- contains a self protective matrix: SLIME LAYER
diseases
- estimates that 65% of ALL diseases are BIOFILM INDUCED
-EX: tuberculosis, cystic fibrosis, bacterial endocarditis, and periodontal diseases
biofilm formation timeline
within minutes:
2-4 hours:
6-12 hours:
2-4 days:
within minutes: free floating bacteria attach to the surface and forms an acquired pellicle
2-4 HOURS: microbes form strongly attached microcolonies (mushroom-shaped attached at narrow base)
6-12 HOURS: extracellular protective matrix/slime layer forms: resistant to antiseptics and antibiotics
2-4 DAYS: fully mature biofilm colonies
4 steps of biofilm growth
- Free-floating bacteria attach within minutes
- Attracts others
- Secrete extracellular slime layer
- Clumps break off and form new colonies elsewhere
mature biofilms
slime layer _____ from ________ and _______ cell penetration deep into the matrix
can block ________ agents
antibiotic resistant bacteria excretes _______ to protect all bacteria present
hibernation AKA ________ makes antibiotics ________; many in the deep layers _____
slime layer PROTECTS from ANTIBODIES and INFLAMMATORY cell penetration deep into the matrix (blocks our fighter cells)
can block ANTIMICROBIAL agents
antibiotic-resistant bacteria excretes PROTECTIVE ENZYMES to protect all bacteria present
hibernation AKA QUIESCENCE makes antibiotics INEFFECTIVE; many in the deep layers HIBERNATE/QUIESCENCE
IN HEALTH
state of ______: live in _____
mostly gram _______
oral biofilm needs constant _____ to prevent ________
define dysbiosis
state of SYMBIOSIS: live in HARMONY
mostly gram POSITIVE
oral biofilm needs constant DISRUPTION to prevent MATURATION
DYSBIOSIS: accumulation of bacteria that promotes a higher host response, inflammation, and eventual tissue damage
BIOFILM DAY 1-3 (early colonizers)
Non-______, free-______, ______, non______, ____gingival
Gram-______ RODS
(2)
Gram-_____ COCCI
(1)
NONMOTILE, FREE FLOATING, AEROBIC, NONPATHOGENIC, SUPRAGINGIVAL BACTERIA
GRAM POSITIVE RODS
- actinomyces viscosus
- actinomyces israelii
GRAM POSTIVE COCCI
- many species of streptococci
BIOFILM MATURATION DAYS 4-7
increase in ______
forms: (2)
increase in gram negative bacteria
forms: vibrios (tails), spirochetes (spiral)
MATURING BIOFILM DAYS 7-14
______ > equal numbers of ____ and ____
Increase in gram-negative forms: (2)
what can be seen?
CHRONIC > equal numbers of gram positive and negative are increasing in gram negative forms
vibrio and spirochetes
clinical inflammation is present
3 forms of oral biofilm:
supragingival
subgingival non attached
subgingival attached
*can be tissue associated or tooth associated
attached biofilm: attached to _____ on the root surface. associated with root ____ and _____, mainly gram positive and negative _____ and _____
nonadherent biofilm: adheres to the _____, can be found in pocket _____, gram negative highly _____, larger number of ______, professional ______ of subgingival biofilm needed
which kind is more dangerous
attached biofilm: attached to TOOTH CEMENTUM on the root surface. associated with root CARIES and CALCULUS, mainly gram positive and negative COCCI and RODS
nonadherent biofilm: adheres to the TISSUE EPITHELIA, can be found in pocket LUMEN, gram negative highly VIRULENT, larger number of SPIROCHETES, professional DEBRIDEMENT of subgingival biofilm needed
free floating bacteria: gram negative road and spirochetes that can destory bone
what are the four stages of PERIODONTAL disease
- initial stage: 2-4 days, initial lesion forms
- early stage: 4-10 days, injury can progress to an early lesion
- established stage: 2-3 weeks, established lesion develops
- final stage: marks the transition from gingivitis to periodontitis
INITIAL STAGE
- increase in tissue _______
- ______ fluid increases
- migration of _______
- 5-10% ________ destruction
- not seen ______
INITIAL LESION
- a________
- ___ days after biofilm colonizes
- Inflammatory cells: ____ pass from BV into the ______
- Release ______
- Destroy gingival __ and provide a path for PMN to _________
INITIAL STAGE
- increase in tissue PERMEABILITY
- CREVICULAR fluid increases
- migration of LEUKOCYTES
- 5-10% COLLAGEN destruction
- not seen CLINICALLY
INITIAL LESION
- ASYMPTOMATIC/SUBCLINICAL
- 2-4 days after biofilm colonizes
- Inflammatory cells: PMNs pass from BV into the GINGIVAL SULCUS
