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Paediatrics > Paediatric Periodontology > Flashcards

Paediatric Periodontology Flashcards

1
Q

What are the aims of the 2021 guidelines for under 18s?

A
  • Detect gingivitis or periodontitis early during routine exams.
  • Provide management guidance, including when to treat in practice or refer to specialists.
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2
Q

What defines periodontal health?

A

– free from inflammatory periodontal disease
– that allows an individual to function normally
– that avoids physical or mental consequences due to current or past disease.

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3
Q

What is periodontal health based on in children?

A
  • absence of gum inflammation and calculus
  • no more than one sextant with plaque
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4
Q

What are the features of periodontal health in children and teenagers?

A
  • Gingival margin several millimeters coronal to the cemento-enamel junction (CEJ).
  • Gingival sulcus 0.5 mm – 3 mm deep on a fully erupted tooth.
  • In teenagers, alveolar crest is situated between 0.4 mm - 1.9 mm apical to CEJ
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5
Q

What are the two types of gingival conditions classified under gingivitis?

A
  • Plaque biofilm-induced gingivitis.
  • Non-plaque biofilm-induced gingivitis (e.g., systemic conditions or immune reactions).
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6
Q

Why does the periodontium get reduced in non-periodontal patients?

A
  • Crown lengthening surgery
  • Recession
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7
Q

Why does the periodontium get reduced in periodontal patients?

A

stable periodontitis

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8
Q

Is attachment loss present in plaque biofilm-induced gingivitis?

A

No, there is no periodontal attachment loss, and the process is reversible.

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9
Q

What are the types of gingivitis?

A
  1. Plaque biofilm-induced gingivitis
    – Intact periodontium
    – Reduced periodontium
  2. Non plaque biofilm-induced gingivitis / gingival lesions
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10
Q

List the four key features of periodontitis.

A
  1. Loss of periodontal attachment to cementum.
  2. Apical migration of the junctional epithelium.
  3. Transformation to pocket epithelium (often thin/ulcerated).
  4. Alveolar bone loss.
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11
Q

What is the immunology of plaque biofilm induced gingivitis?

A
  • As supragingival plaque accumulates on teeth, an inflammatory cell infiltrate develops in gingival connective tissue.
  • Junctional epithelium becomes disrupted
  • Allows apical migration of plaque and increase in gingival sulcus depth
    – Gingival pocket / false pocket / pseudo pocket
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12
Q

What is the most apical extension of the junctional epithelium?

A

CEJ

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13
Q

Where can plaque induced gingivtis occur?

A

Gingivitis can occur on an intact periodontium or on a reduced periodontium in either a non-periodontitis patient or a successfully treated periodontitis patient.

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14
Q

What can non-dental biofilm induced gingival diseases be from?

A
  • Manifestations of systemic conditions
  • Pathologic changes limited to gingival tissues.
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15
Q

What are the sub-classifications of non-dental biofilm induced gingival diseases?

A

1) Genetic/Developmental disorders
2) Specific infections
3) Inflammatory and immune conditions and lesions
4) Reactive processes
5) Neoplasms
6) Endocrine
7) Nutritional and metabolic diseases
8) Traumatic lesions
9) Gingival pigmentation.

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16
Q

What is the aetiology of necrotising periodontal diseases?

A

– fusiformspirochaetal microbial aetiology.
– Socioeconomic factors - developing countries
– risk factors
* Smoking
* Immunosuppression
* Stress
* Malnourishment
* poor diet.
– Local factors
* root proximity
* tooth malposition.
– Systemic factors
* HIV positive status
– underlying undiagnosed pathology in an immunosuppressed host

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17
Q

What are the features of necrotising gingivitis?

A

– Pain
– Necrosis of interdental papillae -
“punched out” appearance
– Ulceration
– spontaneous bleeding
– secondary foetor oris
– pseudomembrane may be present
– +/- lymphadenopathy
– Fever
– may manifest in teenagers
– May progress to Necrotising Periodontitis (NP)

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18
Q

What are the predisposing local risk factors for periodontal disease?

