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,
