Periodontal Diseases in Children

• Definition of periodontal diseases = a group of infections that affect the supporting structures of the teeth:

  • Marginal gingiva
  • Attached gingiva
  • Periodontal ligament
  • Cementum
  • Alveolar bone
• Classification of perio disease - no attachment loss:

  • Acute gingivitis - NUG
  • Chronic gingivitis - plaque-induced, puberty
  • Gingival enlargement - drug-induced
  • Traumatic gingivitis
  • Mucogingival problems
• Classification of perio disease - loss of attachment:

  • Chronic periodontitis - plaque-induced, orthodontic
  • Aggressive periodontitis
  • Periodontitis as part of systemic disease
  • Papillon-LeFevre Syndrome
  • Ehlers-Danlos Syndrome
  • Hypophosphatasia
  • Chediak-Higashi
  • Neutropaenias
  • Langerhans' cell histiocytosis
• Periodontium in children:

  • Marginal gingival tissues more vascular
  • Contain fewer connective tissue fibres
  • Thinner epithelia
  • Less keratinisation
  • Look redder and often mistaken for inflammation
• Periodontium in children - tooth eruption:

  • Localised hyperaemia (excess blood in vessels in a particular area) accompanies eruption of primary teeth
  • Can lead to persistent swollen rounded papillae and >3mm gingival sulcus depth (false pocketing)
  • Eruption of permanent teeth accompanied by migration of the junctional epithelium, leading to large sulcus depths (false pocketing)
  • Care when monitoring gingival status because false pocketing is common
• Gingival stability:

  • After full eruption the junctional epithelium and gingival margin continue to shift
  • At 12 years - lower incisors, 3s, 5s and 6s should be stable - but will have different sulcus depths
  • Further maturation until about 16 years
  • Different levels on different teeth
  • Mistaken for gingival recession
• Primary dentition:

  • Attached gingiva is less variable in width
  • Fewer mucogingival problems
  • Periodontal space is wider (thinner cementum and cortical plates)
  • PDL less fibrous and more vascular
  • Alveolar bone more vascular, fewer trabeculae
  • Enhanced rate of progression of perio disease in primary dentition - often leads to exfoliation of tooth
• Home-based oral hygiene - babies:

  • Toothbrush as soon as first tooth erupts
  • Twice daily with a smear of no less than 1,000 ppmF
  • Adult brushing
  • Allow child to become familiar with brush
  • Small amounts because most will be ingested

  
• Home-based oral hygiene - over 3 years:

  • Twice daily with a smear/small pea of no less than 1,350-1,500ppmF
  • Adult brushing and help until at least 7 years-old, or until manual dexterity sufficient
  • Small amounts because most will be ingested

  
• Home-based oral hygiene:

  • Powered brush
  • Novelty effect
  • Equally as effective as manual especially if highly motivated
  • Helpful in special needs and orthodontics
  • Floss
  • Use is not widespread
  • Specially designed floss holders for children
  • Must be supervised until dextrous
• Acute gingival conditions:

  • Primary herpetic gingivo-stomatitis
  • Necrotising ulcerative gingivitis
• Chronic gingivitis:

  • Plaque-associated
  • Lymphocyte-dominated
  • Can be linked to onset of puberty
  • Potential indicator of future attachment and tooth loss
• Puberty and gingivitis in girls:

  • Oestrogen - increases cellularity of tissues
  • Progesterone - increases permeability of gingival vasculature
• Drug-induced gingival enlargement:

  • Anti-convulsant Phenytoin (epilepsy)
  • Immunosuppressant Ciclosporin (prevent organ rejection)
  • Calcium-channel blocker Nifedipine (used in children post-transplant to reduce nephrotoxicity of ciclosporin)
• Drug-induced gingival enlargement - clinical features:

  • Similar with all drugs
  • Starts 3-4 months after first taking drug
  • Nodular papillae
  • Then becomes diffuse enlargement
  • Encroaches labially
  • Anterior > posterior
  • +/- superimposed gingivitis
  • Overgrowth is due to collagen proliferation
• Phenytoin:

  • Very severe in teenagers
  • Mechanism unclear
  • Probably due to overproduction of collagen
  • Works on particular fibroblasts that naturally make a lot of collagen
• Ciclosporin:

  • 30% of patients show enlargement
  • Children > adults
  • Exact mechanism unknown - maybe
  • Stimulation of fibroblasts
  • Increased collagen production
  • Inhibits collagenase
• Management of gingival enlargement:

  • Oral hygiene and debridement
  • Surgical excision and recontouring - gingivectomy and gingivoplasty
  • Change medication - possibly
  • Tacrolimus can be taken to reduce effects of Ciclosporin

  
• Traumatic gingivitis:

