Chapter 8
Periodontal disease in children
And Pediatric Oral Pathology Soft Tissue Lesion
Section 1 Periodontal disease in children
1 Periodontal diseases
Today, we’ll introduce you periodontal disease in children. What is periodontal
disease? Just as its name implies, periodontal disease comprise a group of infection
that affect the periodontal tissue, we say the supporting structures of the teeth. Then, I
want to ask: what is periodontal tissue or periodontium? We say, periodontium include
four parts: Gingiva, Periodontal ligament, Cementum and Alveolar bone.
2 Anatomy of the periodontium in children
Increasing information emphasizes the relevance of the prevention, early
diagnosis and early treatment of periodontal diseases in children. In order to avoid
erroneous diagnosis and unnecessary treatments, the pediatric dentist is required to
differentiate between pathologic processes and normal changes that take place in the
periodontum with age.
We know the children are in the course of growth and development, so in
different stages, they have their characteristic of physiology and psychology. Then,
what is the different between the periodontium of children and adults? Let’s see.
2.1 Gingiva
2.1.1 Marginal gingival: When we talk about the marginal gingival tissue, you
should pay attention to two key words:vascular and fibers. For children,marginal
gingival tissue around the primary dentition are more highly vascular and contain
fewer connective tissue than tissues around the permanent teeth. The epithelia are
thinner with a lesser degree of keratinization, giving an appearance of increased
redness that may be interpreted as mild inflammation, and it’s easy for marginal
gingiva to be affected
2.1.2 Attached gingival: It may maintain the sulcus depth, resist the functional
stress during mastication, and resist the tensional stress by acting as a buffer
between the gingival margin and the alveolar mucosa. The width of attached
gingival is less variable in the primary dentition, so there is less mucogingival
problem in the primary dentition
2.1.3 Junctional epithelium: When we refer to the gingiva, we can’t help but talk
about junctional epithelium. Because it’s very important in the health of the
periodontium .There is some normal change that take place in junctional
epithelium and we should not treat it as disease. First, let’s see what happens
during eruption of the teeth? It migrates apically. There continue to be an apical
shift when the teeth are fully erupted. So the gingival margins are frequently at
different levels on adjacent teeth that are at different stages of eruption.
Sometimes it gives an erroneous appearance that gingival recession has occurred
around those teeth that have been in the mouth longest. Stability is achieved at 12
years for 1 2 3 5 6, 16 years for the other teeth.
2.2.Periodontal ligament
Periodontal ligament space is wider in children and is less fibrous and more
vascular
2.3 Cementum
Thinner
2.4 Alveolar bone
 Thinner cortical plates(皮质层）
 Larger marrow spaces（骨髓腔）
 Greater vascularity
 Fewer trabeculae
*Clinical significance of the anatomy: Enhance the rate of progression of
periodontal disease
3 A classification of periodontal disease in children
3.1Gingival conditions
Acute gingivitis
Chronic gingivitis
Gingival overgrowth
Factitious（自伤性）gingivitis
Mucogingival problems
3.2 Periodontal conditions
Chronic periodontitis
Early-onset periodontitis
Prepubertal（青春期前的） periodontitis associated with systemic disease
4 Acute gingivitis
4.1 Primary herpetic gingivostomatitis（原发性疱疹性龈口炎）
4.1.1 Definition: An acute infectious disease of the gingiva caused by the
herpesvirus
4.1.2 Pathogeny: Herpes simplex viruses (HSVs)( 单 纯 疱 疹 病 毒 ） Herpes
simplex viruses (HSVs) are ubiquitous, extremely host-adapted pathogens that can
cause a wide variety of illnesses. Two types exist: type 1 (HSV-1) and type 2
(HSV-2). Both are closely related but differ
in epidemiology.Type-1
Gingivostomatitis; Type-2
Genitalia（生殖器）
4.1.3 Transmission: HSV-1 is transmitted chiefly by contact with infected saliva,
Infected saliva from an adult or another child is the mode of infection. whereas
HSV-2 is transmitted sexually or from a mother's genital tract infection to her
newborn.
4.1.4 Prevalence: HSV infection appears to have increased worldwide in the last
2 decades, making it a major public health concern. Many primary infections are
asymptomatic, Herpes simplex infections are asymptomatic in as many as 80% of
patients, but symptomatic infections may be characterized by significant
morbidity and recurrence. Moreover, infections can cause life-threatening
complications, particularly in immunocompromised hosts.
