CSA other topics Flashcards
Effects of Smoking on Periodontium
Tobacco smoking related to:
- Chronic Periodontitis
- Periodontitis that is refractory to treatment
- NUG
* Smoking is a predisposing factor for NUG = painful, acute form of gingivitis, only form of gingivitis treat with antibiotics
Smokeless tobacco related to:
- Localised recession manifesting as attachment loss
- increased oral cancer risk
- severe active periodontal disease
** Current research from cross-sectional and longitudinal studies supports DIRECT effect of smoking on periodontium
E.g: smokers have:
- Greater bone loss & CAL (=irreversible)
- Increased no.s of deep(er) pockets than non-smokers with similar plaque levels
.’. Smoking = risk factor for periodontal disease, namely attachment and bone loss
Clinical Appearance:
- Fibrotic ‘tight’ gingivae (.’. harder to probe)
- Rolled margins
- Less gingival redness + bleeding (nicotine = vasoconstrictor)
- More severe, widespread disease than same age non-smoking control
- Anterior, maxilla palate worst affected
- Anterior recession
- Open embrasures = ‘black triangles between teeth were papilla recession has occurred
- Nicotine staining
- Calculus
Clinical Characteristics:
- Earlier onset, rapid disease progression
- Poorer response to nonsurgical therapy
- Recurrence within 1 year of surgery
- Increased % are refractory to treatment
PATHOGENESIS
- Inhibition of phagocytosis of neutrophils (PMNs)
- Reduction in chemotaxis and migration of oral PMNs exposed to nicotine
- Nicotine adversely affects fibroblast function and penetrates oral epithelium
- Reduced antibody production, serum IgG2
- Altered peripheral blood immuno-regulatory T-cell subset ratios in some studies
- Reduced bone mineralisation
- Cytotoxic, vasoactive constituents
- Adverse effect on micro-circulation, gingival circulation, blood flow
- Possible vasoconstriction of gingival capillaries but evidence inconsistent
- Chronic hypoxia of periodontal tissues
- Fewer gingival vessels in smokers
- High proportion of small blood vessels in smokers compared with large vessels, but no difference in vascular density
- Suppressive effect of smoking on vasculature rather than just simple vasoconstrictive effect
- Overall
Less gingival redness
Less bleeding on probing
Fewer vessels clinically and histologically
Healing response may be affected by impairment of re-vascularisation
MICROBIOLOGY
Some studies have found no difference in microbiology between smokers and non-somkers.
Other studies showed more smokers infected with A.a, P.g and also T. forsythensis and found higher levels in subgingival plaque in the smokers
(Zambon et al 1996 J Perio 67: 1050-4)
T. forsythensis seems to be an important pathogen in smokers
NUG
- Rapid onset, specific features:
- painful, interdental necrosis, bleeding gingivae
- necrotic ulcers affecting interdental papillae
- “punched out” appearance
- ulcers painful, covered by grey slough
- gingival bleeding with little provocation
- possible halitosis, “foetor oris”
- possible lymph nodes involvement
*Predisposing Factors Stress Immune suppression (may be feature of HIV infection) Smoking Malnutrition Poor OH, pre-existing gingivitis Tissue trauma
Clinical Implications of Effects of Smoking on Periodontium
You should advise your patients of the adverse effects of smoking on their oral and periodontal health (+general health)
Record giving advice in patient’s notes (NB medico-legal reasons!)
You should explain poorer response to periodontal therapy
Give smoking cessation counselling
- Brief advice from a health professional can result in up to 5% of patients quitting smoking (Doll R and Crofton J (1996). Tobacco and health. British Medical Bulletin 52(1))
After smoking cessation, time dependent changes:
- recovery of inflammatory response leads to transient increased bleeding (approx 6m)
- return to normal architecture (approx 12m)
Smoking Cessation
- *Suggest
- Free NHS Smoking Helpline 0800 169 0 169
- Nicotine replacement therapy
- Bupropion; a medication primarily used as an antidepressant and smoking cessation aid.
- *Be practical, supportive & encourage: eg 5 As
1. Ask
2. Advise
3. Assess
4. Assist
5. Arrange
SYSTEMIC ANTIMICROBIALS IN PERIODONTAL THERAPY
NB: Antimicrobial resistance major public health issue .’. don’t want to overprescribe
Adjunctive antimicrobials → NEVER used in isolation!
