Systemic Antimicrobials - Part 2 Flashcards

1
Q

Adult periodontitis is called …. As of 1999

A

Chronic periodontitis

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2
Q

Early onset periodontitis is called …. As of 1999

A

Aggressive periodontitis

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3
Q

How to differentiate between chronic and aggressive periodontitis - Old 1999 classification

A

Dependent on
- clinical features
- age of onset
- rate of progression
- pattern of destruction
- signs of inflammation
- relative amounts of plaque / calculus

Multifactorial complex interactions…
- host factors
- microbiology
- genetics
- predisposition - race

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4
Q

Old 1999 classification - features of chronic periodontitis include

A
  • Most prevalent in adults, but can occur inchildren and teenagers
  • Slow to moderate progression + exacerbations
  • Plaque is the main aetiology
  • Destruction consistent with local factors
    (subgingival calculus frequent finding)
  • Modifying factors include:
    local and systemic factors, smoking, stress, poorly controlled diabetes
  • Treat in usual 3 phases - no systemic antibiotics
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5
Q

Old 1999 classification - common features of aggressive periodontitis include

A

Common features generally present:
- except for periodontitis, patients healthy – Non-contributory MH
- rapid attachment loss and bone destruction
- familial aggregation

Localised form (old terminology used to include:
- Localised Juvenile Periodontitis (LJP)
Or
- Localised Early Onset Periodontitis (LEOP))

Generalised form (old terminology used to include:
- Generalised early onset periodontitis (GEOP)
Or
- Rapid progressive periodontitis (RPP)

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6
Q

Clinical and radiographic features of localised aggressive periodontitis

A
  • Localised first molar/incisor presentation
  • Clinical attachment loss (CAL)
  • Deep pockets in association with CAL
  • Gingival inflammation may/not be evident

Alveolar bone loss
- angular defects incisors
- arc shaped bone loss first molars
- often symmetrical distribution right/left

  • Amount of plaque may not be consistent with amount of Periodontal destruction present
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7
Q

Old 1999 classification - secondary features of aggressive periodontitis

A
  • Amounts microbial deposits inconsistent with severity of periodontaltissue destruction
  • Elevated proportions Aggregatibacter actinomycetemcomitans (A. a) and in some populations, P. gingivalis may be elevated
  • Phagocyte abnormalities
  • Hyper-responsive macrophage phenotype, including elevated levels of PGE2 and IL-1Beta
  • Progression of attachm
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8
Q

OLD 1999 CLASSIFICATION – FEATURES OF LOCALISED AGGRESSIVE PERIODONTITIS

A

Specific features:

Circumpubertal onset

Robust serum antibody response to infecting agent
(Aggregatibacter actinomycetemcomitans, A.a)

  • Localised first molar/incisor presentation
  • interproximal attachment loss CAL on at least two permanent teeth, one of which is a first molar, and involvingno more than two teeth other than first molars/incisors
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9
Q

Difference between 1999 and 2018 periodontal disease classification

A

Chronic and aggressive periodontitis is now recognised as the same disease entity however classified according to staging and grading & MIP (molar incisor pattern)

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10
Q

New classification 2017

A
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11
Q

Forms of periodontitis

A

2017 classification now classifies the stages of a diagnosis based on severity and complexity of management as well as the rate of progression

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12
Q

Periodontitis grade

A
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13
Q

1999 classification -
necrotising ulcerative periodontal disease (NUG/P)

Known as what as of 2017 classification?

A

Necrotising periodontal disease

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14
Q

1999 classification -
Periodontitis as a manifestation of systemic disease )

Known as what as of 2017 classification?

A

Periodontitis as direct manifestation of systemic disease

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15
Q

Definition of periodontitis – EFP S3 clinicalguidelines – Mariano Sanz et al 2020

A

A periodontitis case is defined by the loss of periodontal tissue support, which is commonly assessed by radiographic bone lossor interproximal loss of clinical attachment measured by probing.