A

Malocclusion
* Instanding or rotated tooth
* Traumatic occlusion: Low frenal attachments

Traumatic dental injury
* Damage to PDL i.e luxation / intrusion / avulsion

Dental plaque-biofilm retentive factors
* Tooth anatomy e.g talon cusp, cingulum, enamel pearl, enamel defects (pits / grooves)
* Restoration margins / overhangs /cavities
* Orthodontic /prosthodontic appliances (etc).
* Incompetent lip seal -> Oral dryness:
– ↓ saliva flow
– ↓ saliva quality

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19
Q

What are the modifying systemic risk factors for periodontal disease?

A
  • Smoking (Tobacco)
  • Metabolic factors (hyperglycaemia /Diabetes – type 1
  • Pharmacological agents (cyclosporin)
  • Nutritional factors (Vitamin C deficiency)
  • ↑ sex steroids (puberty, pregnancy)
  • Haematological conditions (Leukaemia)
20
Q

What is Molar-Incisor Pattern Periodontitis, and who is commonly affected?

A

Rapid attachment loss around first molars and incisors.
Commonly occurs in adolescents with a family history and no systemic risk factors.

21
Q

What is gingival overgrowth related to?

A
  • systemic and metabolic diseases
  • genetic factors (e.g Hereditary gingival fibromatosis)
  • local factors
  • side effects produced by some medications (cyclosporin, phenytoin and calcium channel blockers).

A greater incidence of gingival overgrowth is seen in puberty and the severity is more intense in children than in adults with similar amounts of dental plaque

22
Q

What is the treatment for gingival overgrowth?

A
  • rigorous home care
  • frequent appointments for professional mechanical plaque removal (PMPR)
  • +/- surgery, especially with drug-induced gingival overgrowth
23
Q

What should you do where the extent of condition is inconsistent with level of oral hygiene observed?

A

-> Consider urgent referral to physician -> haematinic screening

24
Q

Name systemic risk factors for periodontal disease in children.

A

Smoking, diabetes, vitamin C deficiency, and increased sex steroids (puberty).

25
Q

What is periodontitis associated with and characterisied by?

A
  • Associated with dysbiotic (microbial imbalance) plaque biofilms
  • Characterised by progressive destruction of the tooth- supporting apparatus.
  • Multifactoral disease influences:
    – dysbiotic microbiome changes ARE more likely for some patients than for
    others
    – May influence severity of disease.
26
Q

What are the 4 main features of periodontitis?

A

Apical migration of Junctional epithelium beyond CEJ.

Loss of attachment of periodontal tissues to cementum

Transformation of junctional epithelium to pocket epithelium (often thin and ulcerated)

Alveolar bone loss

27
Q

What are the early clinical signs of periodontitis in a substantial proportion of teenagers?

A
  • classified as > 1mm loss of attachment (of cementum to PDL )
28
Q

What pathogens were found in the subgingival microflora of teenagers with periodontitis?

A

– Porphyromonas gingivalis
– Prevotella intermedia
– Aggregatibacter actinomycetemcomitans. (AA)
– Tannerella forsythia (associated with subsequent clinical attachment loss in a 3- year longitudinal study in adolescents)

29
Q

What are the steps to diagnosis of periodontitis?

A

Staging
* Interproximal bone loss at the worst site of bone loss (due to periodontitis)
* Stage I, Stage II, Stage III, Stage IV

Grading
* Rate of progression
* % bone loss / age
* Grade A , Grade B, Grade C

Assess current periodontal status:
* Currently stable
* Currently in remission
* Currently unstable

Risk assessment
* Smoking
* Poorly controlled diabetes

30
Q

What are the features of necrotising periodontitis?

A
  • necrosis/ulceration of the interdental papilla,
  • bleeding of the gingival tissues
  • periodontal ligament loss and rapid bone loss
  • pseudomembrane formation
  • Lymphadenopathy
  • fever
31
Q

What is necrotising stomatitis?

A
  • a severe inflammatory condition
  • necrosis extends beyond gingiva to soft tissues, leading to bone
    denudation
  • severely systemically compromised patients.
32
Q

What are the key features of Molar-Incisor Pattern Periodontitis?