= Adjunctive to mechanical therapy
Not indicated for use in Chronic Periodontitis
– Pathogenic microflora = diverse .’. no one drug can be specific to them all .’. not effective -> no clinical benefit
– Conventional therapy most effective
Rational for adjunctive antimicrobial therapy in Aggressive Periodontitis (AP) and acute periodontal disorders
Periodontitis is a bacterial disease
Not all patients and sites respond to non-surgical therapy (NST)
NST frequently requires repeating
AP cases may be immunedeficient
AP has a specific microbial aetiology
Bacterial invasion may occur in AP
- A.A can colonise soft tissues .’. after debridement can recolonize pocket fro soft tissue lining
- Other non-pocket sites e.g. tongue, floor of the mouth etc. colonised in aggressive periodontitis
Potential to decrease need for surgery
Persistent disease
- Likely around crown margins
- v. deep pockets (6+ mm) – hard to maintain cleanliness for pt & can be difficult for operator to access for debridement
Other Indications:
– NUG
– Periodontal abscess where no local drainage achieved/systemic involvement
– Surgery; to prevent complications
Factors affecting efficacy of systemic antimicrobials in periodontal therapy
Factors affecting efficacy:
– Binding of drug to tissue
– Protection of key organisms by non-target organisms binding or consuming drug
– Bacterial tissue invasion
– Total bacterial load
– Previous drug therapy
– Non-pocket infected sites; tongue, floor of mouth etc
– Choice of bactericidal drug (kills bacteria) versus bacteriostatic drug (prevents growth of bacteria)
– Presence of biofilms –> must disrupt
– Beta-lactamase production
Some bacteria produce beta-lactamase which can inactivate beta-lactam drugs e.g. penicillin
Clavulanic acid = a beta-lactamase inhibitor – sometimes used in combination with amoxicillin to prevent drug inactivation
Mechanisms of action of systemic antimicrobials
One of 4 mechanisms of action:
- Inhibition of cell-wall synthesis e.g. penicillins
- Inhibition of protein synthesis e.g. tetracyclines
- Interference with bacterial nucleic acid synthesis e.g. metronidazole
- Inhibition of bacterial cell metabolism e.g. sulphonamides
Systemic antimicrobials: Review the drug choice and efficacy
**Current regimes adjunctive to mechanical therapy
• Tetracyclines 250 mg (14 days)
• Amoxycillin 250mg + Metronidazole 200mg (7 days)
Drug Choices:
**Amoxicillin: 500 mg, 2-3 times for 8 days Bacteriocidal
(Gram + and Gram –) Penicillinase sensitive
**Amoxicillin and clavulanic acid (combined): 500 mg, 2-3 times for 8 days Bacteriocidal (broader spectrum than amoxicillin alone) Diarrhea, colitis, nausea
**Tetracycline: 500 mg, 4 times for 21 days Bacteriostatic (Gram+ > Gram –) Severe sunburn if exposure to bright sunshine, severe stomach pain and nausea
Non-antibacterial effects:
- Concentrates in GCF
- Binds to root surface
- Slow release
- Fibroblast & odontoblast stimulation -> regenerative properties
- Osseous induction
- Anticollagenase (inhibits matrix metalloproteinases)
**Minocycline: 100-200 mg, 1 time for 21 days Bacteriostatic (Gram+ > Gram -) Bacterial resistance to minocycline
**Doxycycline: 100-200 mg, 1 time for 21 days Bacteriostatic (Gram+ > Gram -)
**Ciprofloxacin: 500 mg, 2 times for 8 days Bacteriocidal (Gram – rods) Nausea, gastrointestinal discomfort
**Azithromycin: 500mg 1 time 4-7 days Bactericidal or bacteriostatic depending upon the dose, broad spectrum Diarrhea vomiting discomfort
**Clindamycin: 300mg 2 times for 5-6 days Bactericidal (anaerobic bacteria) Diarrhea or colitis
**Metronidazole: 500mg 2 times for 8 days Bactericidal to Gram - (Porphyromonas gingivalis and Prevotella intermedia)
Dizzy blurred vision, Headaches
Ineffective for A.actinomycetemcomitans
Management of Periodontal Abscess considerations
– Is the associated tooth vital?
– Can drainage be achieved?
– Is there any systemic involvement?