Other meaningful descriptions of periodontitis include thenumber and proportions of teeth with probing pocket depth over certain thresholds (commonly >4 mm with BOP and ≥6mm), the number of teeth lost due to periodontitis, the number of teeth with intrabony lesions and the number of teeth withfurcation lesions

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16
Q

Why did we change from the 1999 to 2018 classification

A

Absence of universally accepted ‘case’ definitions for aggressive/chronic periodontitis

Difficult to study

Epidemiology, Aetiology, Pathogenesis, Treatment

New ‘case’ definitions proposed

Recent aggressive periodontitis estimates:

1%-15% <35 yrs of age; few studies <20 y

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17
Q

What factors do you base the differences clinically between

aggressive and chronic periodontitis

Generalised and localised

A
  • severity - how severe
  • extent - how widespread in sites/teeth
  • rate of progression - how fast / presence of risk factors (local or systemic)
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18
Q

2018 classification - what does it recognise chronic and aggressive periodontitis as?

A

Current evidence does not support distinction between Chronic and Aggressive periodontitis as two separate diseases

However, substantial variation in clinical presentation exists in terms of extent & severity of periodontitisthro’ age spectrum suggesting population subsets withdistinct disease trajectories caused by differences inexposure and/or susceptibility

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19
Q

Because current evidence does not support distinction between Chronic and Aggressive periodontitis as two separate diseases, the New 2017 periodontitis classification…

A

Chronic and aggressive periodontitis grouped undersingle category of Periodontitis

Further categorised on a multi-dimensional Staging and Grading system

  1. First step is to identify Periodontitis by presenceinterdental Clinical Attachment Loss
  2. Simple matrix of Stage of disease (Severity, Complexity,Extent)
  3. Then Grade (Rate of progression, risk factor)
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20
Q
  1. First step is to identify Periodontitis by presenceinterdental Clinical Attachment Loss
  2. Simple matrix of Stage of disease (Severity, Complexity,Extent)
  3. Then Grade (Rate of progression, risk factor)

Why is periodontitis identified by INTERDENTAL attachment loss?

A

Not buccal or lingual because sometimes there are non periodontal attachment loss in the buccal / lingual regions

  • due to other factors such as aggressive brushing habits / gingival recession
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21
Q

3 steps to staging and grading a pt

A
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22
Q

According to 2017 classification, a patient is a periodontitis case in the context of clinical care if…

A
  1. Interdental CAL is detectable at >2 non adjacent teeth

OR

  1. Buccal or oral CAL >3mm with pocketing >3mm is detectable at >2 teeth

And the observed CAL cannot be ascribed to non-periodontal causes

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23
Q

What is detectable interdental CAL

A

Key to periodontitis case definition is the notion of ‘detectable’ interdental CAL: the clinician being able to specifically identify areas of attachment loss during periodontal probing or direct visual detection of the interdental CEJ during examination, taking measurement error and local factors into account

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24
Q

Can GDP and students measure CAL?

A
25
Q

A periodontitis diagnosis for an individual patient should encompass 3 dimensions

A
  • Definition of a periodontitis case based on detectable CAL lossat two non-adjacent teeth
  • Identification of the form of periodontitis: necrotizingperiodontitis, periodontitis as a manifestation of systemicdisease or periodontitis
  • Description of the presentation and aggressiveness of the disease by Stage and Grade
    (see Appendix B in online Journal of Periodontology
26
Q

NEW 2017 CLASSIFICATION

Classifies individual patient by 2 dimensions beyond Severity and Extent according to … of managing the case and … and/or less predictable … to NST

A

Complexity

Risk of progression

Response

27
Q

NEW 2017 CLASSIFICATION

Acknowledges potential for some cases of periodontitis to influence …

= 2nd most important contributor to systemic inflammatory burden (1st= obesity)

A

Systemic disease

28
Q

NEW 2017 CLASSIFICATION

Proposed … designed to avoid paradox of improvement of … seen after loss/XLA of compromised teeth (because includes knowledge about periodontitis being main reason for loss of > 1 teeth)

A

Staging and Grading

disease severity

This knowledge helps to stage / grade

29
Q

WHAT TO DO ABOUT DIAGNOSING AND MANAGING PATIENTS WHO WOULD FORMERLY BEEN DIAGNOSED AGGRESSIVE PERIODONTITIS?