- Release CYTOKINES
- Destroy gingival CT and provide a path for PMN to JE
EARLY LESION: ACUTE GINGIVITIS (stage 2)
- Infection __ resolved
- Biofilm overgrowth accumulates; about __ week
- Early _____ signs clinically _______
- Inflammatory cells increase– _______ predominate
- More ____ (phagocytic bacteria), ______, _______ (inflammatory mediators)
- 70% _____ lost (reversible thanks to ____)
- May last __ weeks or longer depending on the ____
- May progress to the _______ lesion
- Infection NOT resolved
- Biofilm overgrowth accumulates; about 1 week
- Early GINGIVITIS signs clinically PRESENT
- Inflammatory cells increase: LYMPHOCYTES predominate
- More PMNs (phagocytic bacteria), MACROPHAGES, LYMPHOCYTES (inflammatory mediators)
- 70% COLLAGEN lost (reversible thanks to FIBROBLASTS)
- May last 3 weeks or longer depending on the HOST RESPONSE
- May progress to the ESTABLISHED lesion
ESTABLISHED LESION (CHRONIC GINGIVITIS)
- biofilm moves into ______
- disrupts the most ______ portion of __ and loosens attachment to the root
- destruction of _______ fiber bundles, more ______, still _______
- pocket epithelium appears, __________
- presence of ________ (___, ____)
- more _____ destruction
- what type of pockets are seen
- biofilm moves into GINGIVAL SULCUS
- disrupts the most CORONAL portion of JE and loosens attachment to the root
- destruction of SUPRAGINGIVAL fiber bundles, more PERMEABLE, still REVERSIBLE
- pocket epithelium appears, EPITHELIAL RIDGES
- presence of INFLAMMATORY MEDIATORS (PMNs, LEUKOCYTES)
- more COLLAGEN destruction
- PSUEDOPOCKETS
ESTABLISHED LESION (stage 3)
- _____ gingivitis
- _____ biofilm phase
- lot of _______ and _______
- immune cells increase and release _______, ________, _______
- __ weeks to _______
- self care and immune effects control ______ and ________
- CHRONIC gingivitis
- SUBGINGIVAL biofilm phase
- lot of INFLAMMATORY PMNS and PLASMA CELLS
- immune cells increase and release CYTOKINES (INTERLEUKINS), PROSTAGLANDINS, AND MATRIX METALLOPROTEINASES
- 2 weeks to INDEFINITE
- self care and immune effects control INFECTION RATE and PROGRESSION
ADVANCED LESION (stage 4)
- ______
- ______ tissue destruction
- JE proliferates _______ and invades underlying __
-_______ of the JE, bacteria can now effect __ and ______
- biofilm spreads ______, no longer a ______
- ______, ________, _____ destroy PDL permanently
Loss of __ attachment
_______ shift to destroy CT
________ of epithelium allows bacterial invasion deeper to CT, PDL, bone
________ now destroy bone, starting at the ____
- PERIODONTITIS
- PERMANENT tissue destruction
- JE proliferates EPITHELIAL RIDGES and invades underlying CT
-APICAL MIGRATION of the JE, bacteria can now effect PDL and ALVEOLAR BONE
- biofilm spreads APICALLY, no longer a PSUEDOPOCKET
CYTOKINES, PROSTAGLANDINS, AND MMPs destroy PDL permanently
Loss of CT attachment
FIBROBLASTS shift to destroy CT
ULCERATION of epithelium allows bacterial invasion deeper to CT, PDL, bone
OSTEOBLASTS now destroy bone, starting at the CREST
PERIODONTAL DISEASE is a _______ process
- ______ effects on biofilm
- _____ inflammatory response to biofilm by the host immune response
PERIODONTAL DISEASE is a MULTIFACTORIAL process
- INDIRECT effects on biofilm
- INDIRECT inflammatory response to biofilm by the host immune response
THE CURRENT HYPOTHESIS: DYSBIOSIS MICROBIAL IMBALANCE
- no single ______ dominates in health
- retained _____ matures and brings in bacterial species that elicit a _______
- leads to gingival inflammation, initial _____
- oral dysbiosis: susceptible patients _____ host response causes progression from _____ to _____
- periodontitis: results from an inappropriate __________ to normal microbiome exacerbated by the presence of some _____-associated bacterial species
- no single MICROBIAL STRAIN dominates in health
- retained BIOFILM matures and brings in bacterial species that elicit a STRONGER HOST RESPONSE
- leads to gingival inflammation, initial DYSBIOSIS
- oral dysbiosis: susceptible patients INAPPROPRIATE/EXCESSIVE host response causes progression from GINGIVITIS to PERIO
- periodontitis: results from an inappropriate INFLAMMATORY REACTION to normal microbiome exacerbated by the presence of some DISEASE-associated bacterial species
HOST RESPONSE