A

Rapid attachment loss and bone destruction.
Commonly affects first molars and incisors.
Onset typically occurs around puberty.
Affects otherwise healthy individuals.
May have a family history of the condition.

33
Q

How does the classification of Molar-Incisor Pattern Periodontitis differ from generalised periodontitis?

A

Localised: Limited to first molars and incisors.
Generalised: Affects ≥3 permanent teeth other than first molars and incisors.

34
Q

What systemic diseases can manifest as periodontitis?

A

– Papillon – Lefevre syndrome (PLS)
– Neutropenias
– Chediak-Higashi syndrome
– Leucocyte adhesion deficiency syndrome (LAD)
– Ehlers – Danlos sydndrome
– Langerhans’ cell histiocytosis (LCH)
– Hypophosphatasia
– Down syndrome

35
Q

What pathogen is commonly associated with Molar-Incisor Pattern Periodontitis?

A

Aggregatibacter actinomycetemcomitans (AA).

36
Q

At what age should sBPE be conducted in cooperative children?

A

From 7–18 years old.

37
Q

What is a sBPE performed with?

A

WHO single black band

38
Q

Between 7-11 years old, what are the sBPE codes?

A

0-2

39
Q

What are the sBPE codes from 12-17?

A

all

40
Q

What does a BPE Code 4 indicate in children?

A

Pocketing ≥6 mm, requiring referral to a specialist.

41
Q

What should you do for a BPE code of 3/4?

A
  • 6 point pocket (localised to 3 BPE, or full if 4)
  • Check alveolar bone level.
    – BW’s for posteriors
    – Periapicals for anteriors
    – OPG (esp. if part of orthodontic treatment)
42
Q

What are the key oral health messages to prevent plaque-induced gingivitis in children?

A
  1. Effective toothbrushing (systematic cleaning of all surfaces).
  2. Use of disclosing tablets for improved technique.
  3. Hands-on demonstration of techniques like the modified Bass method.
  4. Fluoride advice for caries prevention.
  5. Smoking cessation, especially important during teenage years.
43
Q

What are the treatment and recall recommendations for a patient with an sBPE Code 2?

A

Treatment: Oral hygiene instruction (OHI), supragingival and subgingival professional mechanical plaque removal (PMPR), manage plaque retention factors.
Recall: Screen at routine recall or within 6 months (whichever is sooner).

44
Q

What are the four steps of the S3 treatment guidelines for managing periodontitis?

A

Step 1: Build foundations (OHI, supragingival PMPR, risk factor management).
Step 2: Cause-related therapy (subgingival PMPR, adjunctive antimicrobials if needed).
Step 3: Management of non-responding sites (surgical interventions for complex lesions).
Step 4: Supportive periodontal care (maintenance with tailored recall intervals).

45
Q

What is the diagnosis for a 19-year-old female with generalised bone loss, stage III/grade C, and currently unstable periodontal status?

What additional questions should be considered in a case like this?

A

Diagnosis: Generalised periodontitis, stage III/grade C, currently unstable.
Follow-up: Systematic periodontal treatment with long-term maintenance.

Any siblings with similar issues?
Evidence of systemic risk factors?

46
Q

What was the diagnosis for the sibling (14-year-old) with bone loss affecting 8 teeth?

A

Diagnosis: Localised periodontitis, stage II/grade C, currently unstable.
Follow-up: Systematic treatment with maintenance and monitoring due to high susceptibility.

47
Q

What are the key conclusions about periodontal screening in children and adolescents?

A
  1. Early detection is critical for accurate diagnosis and optimal treatment outcomes.
  2. sBPE on 6 index teeth is recommended for all cooperative patients under 18.
  3. False pocketing can complicate diagnosis in erupting dentitions.
  4. BPE Codes 4 or * are rare in children and warrant specialist referral.
  5. Periodontal diseases in primary dentition are unusual and require referral if unexplained symptoms like premature exfoliation or gross mobility are observed.

Paediatrics (5 decks)

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