In terms of diagnosis?

A
  • we are continuing to manage cases who would formerly have been diagnosed Aggressive Periodontitis in same way as before but except they will be classified as Stage III or IV and Grade C in new system
30
Q

WHAT TO DO ABOUT DIAGNOSING AND MANAGING PATIENTS WHO WOULD FORMERLY BEEN DIAGNOSED AGGRESSIVE PERIODONTITIS?

In terms of antibiotics?

A
  • Possible use of adjunctive systemic antibiotics at corrective phase of therapy will continue to be carefully considered in line with LDI Protocol for managing Aggressive Periodontitis.

(unless rapid pathway is chosen, then it will be in Initial or cause related therapy)
Or
stage 3 or 4 grade c in younger individuals – aggressive destruction of the supporting bone, which is not proportionate to the amount of local factors

31
Q

NOTES ON DIAGNOSIS OF LOCALISED AGGRESSIVE PERIODONTITIS (stage III/IV -grade C – MIP/ molar incisor pattern)

A
  1. BPE
  2. If 4 even in one sextant then full mouth perio indicies (use periodontal probe PCP10)
  3. Radiographs where indicated/justified
32
Q

Perio screening - simplified BPE in under 18’s

A
  • probe index teeth
  • then carry out full indices based on BPE scores
33
Q

Simplified BPE under 18’s BPE scores

A
34
Q

OLD 1999 CLASSIFICATION – CASE 1 EG OF LOCALISEDAGGRESSIVE PERIODONTITIS ( Stage 4, Grade C, UL6 andLL6

A
35
Q

OLD 1999 CLASSIFICATION – CASE 2 EG OF LOCALISEDAGGRESSIVE PERIODONTITIS ( Stage 3, Grade C, LL6

A
36
Q
A
37
Q

OLD 1999 CLASSIFICATION – GENERALISED AGGRESSIVEPERIODONTITIS

Specific feature?

A
  • Usually affects age <30 yrs, may be older
  • Poor serum antibody response to infecting agents(notably Aggregatibacter actinomycetemcomitans, Porphyromonasgingivalis)
  • Pronounced episodic nature of destruction ofattachment and alveolar bone
  • Generalised interproximal attachment loss CAL-affecting at least three teeth other than first molars
38
Q

1999 CLASSIFICATION - PRINCIPLES OF MANAGEMENT OF AGGRESSIVE PERIODONTITIS

A
  • Early diagnosis is essential - screening!!
  • Establish correct diagnosis - affects therapy
  • Is there an underlying modifying factor orsystemic factor that needs managing?
  • eg poorly controlled diabetes mellitus
  • Referral to a specialist should be considered by GP
39
Q

PRINCIPLES OF MANAGEMENT OF AGGRESSIVEPERIODONTITIS

A

Management is directed to
- suppression of infecting organisms
- providing environment conducive to long-termmaintenance

Therapy in usual 3 phases
- initial cause related (hygiene phase)
- corrective
- supportive

40
Q

DIFFERENCES IN MANAGEMENT OF CHRONIC ANDAGGRESSIVE PERIODONTITIS

A

Initial cause related therapy (scaling/RSD) & (GDP can do both)
- follow same basic principles for both types

Corrective therapy* (Consider Specialist for AggressivePeriodontitis / stage 3 or stage 4 Grade C in younger individuals or disproportionate bone loss to the amount of plaque and calculus)
- consider adjunctive systemic antibiotics in conjunction with furthernon-surgical therapy or periodontal surgery

Supportive (maintenance) therapy* (GDP can do both
- more freq recalls for aggressive perio