– Can the occlusal force be reduced
When to use systemic antimicrobials in terms of treatment planning
Treatment Planning
• Non-surgical therapy:
Decrease bacterial load
May produce resolution – review within 6 weeks; may have recolonized pockets
• Monitor response:
Resolved → PPD reduced, no BOP
Active → Repeat NST + adjunctive antimicrobial decontamination type protocol
Surgical phase
Microbial Testing
- Bacterial culture: cost, time, not all pathogens culturable
- Molecular biological methods using bacterial genome
E.g. Checkerboard hybridisation (43 species tested at a time, = research tool)
Genome tests don’t require viable bacterial cells
Expensive and laboratory based genome tests
Potential benefits of microbial testing
– May assist CP v AP diagnosis
– Identify specific bacteria for selection of antibiotic adjuncts
– Performed as part of risk assessment
Reasons for antimicrobial therapy failure
- Lack of culture and sensitivity
- Failure to achieve drainage
- Non-bacterial causative agent e.g. in HIV + patients often fungal element involved
- Incorrect drug duration or dose
- Lack of compliance
- Defective host response
- Persistent risk factors e.g. smoking
- Lack of substantivity of local agents
- Drug resistance
- Failure to achieve suitable debridement
Types of diabetes
DIABETES MELLITUS (DM) = Common group of metabolic disorders characterised by chronic hyperglycaemia resulting from insulin deficiency or impaired utilisation of insulin (insulin resistance)
**Type 1
Aetiology:
- autoimmune process -> destruction of ß cells in islets of Langerhans
- genetic predisposition; Human Leukocyte Antigen genes on chromosome 6 are key- encode molecules crucial to immune system
- abrupt onset; most often children and teens
Treatment:
Insulin injections/insulin pump
Balance carbohydrate intake & insulin
New technology includes transplantation of pancreatic Islets of Langerhans cells
**Type 2
Aetiology:
- Defect in ß cells (insufficient insulin produced) and insulin resistance
- Usually manifests mid life and is common
- Small number of children affected
- Genetic influence, several genes likely
- Increased risk with obesity, sedentary lifestyle, close relative with DM, Asian/Afro-Caribbean
- Complications possible before diagnosis
Treatment:
- Diet
- Diet + Oral hypoglycaemic drugs + exercise
- 25% may go on to need insulin injections
**MODY (Maturity Onset Diabetes in the Young)
Aetiology:
- Rare, young age of onset, usually
Diabetes Diagnosis
Random venous plasma glucose > 11.1 mmol/litre, or fasting venous plasma glucose concentration > 7.0 mmol/l
[N.B. Normal blood glucose is 4–5.5mmol/l before meals,
Complications of Diabetes
Macrovascular:
- Cardiovascular disease - major cause of death & peripheral vascular disease - amputations
- Cerebrovascular disease & stroke
Microvascular:
- Retinopathy – blindness
- Nephropathy – renal failure
- Neuropathy – painful nerve damage
Diabetes and Periodontal disease
Periodontal disease is a clinical complication of diabetes (Lamster & Lalla, 2001)
With similar levels of plaque, poorly controlled Type 1 diabetics lost more attachment and bone
- Increased risk of perio disease with increased age
- Increased severity with increased diabetes duration
‘Diabetes mellitus associated gingivitis’ consistent feature in children with poorly controlled Type 1 DM
Inflammatory response of gingiva to plaque aggravated by poorly controlled plasma glucose levels
- In UK (2011-12) 82.6% did not meet NICE HbA1c target
- Psychological issues, peer pressure, puberty
Diabetes ->
Increased inflammation and CAL
***Inflammation is central feature of pathogenesis of DM and periodontitis -> 2-way relationship
Periodontal Infection => Increased levels of Inflammatory mediators (TNF-a, IL-6, C-reactive protein) => Other inflammatory diseases CHD/CVD, renal disease
o Increased IL-1ß may have role in Type 1 DM
- Increased IL-1ß -> Protein kinase C activation -> Pancreatic ß cell destruction
o TNF-a may have role in Type 2 DM
- Increased TNF-a alters intracellular signalling -> Insulin resistance
- In obesity, IL-6 stimulates TNF-a
o Diabetic patients with periodontitis may have:
Increased IL-6, increased TNF-a and increased C-Reactive Protein (can increase insulin resistance, aggravate glycaemic control)
HYPERGLYCAEMIA =>
- decreased collagen synthesis and glycosaminoglycans (GAGs)
- increased collagenase activity
- Collagen undergoing non-enzymatic glycation to Advanced Glycation End products (AGEs)
- > up regulates periodontal inflammation
- > production of ROS & enhance oxidant stress -> endothelial damage found in diabetic complications
- > Enhance PMNs respiratory burst (increased local perio tissue damage)
- > adverse effects on bone metabolism
AGES activate Receptor for AGEs = RAGEs
Interaction of RAGEs & AGEs perturbs vascular & inflammatory cell function
-> Microvascular & macrovascular diabetes complications
-> Accelerated periodontal tissue destruction
PMNs first line of defence, but in DM:
Decreased PMN function, increased periodontitis
Decreased Chemotaxis
Decreased Adherence
Decreased Phagocytosis
Enhanced respiratory burst
Delayed apoptosis, increased tissue destruction
Poorer wound healing in DM
Precise mechanisms uncertain, but may relate to:
- Decreased collagen due to increased collagenase
- Inhibition of attachment and spreading of fibroblasts in the wound
- Altered late inflammatory response
No specific microbiological characteristics
Systematic review of current evidence suggests that periodontal diseases adversely affect diabetes outcomes:
- Control
- Complications
- Incidence
Patients with DM should be told:
- At increased risk of periodontitis
- Glycaemic control may be more difficult
- At higher risk of other complications eg cardiovascular disease
And should:
- Receive thorough oral/perio exam (adults and children)
LOCALLY DELIVERED ANTIMICROBIALS - what are they and why used.