  • Gingivitis artefacta/Factitious gingivitis - continuous picking of the gingivae
  • Minor and major variants
  • Self-inflicted
  • Habitual
  • Psychological issue - particularly if dermatitis artefacta evident too (picking at skin)
  • Can produce loss of attachment and so traumatic periodontitis

  
• Traumatic gingivitis:

  • Gingivitis artefacta/Factitious gingivitis - continuous picking of the gingivae
  • Minor and major variants
  • Self-inflicted
  • Habitual
  • Psychological issue - particularly if dermatitis artefacta evident too (picking at skin)
  • Can produce loss of attachment and so traumatic periodontitis

  
• Width of keratinised gingivae:

  • A narrow zone of keratinised gingivae can be healthy
  • A wider zone may be better to withstand inflammation, trauma, toothbrushing and muscle pull
• Gingival recession in children:

  • In children tooth position important - permanent incisors with recession are very often labially displaced
  • Labial tipping of roots in orthodontics
  • Oral hygiene support essential
  • Monitor until maturation complete
  • Cautious approach in children
• Screening: the modified BPE:
• Screening: The Modified BPE

  • BSP/BSPD
  • Used when under 18 years
  • 6 index teeth
  • 16, 11, 26, 36, 31, 46
  • Use codes 0, 1 and 2 for 7-11 year-olds
  • Use full range of codes for 12-18 year-olds. If codes 3-4 found - radiographs
  • Use BPE for pre-orthodontic screen

  
• Local risk factors for perio conditions and diseases:

  • Malocclusions
  • Traumatic dental injuries
  • Plaque-retentive factors
  • Dental anomalies
  • Iatrogenic
  • Ectopic eruption
• General risk factors for perio conditions and diseases:

  • Inherited conditions
  • Papillon-LeFevre Syndrome
  • Chediak-Higashi Syndrome
  • Leukocyte Adhesion Deficiency
  • Ehlers Danlos
  • Hypophosphatasia
  • Systemic conditions
  • Diabetes mellitus
  • Poorly controlled Type 1
  • Both diabetes and perio are inflammatory conditions
  • PMNL (polymorphonuclear leukocyte) defects (chemotaxis, phagocytosis and adherence)
  • Disrupted immune networks (cytokine IL-6)
  • Upregulation of cytokines - local damage
  • Tobacco smoking
• Aggressive periodontal disease:

  • Recently reclassified from 'prepubertal' and 'juvenile'
  • Can affect primary and adult dentitions and be local or general
  • Rare, rapidly progressing
  • Prevalence 0.1%-5%
  • More prevalent in UK within Asian and Afro-Caribbean cohorts
  • Specific microbes and inherent host immune defect
• Treatment of periodontal diseases in the primary dentition:

  • Intense treatment (debridement +/- amoxicillin/metronidazole)
  • If general, may render child edentulous before eruption of adult teeth as this is thought to remove aggressive pathogens
  • Monitor permanent dentition very closely and culture subgingival flora to ensure permanent dentition aren't affected
• Permanent dentition:

  • Severe perio destruction with onset at puberty, PMNL (polymorphonuclear leukocyte) functional defects
  • Plaque-control doesn't equal level of destruction
  • Localised: otherwise healthy involving 1s and 6s
  • Generalised can also occur in healthy children but >14 teeth (whole arch or entire dentition)
  • Microbes
• Treatment of periodontal diseases in permanent dentition:

  • Regular scaling and PMPR
  • 2/52 course of tetracycline or amoxicillin and metronidazole for 1/52
  • Occasionally radical flap surgery and antimicrobials
• Aggressive perio and genetic factors:

  • Ethnic groups and family histories
  • Functionally defective PMNLs (polymorphonuclear leukocytes)
  • Links with other inherited conditions displaying PMNL defects, enzyme reactions or collagen synthesis
  • Rare
  • Often autosomal mode of inheritance
• Systemic disorders with periodontal features:

  • Papillon-LeFevre Syndrome
  • Autosomal recessive
  • Cathepsin C gene, affects immune and inflammatory responses
  • Periodontitis and palmar plantar hyperkeratosis
  • Acitretin now used to reduce symptoms
• Systemic disorders with periodontal features:

  • Neutropaenias (familial or cyclic)
  • Cyclic neutropaenia
  • Gene encoding neutrophil elastase
  • Varies according to bone marrow activity
  • 3 week cycles
  • Chediak-Higashi Syndrome (reduced phagocytosis)
  • Gene mutation - phagocytosis disrupted
  • Lots of pyogenic infections
  • Ocular-cutaneous albinism
  • No phagocytosis -> periodontitis
• Systemic disorders with periodontal features:

  • Leukocyte Adhesion Deficiency Syndrome
  • Ehlers-Danlos Syndrome Type VIII (collagen)
  • Langerhans' Cell Histiocytosis
  • Papillon-LeFevre Syndrome
  • Neutropaenias (familial or cyclic)
  • Chediak-Higashi Syndrome (reduced phagocytosis)