41
Q

CORRECTIVE THERAPY FOR AGGRESSIVE PERIODONTITIS : CONSIDER USE OF ADJUNCTIVE SYSTEMIC ANTIBIOTICS

A

Microbial aspects
- Initial therapy should decrease microbial load

Corrective therapy, need to disrupt biofilm on root surfaces (Root Surface Debridement), in conjunctionwith adjunctive systemic antibiotics
- Workable regime: 2 visits for half-mouth RSD one week apart. Debate aboutstarting antibiotics, where indicated, at first visit (forconvenience/compliance) OR prescribing antibiotics at end of 2nd visit(avoids monotherapy) (6th European Workshop 2008)
- LDI protocol: prescribe adjunctive antibiotics at end of 2nd visit
- Microbial sampling in theory can be useful before hand to identify periodontal pathogens, but not routinely done

42
Q

CORRECTIVE THERAPYADJUNCTIVE SYSTEMIC ANTIBIOTICS

What do we use and what dose

A

LDI protocol, metronidazole 400mg + amoxycillin 500mg, t.i.d

If allergy - Azithromycin 500 mg o.d, for 3 days

43
Q
A
44
Q

EFP S3 Clinical guidelines 2020 on the use of subantimicrobial dose doxycycline

A

Understand this

45
Q

LDI protocol

A
46
Q

Prognosis (treatment outcome) for aggressive periodontitis

A

Improves with

  • early,correct diagnosis;appropriate therapy
  • frequent recall/monitoring after therapy
  • Elimination of associated microorganisms isrequirement of success
  • Extractions may be indicated
  • Burn out MAY occur without therapy
  • unpredictable - therefore TREAT
47
Q

WHAT IS PERIODONTITIS?

A

Periodontitis is a chronic inflammatory diseaseassociated with dysbiotic plaque biofilms andcharacterised by progressive destruction oftooth supporting apparatus.

Primary Features: loss of periodontal tissuesupport manifest through clinical attachmentloss (CAL); radiographically assessed bone loss;presence of periodontal pocketing; gingivalbleeding

48
Q
A
49
Q

What is NECROTIZING PERIODONTAL DISEASE

A

Acute periodontal infection

50
Q

Rationale – why systemic antibiotics innecrotizing periodontal diseases?

A

• Necrotizing ulcerative gingivitis (NUG) is a mixedbacterial infection caused by a group ofanaerobes – spirochaetes and fusiform bacteria(fusospirochaetal complex)

• These microorganisms found in LARGENUMBERS in the slough and necrotic tissue atthe surface of the ulcer and also invadesgreatest distance in the underlying intact tissueat the base of the ulcer. This is evidenced byelectron microscopy

51
Q

Management of Necrotizingperiodontal disease

A

Acute phase treatment:

  1. Removal of supra and sub gingival deposits –ultrasonic scaling.
  2. Systemic antibiotic –Metronidazole tablets 200mg, threetimes daily for 3 days
  3. Chlorhexidine mouth rinse

Maintenance phase

52
Q
A
53
Q

Diabetes considerations – poorly controlled

A

Infection mediated upregulation cycle of cytokine synthesis andsecretion by chronic stimulation from LPS and products ofperiodontopathogenic organisms may amplify the magnitude ofadvanced glycation end product (AGE) -mediated cytokine responsein diabetes mellituus

54
Q

Other indications of systemic antibiotics requirement

A

Pericoronitis with the evidence of systemicinvolvement or spread of infection

55
Q

Infective endocarditis

A

Endocarditis

NOTE - Antibiotic prophylaxis against infectiveendocarditis no longer indicated according to NICEguidelines, March 2008

August 2018: Antibiotic Prophylaxis AgainstInfective Endocarditis: Implementation Advice;

The vast majority of patients at increased risk of infectiveendocarditis will not be prescribed prophylaxis. However, for avery small number of patients, it may be prudent to considerantibiotic prophylaxis (non-routine management), inconsultation with the patient and their cardiologist or cardiacsurgeon

56
Q

NICE RECOMMENDATIONS ON ANTIBIOTICPROPHYLAXIS

A

We dont do this anymore

57
Q

Doxycline dose

A

Not recommend currently

58
Q

Tetracyclines no antibacterial effect

A
59
Q
A