Periodontal health can be maintained if the pathogen level is ___, and the host response is sufficient with ___ and __________ care
_____ and ________ hold disease in check
When plaque biofilms become pathogenic then host compromised ________ will result
________ reaction
Periodontal health can be maintained if the pathogen level is LOW, and the host response is sufficient with SELF and PROFESSIONAL care
PMNS and FIBROBLASTS hold disease in check
When plaque biofilms become pathogenic then host compromised INFLAMMATION will result
HYPERINFLAMMATION reaction
as clinicians what can we do to impact the host response
- refer pts to a nutritionist
- inform pts about stress/diet/water intake/exercise
- tobacco cessation
- encourage diabetes to maintain control of hba1c
Dysbiosis hypothesis/Ecological plaque hypothesis/microbial homeostasis-host response hypothesis/Keystone pathogen hypothesis
Changes in _______ environment > ______ environment > favors an ______ in pathogenic bacteria > _______
Shift in _____ environment shifts biofilm to a ________ state
______ now considered
Changes in SUBGINGIVAL environment > ALTERED environment > favors an INCREASE in pathogenic bacteria > DAMAGE
Shift in LOCAL environment shifts biofilm to a PATHOLOGIC state
HOST RESPONSE now considered
PATHOGENIC BACTERIA
What we are confident in: ______ bacteria are present in ________
No evidence to say they are the _______—but they are key players
_________ is certainly part of it and risk factors to that host response are key to ____
What we are confident in: SPECIFIC bacteria are present in PERIODONTITIS
No evidence to say they are the INITIATORS but they are key players
HOST RESPONSE is certainly part of it and risk factors to that host response are key to PROGNOSIS
what 5 major bacterias are associated with PD
- porphyromonas gingivalis (PG)
- invades soft tissue
- aggressive gram negative
- transmitted within families - aggregatibacter actinomycetemcomitans (AA)
- invade soft tissue
- aggressive gram negative
- transmitted within familes
- destroy CT and bone - tannerella forsythia (TF)
- aggressive gram negative - tremponema denticola
- gram negative
- associated with disease progression and improvement with elimination - prevotella intermedia (PI)
- gram negative rod
- associated with subgingival plaque
what SPECIES are associated with PD
- eubacterium
- fusobacteriam nucleatum and nigrescens
- peptostreptococcus micros
- not all bacteria is bad, dysbiosis is what causes trouble
RED COMPLEX
- dominate in the _____ biofilm
- lots of research on its role in perio, conflicting data if _____ effects
- which bacteria are included
- i________
- orange complex is also very ______
- dominate in the LATE STAGE (MATURE) biofilm
- lots of research on its role in perio, conflicting data if CASUAL effects
- PORPHYROMONAS GINGIVALIS, TANNERELLA FORSYTHIA, AND TREMPONEMA DENTICOLA
- INTERDEPENDENT
- orange complex is also very PATHOGENIC
All ________ is preceded by ________, but not all _______ is followed by _______
All periodontitis is preceded by gingivitis, but not all gingivitis is followed by periodontitis
disease progression is
-non______
-periods of _______
-periods of ________
- complex interactions between the ______, _________, and _______
- NONLINEAR
-periods of EXACERBATION
-periods of QUIESCENCE - complex interactions between the MICROBIOME, HOST SUSCEPTIBILITY, and ENVIRONMENTAL FACTORS (diet/systemic conditions/diabetes/habits/stress)
CYTOKINES
- ___ to progression
- ______ molecules
- signal from one ____ to another
- call ________ to the site of infection
- recruits leukocytes such as ___ and ______
- increases ________ to help fighter cells and _______ get in, bacteria causes ________
- allows _____ and ______ cells to move into tissues
- KEY to progression
- PROTEIN molecules
- signal from one CELL to another
- call PHAGOCYTIC CELLS to the site of infection
- recruits leukocytes such as PMNs and MACROPHAGES
- increases VASCULAR PERMEABILITY to help fighter cells and BACTERIA get in, bacteria causes EXUDATE
- allows IMMUNE and COMPLEMENT cells to move into tissues
IN HIGH LEVELS OF CYTOKINES
- high levels of other inflammatory mediators (______ and _______)
- Bacterial challenge results in high levels of ______ from the ___ on gram neg. bacterial walls
- body chooses to lose the tooth to control infection > immune systems way of protecting the host