4.1.5 Clinical features:
1) Age: 6 months to 3 years
2) Incubation period(潜伏期): 1 week
3) Prodrome:
A Febrile（发烧的） illness
B Headache, malaise, oral pain, mild dysphagia（吞咽困难）
C Cervical lymphadenopathy(淋巴结病）
4) Symptom
A Gingivitis: Gingivitis is the most striking feature,with markedly swollen,
erythe-matous, friable gums
B Vesicular lesions: Vesicular lesions develop on oral mucosa ,lip and
tongue , can occur anywhere in the oral cavity, on the perioral skin, on
the pharynx
4.1.6 Prognosis
Oral lesions heal without scarring
4.1.7 Course: Acute disease lasts 5-7 days, and the symptoms subside in 2
weeks. Viral shedding from the saliva may continue for 3 weeks or more. Adults
also may develop acute gingivostomatitis, but it is less severe and is associated
more often with a posterior pharyngitis.
4.1.8 Diagnosis: According to Clinical features,History and age
4.1.9 Treatment: The availability of effective chemotherapy underscores that the
prompt recognition of the infection and early initiation of therapy are of utmost
importance in the management of the disease. The goals of treatment are to make
the patient comfortable and to prevent secondary infections or worsening systemic
illness. It includes:
1) Pharmacotherapy(药物疗法) :
A Antiviral treatment : Overall, medical treatment of HSV revolves
around specific antiviral treatment. Patients should be advised about the
potential for autoinoculation if they touch the herpetic lesion and then
touch a mucous membrane or an eye. Controlling autoinoculation can be
a challenge if the patient is a young child.
B Symptomatic treatment : In situations in which constitutional effects
such as fever occur, symptomatic treatment can be used. Analgesics,
such as acetaminophen, may make the patient more comfortable. Aspirin
should be avoided in pediatric patients because of the possibility of Reye
syndrome. Topical anesthetics and coating agents may make the patient
more comfortable and may aid in the consumption of food; however,
they do not speed healing. Appropriate wound care is needed, and
treatment for secondary bacterial skin infections may be required.
2) Supporting treatment:
A Bed rest
B Soft diet
C Be kept well hydrated: The patient should maintain fluid intake and a
balanced diet with the use of liquid food replacement if necessary
4.1.10 Warnings to parent:
A Children are highly contagious
B No school, day care etc.
C Sterilize eating and drinking utensils
D Disease is self-limiting; 10-14 days in duration
4.2 Acute necrotizing ulcerative gingivitis(ANUG)
4.2.1 Aetiology:
Broad anaerobic infection
Causative organism: Fusiform bacteria ,
Spirochaete（螺旋体）
Other Gram-negative(革兰氏阴性)anaerobic organism
4.2.2 Clinical features:
A Necrosis and ulceration : Interdental papillae marginal gingival
Covered by yellowish-grey pseudomembranous( 假 膜 ) slough, Acute
stage enters a chronic phase after 5-7days. Recurrence of the acute
condition is inevitable
B Pre-existing gingivitis
C Distinctive halitosis
D Acute-chronic clinical course: If acute-chronic cycle continues, the
marginal tissues lose their contour and appear rounded. Eventually,
involve the alveolar crest
4.2.3 Treatment
A Intense oral hygiene
B Oxidant: hydrogen peroxide
C Mechanical debridement
D Metronidazole
5 Chronic gingivitis
Chronic gingivitis is a common condition. In fact, gingivitis affects over 90%
of the population of the United States. If treated, the prognosis for those who have
gingivitis is good. Untreated, gingivitis may progress to gum disease or
periodontal disease. Gingivitis is painless in the early stages, but may lead to
bleeding gums and other oral problems. Bleeding gums are only one sign of
gingivitis. Gums become red and swollen, teeth may become loose or may
eventually fall out.
Prevalence: increases steadily between the ages of 5 and 9 years, peaks at 11
years and decrease slightly with age to 15 years.
Etiology: Closely associated with the amount of plaque, debris and calculus
present.
