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5 Modes of action of fluoride
replaces hydroxyapatite with flurapetite
Critical pH 4.5
Bacteriostatic - inhibits bacterial growth specifically strep. Mutants
Lowers plaque acid production
Systemically: flatter + wider cusps, flourosis
describe initial lesion
24-48 hrs after plaque accumulation
vasodilation occurs which allows neutrophils to arrive at the side of infection via chemotaxis
GCF increases to flush out bacteria starting to form
describe early lesion
1 week after plaque accumulation
Increase in inflammatory infiltrate lymphocytes (esp T) + PMNs
fibroblasts and collagen loss near the sulcus
more inflammatory cells reqruited via chemotaxis - macrophages, Ig, complement
GCF increases
describe established lesion
2-3 weeks of plaque accumulation / gingivitis
junctional epithelium is leaky and ulcerated = BoP
apical migration of plaque
continued loss of collagen
rete pegs start to form
red complex bacteria begin to colonise
describe advanced lesion
this is periodontitis
junctional epithelium migrates apically = pocket
collagen loss up to 90% in the base of the pocket
bone resorption due to cytokine release
rete pegs infiltrate connective tissue - epithelial extensions which create more surface area and epithelial permeability for inflammatory cells to migrate to site of infection
orange and red complex
orange
prevotella intermedia
fusobacterium nucleatum
red
tanerella forsythia
treponema denticola
porphynomas gingivalis
what does p. gingivalis produce
gingipains
(proteolytic enzymes) that help p.gingivalis colonise and dominate subgingival plaque by inhibiting neutrophils cell apoptosis facilitating inflammation, bone loss and destruction
whats the difference between gram +ve and -ve bacteria
+ve has single membrane layer and stains pink
-ve has double membrane layer (less permeable to host defences) and stains purple)
describe healing process after RSD
from 24-48hours you get acute inflammation, 5 symptoms
redness (rubor),
swelling (tumor),
Heat (calor)
Loss of function (functino leasa)
Pain (Dolor)
Neutrophils are the 1st responders that release cytokines + GCF increases
LJE starts to form and basement membrane forms on the root surface
These 2 things join together by hemidesmosomes to form NEW ATTACHMENT!!
No PDL fibres or sharpies fibres
Fibroblasts start laying down collagen: strengthening tissue attachment and tightens gingival cuff Resulting in SHRINKAGE Occurs because inflammation has subsided = reduced PPD, BOP
How does stress affect the periodontium
reduced salivary flow → dry mouth → plaque buildup
Increased cortisol → altered/weakened immunity making it difficult to fight off bacteria
Disturbed routines → poor OH
Potential bruxism
Pre disposing factor for NG
How does diabetes affect periodontal disease?
bidirectional relationship, each condition worsen the other
only poor controlled diabetes has this effect
altered immune cell function - less effective neutrophils
poor fibroblast function which decreases collagen and tissue regeneration
exaggerated inflammatory response leading to prolonged, intense inflammation that damages host tissues
How does bone resorb
pathogens (p.gingivalis) releases toxins that trigger an immune response that release cytokines:
IL1: originate from epithelium: Pro inflammation and osteoclast activation.
TNF(a): originates from neutrophils: causes bone resorption + tissue damage
these cytokines stimulate osteoclasts that breakdown alveolar bond by releasing acid and enzymes
What are the different types of periodontal disease
inflammatory conditions
Gingivitis → no attachment loss
Periodontitis → attachment loss
Clinical presentation
Acute eg necrotising gingivitis
Chronic most common form of
By cause
Plaque induced vs non-plaque induced (rare, genetic, systemic)
how does smoking effect perio/mouth
Smoking is a major risk for periodontal disease as it affects immune response and tissue healing
Vasoconstriction → Reduced blood flow, less BoP = delayed detection of disease. limits number of neutrophils that can reach the periodontium effectively
Neutrophils → they are needed as they are the first line of defence in the inflammatory process = this weakens the immune response allowing bacteria to multiply and cause more severe disease.
chemotaxis is impaired. this is the process by which cells like neutriphils move towards site of inflammation in response to chemical signals released by bacterial toxins
Keratinisation → keratinisation of epithelial soft tissues causing them to become thick and hard
Collagen → smoking inhibits fibroblasts and their ability to produce collagen, poor would healing after tx, weaker tissues = increased pocket formation
clinical presentation of smokers
Deeper periodontal pockets
More calculus and plaque
Less bleeding on probing (masks disease)
Vertical bony defects
More keratinised tissue
Tooth mobility
Xerostomia (dry mouth)
Increased risk of oral cancer and tooth loss
reasons for perio treatment failure
incomplete RSD
Poor OH
Anatomical challenges (Narrow pockets, difficult access)
Medical/social history (smoking, medication)
Clinical skill level
Inappropriate tx planning
lack of motivation
restoration deficiencies/overhangs
local factors like crowding of teeth
impaired would healing
increased susceptibility
treatment options after failure of RSD
Repeat another course of tx
chemical adjuncts:
local:
Anticeptic: chlorhexidine: gel, mw + periochip (lasts 100 days)
Antibiotic: Tetracycline/metronidazole gel/fibres (eg actisite)
systemic: Antibiotics
metronidazole
tertracycline
doxacylin (subclinical dose): low dose for 3-12months
surgical:
furcation:
furcationplasty - remove part of bone to make furcation bigger but not all the way through to make more accessible
Hemisection (root and a bit of crown removed)
tunnel prep (esp for grade 3 furcation = remove bone so can clean)
open flap surgery (flap raised to expose root, debridement of root and then flap sutured)
gingevectomy (removes excess gingival tissue)
root resection - remove a root to make to easier to clean
guided tissue regeneration: aids PDL and bone formation by excluding epithelium using a membrane.