- high levels of other inflammatory mediators (PROSTAGLANDINS and MMP)
- Bacterial challenge results in high levels of IMMUNE RESPONSE from the LPS on gram neg. bacterial walls
INFLAMMATORY MEDIATORS
Cytokines:
> _______ (IL-1) is secreted by ___, ____, ____ cells, and ____; stimulates ___ and ____
> ____ (TNF) secreted by ____; produces ____ and causes __ and ____ destruction
Prostaglandins (PGE):
>Secreted by ___ and _____; causes secretion of ___ and bone ______ through osteoclasts
Matrix metalloproteinases (MMPs)
> Family of __ enzymes associated with destroying ________
Cytokines:
> INTERLEUKIN-1 (IL-1) is secreted by PMN, LYMPHOCYTES, EPITHELIAL cells, and MACROPHAGES; stimulates PROSTAGLANDINS and OSETOCLASTS
> TUMOR NECROSIS FACTOR (TNF) secreted by PMN; produces MMP and causes CT and BONE destruction
Prostaglandins (PGE):
>Secreted by PMN and MACROPHAGES; causes secretion of MMP and bone RESORPTION through osteoclasts
Matrix metalloproteinases (MMPs)
> Family of 12 enzymes associated with destroying COLLAGEN
what 3 things is destruction characterized by
where is bone levels in health
- apical migration of the JE
- loss of attachemt
- loss of bone
crest of the bone is 2mm apical to the CEJ (3 is considered okay due to radiograph distortion)
suprabony pocket vs infrabony pocket
SUPRABONY
- base of the pocket is coronal to the bone
- horizontal bone loss (stage 1 or2 perio)
INFRABONY
- base of the pocket is apical to the bone
- vertical bone loss (stage 3 or 4 perio)
why do we see different clinical patterns of destruction (5)
- microbiome pathogenicity
- host risk factors
- elimination and control of risk factors
- self and professional care
- periods of exacerbation and quiescence
what is included with the perio assessment (5)
- IAG - attached gingiva
- FGM - 000
- probing - 1-3mm
- BOP - less than 10%
- attachment level - auto calculated
when is recession considered loss due to PD
when there is recession in the interproximals
recession on just the facial is likely due to a bad brushing habit
classes of recession (4)
miller class I: isolated to the facial
miller class II: isolated to the facial but extends to or beyond the MGJ
miller class III: damage is broad and includes the papilla from disease progression, MDJ is also involved
miller class IV: damage is broad, damage is severe in the interdental papilla, MGJ is involved
what are the classes of furcation
class I: concavity is just above the furcation entrance, bone is still intact between the root
class II: probe can enter the furcation but not go all the way through
class III: probe enters the furcation through and through but it is covered by the gingiva
class IV: probe enters the furcation through and through and there is recession making the furcation clinically visible
millers classifcation of tooth mobility
class I: tooth can be moved less than 1mm
class II: tooth can be moved more than 1 mm, no vertical mobility
class III: tooth can be moved more than 1mm and can be depressed in the socket (vertical mobility)
stage 1 periodontitis (initial)
cal
rbl
tooth loss
PD
type of BL
CAL: 1-2mm greater than health
RBL: 15% in the coronal third
0 tooth loss to PD
4mm or less PD
horizontal bone loss
what is considered direct/indirect evidence
what is the main thing that determines if perio is stage 3 or 4
direct: radiographs!! radiographic bone loss
indirect: clinical attachment loss
tooth loss
stage 2 periodontitis (moderate)
cal
rbl
pd
tooth loss
type of bone loss
CAL: 3-4 mm greater than health
RBL: 15-33% in coronal third
PD 5mm of less
no tooth loss due to perio
horizontal bone loss
stage III (severe)
cal
rbl
PD
tooth loss
type of bone loss
furcations
CAL: 5mm or more
RBL: greater than 33% extednign from middle third and beyond
PD: 6mm or more
1-4 teeth lost due to perio
vertical bone loss of 3mm or more
class 2-3 furcations
stage IV periodontitis (severe)
CAL
RBL
teeth lost
PD
additional modifiers
CAL: 5mm or more
RBL: greater than 33%
PD 6mm or more
5 or more teeth lost due to perio
masticatory dysfunction, secondary occlusal trauma, severe ridge defects, bite collapse, pathologic migration of teeth, less than 20 teeth remaining (10 opposite pairs)
localized vs generalized periodontal disease
localized: less than 30% involved
generalized: more than 30% involved, must have two nonadjacent areas.
