periodontology Flashcards
gingivitis
accumulation of plaque in the mouth causing reversible inflammation of the surrounding soft tissue
causes of microbial challenge
- local plaque retentive factors
= calculus, crowding, overhangs and margins, mouth breathing - systemic modifying factors
= hormones and medication
diagnosis of healthy gums
- well defined, knife edge margins
- pointed papillas
- stippling in some
- healthy pink colour
healthy gingival turnover
4-5 days
what bacteria will predominate in healthy gingiva
aerobes
gingivitis signs
- puffy rolled gingival margins
- loss of stippling
- redness
- local bacterial plaque changes
- bleeding gums
what is amplified in the disease state
the immune response
what leads to bleeding on probing
the epithelium proliferates quickly which can lead to ulcerations and ultimately bleeding
what happens in early gingivitis
- slightly increased infiltration of immune cells
- proliferation of junctional epithelium
- very few plasma cells infiltrate
- blood vessels dilate
what happens in established gingivitis
- greatly increased leukocyte infiltration
- lots of increased proliferation of the junctional epithelium meaning false pockets form
- plasma cells constitute 20-30% of infiltrating cells
false pockets
- epithelium has proliferated
- inflammatory exudate causes swelling and therefore the illusion of a pocket is created as the probe end disappears
- however there is NO LOSS OF ATTACHMENT
true pockets
- apical migration of the junctional epithelium as the source of inflammation is not removed
- exposes cementum as a site for biofilm accumulation
- loss of attachment is rarely regained and can result in healthy looking gingiva having deep pockets
loss of attachment can be
continuous or periodic
general rate of loss of attachment
- 05-0.1mm/year
- greatly variable among patients
the biofilm
one or more communities of microorganisms embedded in a glycocalyx, attached to a solid surface
glycocalyx
glycoprotein and glycolipid covering surrounding the cell membranes of bacteria
properties of the biofilm
- provides protection for colonising species against environmental pressures and competition
- facilitates the uptake of nutrients and expulsion of metabolic waste (plaque acid)
- develops a physiochemical environment to favour bad bacteria (lowers pH and O2 concentration)
- allows communication between bacteria
bacterial virulence
the ability to colonise and compete in an ecological niche and to evade host defences to survive
ways bacteria evade the host immune system
- degrade host immunoglobulin and complement
- leucotoxin production
- tissue invasion
- inhibition of antibody synthesis
how are oral bacteria equipped to cause periodontal disease
they easily break down antibodies and cytokines
evidence which would support bacteria being the causation
- associated bacteria reside in higher concentration in diseased sites
- reduced numbers of bacteria following periodontal therapy
- presence of an elevated specific immune response
- production of virulence factors to evade host defences and invade tissues
what is red complex bacteria
identified bacteria highly associated with the presence of periodontal disease
synergistic infection
- relates to the interaction or cooperation of two or more organisations, substances or other agents to produce separate effects
- gingivitis and periodontal disease are exmaples
the theory behind the causation of PDD
- presence of bacteria in the biofilm causing inflammation
- the extent of the disease is caused by the interaction of the bacteria and the host immune response
mechanisms of the host immune response in the oral cavity
- saliva
- epithelium
- gingival crevicular fluid
- inflammatory and immune cells
describe the host immune response to bacterial plaque in periodontitis
- initial periodontal lesion is composed of mainly T lymphocytes which secrete the cytokines to tell other cells what to do
- the B cells and plasma cells driven by the cytokines arrive
- antibody is produced locally to the site of infection and is usually protective
protective functions of the antibody
- inhibition of adhesion and invasion
- complement activation
- neutralisation of toxins
- opsonisation and phagocytosis
matrix mellatoproteinases
- family of zinc and calcium dependent proteolytic enzymes
- break down connective tissue causing tissue destruction
3 patterns of bone loss in periodontal disease
- horizontal
- vertical
- furcation
measuring bone loss in PDD
should look at % of bone lost in relation to length of root
usually the bone sits 1-2mm below the ADJ
some people have short roots however
horizontal bone loss
- usually in thinner areas of bone
- bone is lost at an even plane across the teeth
- harder to regenerate due to lack of additional adhesive surfaces for bone to grow from
vertical/angular bone loss
- usually in thicker areas of bone
- same pattern of loss as horizontal however it doesn’t go all the way through the bone resulting in deeper loss in some areas
- easier to regenerate
reasons for different patterns of bone loss
initial shape and thickness of bone
- destruction begins from the most apical point in the plaque
- depends on the thickness of the bone
general risk factors for periodontal disease
- smoking
- diabetes
- stress
- drugs
- systemic disease
- nutrition
anatomical risk factors of periodontal disease
- enamel pearls and projections
- grooves
- furcations
- gingival recession
tooth position risk in PDD
- malalignment creating difficult to clean areas
- crowding
- tipping of teeth
- migration
iatrogenic risk factors of PDD
- restorative margins and overhangs