Prognosis and maintenance of periodontitis
Once pt has periodontitis, they always have it
Once the disease is stabilised, they go on the supportive periodontal therapy (SPT) = maintenance phase post tx
focuses on long term monitoring, OHI reinforcement and early intervention
types of ultrasonic
Magnetostrictive - magnetic stack creates vibrations, tip move back and forward
Piezoelectric - crystals deform under electric current causing vibrations, tip moves eliptically
modes of action of ultrasonic
Acoustic streaming – movement of fluid around the tip which breaks up the biofilm
Cavitation – produces bubbles that implode, releasing oxygen, which kills anaerobic bacteria (those that cant survive in oxygen)
Mechanical Vibration – tip vibrates at a high frequency to mechanically disrupt plaque and calculus
Types of mouthwashes
phenolic compounds + essential oils = listerine
Antiseptic = chlorhexidine (stains), bisbiguanides
Fluoride rinse = 225ppm
Oxygenating (hydrogen peroxide) = NG, helps by releasing oxygen
what are the dental affects of hypertension
increased risk of bleeding - if uncontrolled
medication related side effects eg CCB Cause gingival overgrowth
xerostomia eg some meds cause xerostomua (diuretics, ACE Inhibitors) = higher risk for perio, caries and candida
delayed healing
smoking cessation
brief intervention 3-5 min chat
When patient isn’t motivated - 5Rs
Relevance, Risks, Rewards, Roadblocks, Repetition
When patient is ready - 5As
Ask, Advice, Assess, Assist, Arrange
Toothbrushing Techniques
Bass Technique → 45 degrees towards sulcus, short, vibratory back and forth motion
Stillman Technique → 45 degree angle, half on tooth and half on gum, gentle vibratory motion
Modified bass → Same as bass but adds a sweeping motion at the end of the vibratory strokes
modified stillman → 45 degrees but adds a sweeping or circular motion at the end of the stroke
Roll Technique → Brush placed at gingivae and rolled downwards(away from gumline) Good for pts with abrasion and recession
Mini scrub → Back and forth scrubbing, can cause abrasion and recession
Gingivitis case studies
Lose study
dental students stopped brushing for 20 days to allow plaque accumulation = gingivitis
When they started brushing = reversed
Study shows that gingivitis is reversible
what are the acute perio conditions
necrotising gingivitis
acute herpetic gingivostomatitis
periodontal abscess
endodontic abscess
Necrotising gingivitis
Treponema + f. nucleatum
necrotic ulcers, grey pseudomembranous sloth, halitosis, bleeding, metallic taste, pain
Side effects - necrosis and tissue destruction, necrotising fasciitis (a rapidly progressing "flesh-eating" condition), cancrum oris (a severe form of necrotising infection in the orofacial region, creating large tissue defects), Lymphadenopathy (swollen lymph nodes), cellulitis, Ludwig's angina
Acute herpetic gingivostomatitis
herpes simplex 1
vesicles fill with fluid which burst and form ulcers: EO + IO
Systemic: fever, malaise, lymphadenopathy
Erythema + Odema on the gingiva
tx: analgesics (paracetamol), soft diet rest
Secondary: herpes labialis (cold sores)
Periodontal abscess
acute infection in the perio pocket, due to blockage, incomplete RSD
Pulp is vital but infection may enter via the accessory canals
local swelling, pus, tender tooth
tx - drainage, rsd, abx if systematic
endodontic abcess
pulpal infection due to deep caries/trauma → necrosis → infection spreads to periapical tissues
non - vital tooth, PA radiolucency, swelling at apex, TTP
tx - RCT, XLA
nicotine replacement therapy
provides low doses of nicotine without harmful tobacco chemicals
Aims to reduce withdrawal symptoms and help pts quit
Examples
patches
Gum
Lozenges
Micro tabs (under the tongue)
Inhalers
Nasal spray
Mouth spray
Non nicotine replacement therapy
Champix - works on acetylcholine receptors in the brain where nicotine binds. Reduces cravings and withdrawal symptoms and blocks nicotine to make smoking less enjoyable
Dummy cigs
Hypnotherapy
BPE
BPE (Basic Periodontal Examination)
Screening tool; scores:
0 = Healthy
1 = Bleeding on probing only
2 = plaque retentive factors (eg calculus/overhangs), black band fully visible
3 = black band partially visible
4 = black band not visible
Children: only codes 0–2 up to 11 years.
Children sites examined UR6, UR1, UL6, LL6, LL1, LR6