grading
Grade A
- RBL or CAL
- % bone loss / age
- case pheonotype
- risk factors
Grade B
- RBL or CAL
- % bone loss / age
- case pheonotype
- risk factors
Grade C
- RBL or CAL
- % bone loss / age
- case pheonotype
- risk factors
Grade A
- RBL or CAL: no loss over 5 years
- % bone loss / age: less than .25%
- case pheonotype: heavy biofilm, low destruction
- risk factors: nonsmoker, nondiabetic
Grade B
- RBL or CAL: less than 2mm over 5 years
- % bone loss / age: .25-1.0%
- case pheonotype: equal biofilm and destruction
- risk factors: smokes less than 10 cigs a day and hba1c less than 7
Grade C
- RBL or CAL: 2mm or more over 5 years
- % bone loss / age: over 1%: destruction exceeds biofilm expectations
- case pheonotype
- risk factors: smokes more than 10 cigs a day and hba1c over 7
local risk factors
- biofilm _______
- increases _____ biofilm and ________
- can directly ______ the periodontium
- biofilm RETENTION
- increases MATURE biofilm and PATHOGENICITY
- can directly INJURE the periodontium
CALCULUS
- ______ surface
- retains ______ which causes ______
- contributes to _______ and ________
- does NOT cause _______
MECHANISM OF CALC
- Mineralization of plaque begins from ____ up to _____ after plaque initiation. Depends on _______ and ________
- Covered with pathogenic bacteria on the _____ layer, is bacteria hibernating within?
- ROUGH surface
- retains BIOFILM which causes PD
- contributes to CHRONICITY and PROGRESSION
- does NOT cause PD
- Mineralization of plaque begins from 48 HOURS up to 2 WEEKS after plaque initiation. Depends on SALIVA COMPONENTS and GENETICS
- Covered with pathogenic bacteria on the OUTER layer and also hibernates within
secondary factors regarding calculus
- _______
- reservoir for _______
- interferes with ______
- POROUS
- reservoir for ENDOTOXINS
- interferes with SELF CARE
OVERHANGING RESTORATIONS
- _______ factor
- retains _______
- food ________
- marginal issues (3)
- IATROGENIC factor
- retains PLAQUE BIOFILM
- food IMPACTION
- marginal issues: subgingival margins, roughened margins, and gaps between teeth
occlusal disharmonies
- Due to ________ of teeth
- Poor restorations that alter ______ and cause pressure during mastication
- Tooth ______ contributions
- what kinds of trauma?
- Due to MISALIGNMENT of teeth
- Poor restorations that alter OCCLUSION and cause pressure during mastication
- Tooth ANATOMY contributions
- PRIMARY: getting hit; SECONDARY: weakened periodontium results in trauma
signs and symptoms of trauma (5)
- tooth mobility
- sensitivity due to pressure (trauma) not hot and cold (recession)
- migration of teeth
- enlarged funnel shaped PDL space
- alveolar bone resorption
The role of _______ in the progression of periodontal disease remains _______
Not _______ due to the inability to perform an ______ controlled clinical trial
Current data: occlusal discrepancies and certain types of occlusal contacts contribute to the _________ of periodontal disease
Treatment of occlusal discrepancies has a __________ therapeutic effect
The role of OCCLUSION in the progression of periodontal disease remains CONTROVERSLE
Not DEFINITIVE due to the inability to perform an ETHICALLY controlled clinical trial
Current data: occlusal discrepancies and certain types of occlusal contacts contribute to the PROGRESSION of periodontal disease
Treatment of occlusal discrepancies has a BENEFICIAL therapeutic effect
appliances
- poor fitting ________
- _________
mouth breathing
- mostly impacts ________
- these pts have more ____ and _____
- does not response well too ________
Oral piercings
- Habits like _______ it against teeth causes the worst damage
- ______ surface that retains plaque
grinding/clenching
- _________ habit
- how do pts. know they do this
appliances
- poor fitting PROSTHETICS
- ORTHODONTICS
mouth breathing
- mostly impacts MAX ANTERIOR
- these pts have more PLAQUE and CALCULUS
- does not response well too CONVENTIONAL THERAPY
Oral piercings
- Habits like RUBBING it against teeth causes the worst damage
- ROUGH surface that retains plaque
gridning/clenching
- parafunctional habit
- jaw/mouth pain, headaches, TMJ clicking