- defective crown margins
- poorly designed partial dentures
- orthodontic appliances
normal physiological response to infection or injury of the gingiva
gingivitis
pathological inflammatory response associated with tissue destruction
periodontitis
early colonisers
commensal aerobes
late colonisers
gram negative anaerobes
colonisation
microbial presence on a body surface without clinical signs of inflammation or disease
- usually commensal organisms
infection
microbial invasion of host tissues causing a reaction
asaccharolytic
bacteria metabolism which doesnt break down carbohydrates but proteins and peptides instead
gingipains
proteases produces by P.gingivalis which
1. degrade host enzymes
2. activate MMP’s
virulence factors of P.Gingivals
- asaccharolytic
- gingipains
- atypical LPS
- inflammophillic
inflammophilic
thrive in inflammatory conditions
red complex bacteria
- porphyromonas gingivalis
- tannerella forsythia
- treponema denticola
why can lesser pathogens (orange complex) cause PDD
- some factors produced by the bacteria reduce host inflammatory response
- therefore they cause the disease easier
contents of saliva which protect the teeth
- S-IgA
- lysozyme
- peroxidase
- lactoferrin
- mucins
- cystatins
- histamines
immune defences in the GCF
- AMPs
- cytokines
- chemokines
- lactoferrin
- IgG
pathogenesis in the development of periodontal disease
- healthy biofilm is symbiotic and lives next to host tissues
- inflammation is subclinical in health
- any microbial challenge may disrupt this
1. if controlled, health will return
2. if uncontrolled then the inflammation will continue and a dysbiosis will occur
disease state of gingivitis
- increased TLR stimulation
- increased production of pro-inflammatory mediates
- redness, swelling, bleeding, vasodilation, cell migration
- neutrophils remain the predominant cell type
- monocytes are recruited and active to differentiate into macrophages
- lymphocytes recruited later on to fine tune the immune response
factors that may cause the symbiosis of the oral microbiome
- antibiotics
- diseases e.g. diabetes
- genetics
- activity of salivary proteins
- salivary flow rate
- innate/adaptive immune factors
- oral hygiene
- diet
- smoking
hallmark clinical signs of periodontitis
- increased pocket depth
- apical migration of junctional epithelium
- loss of attachment
problems with a lack of neutrophils
- patients with leukocyte adhesion deficiency
- trouble getting neutrophils from the BV to the tissues
- prone to PDD from a young age as they are the predominant species of immune cells
problems with too many neutrophils
- main source of tissue MMPs
- can increase the tissue breakdown associated with chronic inflammation
- leads to excessive bone and attachment loss
adaptive immune system in periodontal destruction
- B and T lymphocytes present in the early lesion
- aggregations of CD4 T cells and B cells and dendritic cells
- unable to regulate symbiotic biofilm so does 2 things
1. protects by stopping the infection becoming systemic
2. destructive as the inflammation is induced and increases alveolar bone loss
process of alveolar bone loss
- RANK receptors are expressed on monocytes
- in the gingival tissues, B and T cells release RANKL which is free to bind to the osteoclasts which are being brought into the tissues by chronic inflammation
- when the monocytes bind RANKL, they differentiate into osteoclasts and destroy the bone
- this is because in chronic inflammation there are low levels of OPG to increase bone formation
= net loss of alveolar bone
chronic periodontitis
- destruction of junctional epithelium and connective tissue attachment
- bone destruction and pocket formation
- progressive disease which affects the amount of bone loss
aggressive periodontitis
- severe condition usually affecting younger patients
- may be associated with family history
- progression is rapid
- loss of bone attachment is severe
- plaque levels may be incosistent with disease progression
necrotising ulcerative gingivitis
- NUG
- painful ulceration of the tips of the interdental papillae
necrotic tissue is visible
- associated halitosis
necrotising ulcerative periodontitis
- same as NUG but with the presence of connective tissue attachment and bone loss
periodontal abscess
infection in a periodontal pocket
can be acute or chronic
gingival enlargement
- thickingin of the gingiva
- can occur in response to irritation by;
- plaque or calcuclus
- friction or trauma
- fluctuations in hormones
smoking and periodontal disease
- no bleeding on probing as the vessels are constricted by the nicotine
- impaired wound healing
- production of inflammation mediating cytokines
drugs which can increase periodontal disease risk
calcium channel blockers
actions to take when a patient scores BPE3 or above
- treat entire sextant and take 6PPC for completed sextant AFTER completion of treatment
OR - complete 6PPC BEFORE and AFTER treatment and conduct RSD on teeth scoring BPE3
other terms for non-surgical management of PDD
cause related therapy
hygiene phase therapy
aims of non-surgical management of PDD
- arrest the disease process
- regenerate lost tissues
- maintain periodontal health in the long term
- to preserve a functional dentition for life
stages in the treatment plan
- emergency care
- disease control
- re-evaluation
- reconstruction
- supportive care
disease control
- extract hopeless teeth
- hygiene phase therapy
- caries management
- endodontic therapy
- provisional prosthesis
periodontal therapy in the clinic
- supra and sub gingival plaque control
- root surface debridement
- removal of plaque retentive factors
periodontal therapy at home