=> Role in treatment of Chronic Periodontitis
Antimicrobials ALWAYS an ADJUNCT to mechanical therapy
Why sub gingivally applied antimicrobials help:
GCF – low volume but high flow rate; 0.5 microlitres GCF renewed 40x/hr .’. rapid clearance .’. liquid antimicrobials such as Chlorhexidine have little effect
.’. need a device to ensure retention of antimicrobial in pocket long enough to have an effect
Limitations of mechanical therapy
o MT poorer treatment outcomes for sites with furcation involvement compared to molar flat surfaces and non molar teeth
o MT may fail to remove periodontal pathogens
– Sub epithelial gingival tissue – out of instrumentation reach
– Crevicular epithelial cells
– Located in connective tissue
– Reside in altered cementum and dentinal tubules
– Sub gingival calculus
– Anatomical features
– Colonisation of dorsum of tongue, tonsils and oral mucosa
Local Antimicrobials; What systems are available:
o Actisite
– EVA fibre containing 25% tetracycline HCl
– Not resorbable!
– No longer used
o Periochip
– Chlorhexidine gluconate (2.5mg) in hydrolysed gelatine
– Biodegradable gelatine chip, placed in pocket after scaling and RSD
– Resorbable
– Diffusion 24 hrs 1000ppm
– Matrix degradation 3-10 days 100-500ppm
– NB: risk of lateral periodontal abscess formation as blocking route for any exudate or build up of pressure to be released
– Resulting in approx. +0.5mm CAL than control
o Dentomycin – Minocyline 2% lipid gel – Resorbable – Injected into pocket – Multiple visits needed to apply
o Elyzol
– Metronidazole 25% in a mono/triglyceride gel
– Resorbable
– No longer used
o Atridox
– Doxycycline hyclate (8.8%) resorbable gel
o Arestin
– Minocycline HCl (1mg) encapsulated microspheres
– Resorbable
Indications for local antimicrobials:
- Pocket depths >5mm with BOP
- Adjunct to mechanical therapy
- Non-responding sites after initial therapy
- Choice of product influenced by number of pockets to be treated – many pockets use gel, singe pockets use chip
- NOT indicated in aggressive forms of periodontitis
NB: Site Risk Assessment:
Absence of BOP = a reliable indicator of periodontal stability even in deep pockets
Give reasons why antimicrobials may be useful in periodontics.
Periodontitis is a bacterial disease
Mechanical therapy may fail to recognise pathogens that are:
Invading sub epithelial gingival tissue
Invading crevicular epithelial cells
Located in the connective tissue
Present in altered cementum and in dentinal tubules Present on sub gingival calculus
In anatomical features such as furcation areas
Colonising the dorsum of the tongue, tonsils or oral mucosa
Not all patients and sites respond to non-surgical therapy, which frequently requires repeating
In aggressive periodontitis cases there is a deficient immune response and a specific microbial aetiology
Using antimicrobial agents may decrease the need for surgery
Summarise the arguments against the use of antimicrobial agents in periodontics.
Use of antibiotics results in antimicrobial resistance
Allergic reactions are possible and can be life-threatening
Suppression of commensal bacteria can result in fungal superinfection
Drugs are costly
The efficacy of local and systemic antimicrobial agents in periodontitis is questionable.
Results are often only marginally better than with mechanical therapy alone.
What are the indications for the use of systemic and topical antimicrobial agents in periodontics?
Always as an adjunct to mechanical therapy Systemic
In aggressive periodontitis
In necrotising ulcerative gingivitis
In periodontal abscess where no drainage can be achieved or the patient is unwell
As per-operative/perioperative medication in periodontal surgery to prevent complications
Local delivery
In pocks exceeding 5mm, with BOP and which have failed to respond to initial therapy.
Topical
As an aid to plaque control after surgery or in other situations where mechanical plaque control is difficult
