Gingival and periodontal health in children: an overview Flashcards
Visual assessment of plaque 2013 (national statistics)
Visible plaque present in:
- 46% of 5 year olds
- 71% of 8 year olds
- 50% of 15 year olds
Visual assessment of calculus 2013 (national statistics)
Calculus detected in
- 9% of 5 year olds
- 28% of 8 year olds
- 46% of 15 year olds
Exceptions: children who would not have plaque or calculus
Children who are fed only by a gastrostomy tube (PEG)
Gingival bleeding on probing (BPE for 6 teeth) amongst 15 year olds
Present in 40%
Periodontal pocketing
Predominantly in mild category 3.5-5.5mm
Gingivitis less prevalent where?
Left than right side of mouth
Differences according to social class
No
Differences between boys and girls
Generally no significant differences except plaque & calculus scores for 12 year olds
- 72% of boys and 56% of girls had visible plaque
- 46% of boys and 31% of girls had visible calculus
Gingival disorders in children
- Chronic gingivitis (plaque-induced)
- Gingival hyperplasia
- Traumatic lesions
- Acute gingivitis (infective)
Chronic Gingivitis
Common
Reversible with improved oral hygiene
Painless, red, swelling of gingiva, no loss of function
Cultivable flora similar to that in adults
-gram +ve rods and cocci
-gram -ve anaerobic rods and spirochaetes
May be exacerbated by exfoliating teeth, malocclusion or presence of orthodontic appliances
Challenges to toothbrushing
Retroclined teeth in cleft lip and palate pxs
Abnormalities of tooth morphology
Orthodontic appliances
Sensitive teeth - amelogenesis imperfect
Physical disabilities e.g. Cerebral palsy, hemiplegia
Learning disabilities e.g. Down syndrome, autism
Localised gingival recession
Stillman’s cleft
10% of children < 10 years of age
Usually labial to lower incisors
Associated with malaligned teeth, self-inflicted injury, toothbrushing habits
Need to educate and improve plaque control, orthodontic therapy
Gingival hyperplasia: drug induced
Phenytoin (anti-epileptic)
Cyclosporin (immunosuppressant)
Nifedepine (calcium channel blocker)
Cyclosporin
Selective immunosuppressant - inhibits T lymphocyte proliferation
Used mainly to prevent graft rejection
Gingival hyperplasia in around 30% of cases
Hyperplasia is exacerbated by poor OH
Effects fibroblasts promoting protein synthesis and collagen formation
Recurs after gingival surgery
Gingival hyperplasia: systemic disease
Carcoid
Cyclic neutopenia
Traumatic gingival injury: self-inflicted injury
Type A: injuries superimposed upon pre-existing source of irritation
Type B: injuries are secondary to another established habit
Type C: injuries are of complex aetiology and are a physical manifestation of an underlying emotional disturbance - resistant to conventional treatment
Acute gingival conditions and infections
Acute herpetic gingivostomatitis
Necotising ulcerative gingivitis
Hand, foot and mouth
Herpengina
Acute herpetic gingivostomatitis
Common in childhood
HSV type I infection
Can present as subclinical infection, febrile illness, encephalitis/ meningitis
5-7 day incubation period
Signs/ symptoms of AHGS
Pyrexia, >39 degrees C Lymphadenopathy Malaise and irritability Profuse salivation Refusal to eat Sore throat and mouth Symptoms for 7-10 days
Clinical features of AHGS
Multiple small irregular ulcers on gingiva, tongue and palate Erythematous gingiva Occasional extra-oral lesions Salivation Lymphadenopathy Recurrence as herpes labialis in 30%
Management of AHGS
Symptomatic and supportive
- fluids & soft diet
- analgesics & antipyrexics
- isolation of eating/ drinking utensils
- OHI - chlorhexidine and sponges, soft toothbrush
- rest
- reassurance and review
- not acyclovir (unless immunocompromised)
Who does necrotising ulcerative gingivitis/ periodontitis affect?
Affects young adults and HIV+ in Western contries (0.7-7%)
-risk factors = smoking and stress
More commonly affects children in developing countries - with underlying malnutrition and infections (HIV) up to 20%
Necrotising ulcerative gingivitis: symptoms, clinical and treatment
Characterised by necrosis and ulceration -usually interdental papillae, gingivae bleed profusely, distinctive halitosis
Broad anaerobic infection
Treatment with oral hygiene, hydrogen peroxide mouthwash, metronidazole 3-days
Can spread rapidly to facial tissues –> cancrum oris
Systemic conditions that may present with gingival changes e.g. bleeding, ulceration
HIV Chrons' disease Leukaemia Langerhans' cell histiocytosis Scurvy
Periodontal disease in children
Loss of tooth tissue attachment very uncommon in children
Clinical features of aggressive periodontal disease in children
~0.1% of white Caucasians and 2.6% of black Africans may suffer from localised aggressive forms of periodontitis
Onset ~ puberty
May present with tooth mobility, drifting or periodontal abscess
Rapid periodontal attachment loss, usually incisors and first permanent molars
Often a positive family history
Healthy apart from periodontitis
Progression of attachment loss and bone loss may be self-arresting
Clinical features of aggressive periodontal disease in children (Microbiology)
Amounts of microbial deposits inconsistent with severity of destruction Elevated proportions of A. actinomyecetemcomitans and in some populations, P.gingivalis Phagocyte abnormalities (host defence defects): hyper-responsive macrophage phenotype, including elevated levels of PGE2 and IL-1β
Management of aggressive periodontal disease in children
Refer to specialist: early diagnosis and interventions critical for better outcome
- standard mechanical periodontal therapy
- systemic or local drug therapy (metronidazole AND amoxicillin tds 1 week)
- maintenance therapy
- periodontal surgery
Systemic/ genetic conditions in which periodontal disease is exacerbated
Insulin-dependant diabetes Down syndrome Papillion-lefevre syndrome Enlers-Danlos syndrome Langerhans' cell histocytosis Neutropenias Hypophosphatasia
Papillion-Lefevre syndrome
Itchy feet (hyperkeratosis of soles) Loose teeth (generalised gingival recession) Hyperkeratosis of palms of hands