- demonstration of how to use oral hygiene aids
- tooth brushing advice
- toothpaste recommendations
things assessed to determine level of dental health education
- evaluate the patients reasons for attendance
- assess their attitude towards healthcare and their motivation to improve their oral health
- explain the nature of the patients disease using visual aids
- discuss the findings of the examination
- demonstrate the healthy dentition and diseased state in the patients mouth
- explain the nature of the treatment and the consequences
scaling
the removal of plaque and calculus from the tooth surface
root surface debridement
- the actor removing dead, contaminated or adherent tissue or foreign material from the root surface
- instrumentation encompasses scaling and root planing
root planing
the removal of contaminated cementum, leaving the tooth root surface hard and smooth
scaling instruments
hand instruments (manual) and sonic and ultrasonic instruments
rotating and reciprocating instruments
advantages of hand instruments
- no cavitation and flushing effect from water coolant
- powered instruments produce aerosol
- powered instruments tend to leave the surface rougher
- there is greater tactile sensitivity with hand instruments
advantages of powered instruments
- may allow better access to furcation regions
- may be faster
- less demanding on the operator (hand fatigue)
- less unwanted tooth tissue removal
assessing treatment
- inflammation levels
- bleeding on probing indices
- reduction in probing depth
- gain in attachment level
probing depth indicates
indicates the difficulty of the treatment and the likelihood of recurrence
attachment levels indicate
a measure of the tissue destruction pre treatment and the extent of repair post treatment
things which can influence manual probing depths
- resistance of the tissues
- size, shape and diameter of the probe
- site of insertion
- angle of insertion
- presence of obstructions e.g. calculus
- patient discomfort
effects of supra gingival plaque control alone
- decreased gingival inflammation
- limited effect on probing depth
- no change in clinical attachment level
- no alteration in the sub gingival microflora in deep pockets
effects of RSD without supra gingival scaling
- initial reduction in pocket depth and inflammation
- pockets re-colonised by supra gingival plaque species
- disease recurrence
effects of RSD combines with supra gingival scaling
- decreased gingival inflammation
- reduction in pocket depth
- gain in probing attachment levels
- marked changes in the sub gingival microflora
healing time after PDD treatment
- greatest changes observed in 4-6 weeks after treatment
- gradual repair and maturation of the tissues over the next 6-12 months
full mouth disinfection
- aims to prevent treated pockets becoming recolonised by bacteria
- use of chlorohexidine mouth wash for sub gingival irrigation
- tongue brushing
- mouth rinsing
effects of RSD
- reduces microbial challenge
- decreases inflammation
- inoculation with plaque organisms can boost the immune response
re-evalutaion should look at
- patient plaque control
- bleeding on probing
- residual probing depth and attachment levels
what suggests success of non surgical PDD therapy
- good OH
- no bleeding on probing
- no pockets greater than 4mm
- no increasing tooth mobility
- a functional and comfortable dentition
why does periodontal treatment fail
- poor compliance
- inadequate debridement
- host factors mainly smoking
limitations to non-surgical therapy
- root morphology preventing clearing
- furcation involvement
- deep pockets
- skill level
- time
supportive care
- maintain periodontal health
- detect and treat the recurrence of disease
- maintain acceptable levels of the disease
- manage and prevent tooth loss
SHOULD BE EVERY 3 MONTHS
what can be assessed in a 6PPC
- probing depth
- bleeding on probing
- gingival margin height
- loss of attachment
- mobility
- furcation involvement
what is the minimum requirement of a 6PPC
to record all sites greater than or equal to 4mm or more probing depth and bleeding on probing
what is probing depth a measure of
the base of the gingival crevice to the gingival margin
what is recession measure from
the gingival margin to the cej
how is loss of attachment a measured
probing depth + recession
is the value for gingival margin + or - in a 6PPC if it goes above the CEJ
-
is the value for gingival margin + or - in a 6PPC if it goes below the CEJ
positive
how should the PCP probe be inserted to measure accurately
parallel to the long axis of the tooth while maintaining contact with the end of the probe to the tooth
how many sites around the teeth are recorded on 6PPC
6 points
3 buccal 3 palatal
grade 1 furcation involvement
initial involvement
- furcation can be felt on probing
- there is less than one third of the tooth width involved
grade 2 of furcation involvement
partial furcation involvement
loss of support exceeds one third of the tooth width but does not include the total width of the furcation
grade 3 furcation
through and through involvement
the probe can pass through the entire furcation
grading tooth mobility
0-3
grade 0 tooth mobility
physiological mobility at crown level
tooth as only moved 0.1-0.2mm in the horizontal direction
grade 1 tooth mobility
increased mobility of the crown of the tooth at most 1mm in horizontal direction
grade 2 tooth mobility
visually increased mobility of the crown exceeding 1mm in a horizontal direction
grade 3 tooth mobility
severe mobility of the crown of the tooth in both horizontal and vertical direction impinging on the function of the tooth