5.1 Eruptive gingivitis
Cause：
1）Trauma of gingiva
2） Debris and food residue
Clinical feature:
1）Site: Primary teeth and the 1st permanent molar
2）Symptom：
Treatment：Oral hygiene
5.2 Filth gingivtis(不洁性龈炎)
Cause：
Clinical feature:
Age: 3Y~5Y
Site：Buccal, Papi
Symptom：redness, bleeding
Treatment:
1）Local cleaning, antiinflection
2）Oral hygiene
5.3 Crowding gingivitis (牙列拥挤性龈炎)
Cause
Symptom: Redness and thickness
Treatment: A: Oral hygiene B: Orthodontic treatment
5.4 Puberty gingivitis(青春发育期龈炎)
Cause: Increase of sex hormones in circulating levels
*sex hormones :
Oestrogen( 雌 激 素 ): Increases the cellularity of tissues and provides
suitable growth condition for species associated
with established gingivitis
Progesterone ( 黄 体 酮 ):Increases the permeability of the gingival
vasculature
Clinical features：
Good oral hygiene, but the gum tends to bleed and hyperplasia
Bad oral hygiene
Treatment：
5.5 Catarrh gingivitis (卡他性龈炎)
Cause：The infection of hemolytic streptococcus(溶血性链球菌感染)
Clinical features：
1）Oral lesion：soft and
hematose gum, but no vesicles or ulcers
2）Systemic reaction：fever，headache，myalgia, arthralgia（关节痛）
Treatment：
1）Local: Rinse
2）Systemic treatment:
Penicillin
6 Drug-induced gingival overgrowth
6.1 cause:
Drug: Phenytoin , Cyclosporin
1) Phenytoin
A An anticonvulsant used in the management of epilepsy
B Rate: occur in about 50% of subjects taking the drug
C Be most severe in teenagers
D Associated with a deficiency of folic acid
2) Cyclosporin
A An immunsuppressant drug
B Rate:30%
C Children: more susceptible
6.2 Clinical feature:
1) The clinical changes of drug-induced overgrowth are very similar
irrespective of the drug involved.
2) The first signs of changes are seen after 3-4months of drug
administration.
3) Progress: The interdental papilla become nodular before enlarging
more diffusely to encroach upon the labial tissue
4) Site:The anterior part is most severely and frequently involved
5) Sypmtom: with a good standard of oral hygiene, overgrowth gingiva is
pink,firm and stippled, When there is a pre-exiting gingivitis the
enlarged tissues compromise an already poor standard of plaque
control.the gingiva then exhibit the classical signs of gingivitis
6.3 Management
1)A strict programme of oral hygiene instruction, scaling and polishing
must be implemented.
2) Severe cases of gingival overgrowth inevitably need to be surgically
excised and then recontoured to procedure an architecture that allows
adequate access for cleaning
3)A follow-up programe is essential to ensure a high standard of plaque
control and to detect any recurrence of the overgrowth.
4)To modify or change the anticonvulsant therapy if phenytion-induced
overgrowth is refractory
5)Indefinite oral care if there is no alternative.
7 Factitious gingivitis
7.1 Minor form
Etiology: Rubbing or picking the gingiva using the fingernail, or from
abrasive foods
Management: correct the habit and remove the source of irritation
7.2 Major form
The injuries are more severe and widespread , can involve the deeper
periodontal tissues. Other areas of the mouth such as the lips and
tongue may be involved. Extraoral injuries may be found on the scalp,
limbs or face.
Management
A Dressing and protection of oral wounds
B No lying with dentists
C Psychological or psychiatric consultation
8 Chronic periodontitis
A number of epidemio-logical studies have investigated the prevalence of
chronic periodonditis in children. The prevalence of the study varied due to
different methods of diagnosing and different cut-off value in different studies.
Prevalence
At 1-11%,
The chronic periodontitis initiates and progresses during the early teenage
years
9 Periodontal complications of orthodontic treatment
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Gingivitis
Gingival overgrowth
Attachment and bone loss
Gingival recession
Trauma
10 Early-onset aggressive periodontal disease
Prepubertal periodontitis: mainly influences primary dentition immediately
after the teeth have erupted. It includes generalized form and localized
form:
Generalized form
A Gingiva:fiery red,swollen,and haemorrhagic
B Tissue: hyperplastic with granular（粒状的） or nodular（节结状的）
proliferation
C Gross deposits of plaque
D Progress: extremely rapidly, primary teeth loss:3-4 years
E Bone loss: may be restricted to one arch
Localized form
A Progresses more slowly
B Bone loss affects only incisor-molar teeth
C Plaque levels are low
Treatment
A Intense oral hygiene at frequent intervals
B Antibiotic
C Extraction of the teeth
Section 2 Pediatric Oral Pathology Soft Tissue Lesion
1 Infection:
1.1 Viruses:
1) Herpetic infention: Primary herpes simplex infection
Secondary herpes simplex infection
2) Hand, foot，mouth disease
Cause: Coxsackie virus A16
Signs and symptoms
Prodrome: Fever, malaise, lymphadenopathy
Skin lesion : Maculopapule(斑丘疹）on the hands and feet
Oral lesion: vesicles
ulceration
Course: 10-14 days
3) Herpangina（疱疹性咽峡炎）
Cause: Coxsackie virus A4
Signs and symptoms
A Light systemic reaction and prodrome
B Vesicles in the tonsillar or pharyngeal region ulcers, no coalesce
for large areas of ulceration
C Short-lived
1.2 Bacteria
1) Staphylococcal infections impetigo
2) Streptococcal infection
3) Congenital syphilis
1.3 Fungi or protozoa（原生动物）
Oral Candidiasis
Candidiasis describes a group of yeastlike fungal infections involving the skin
and mucous membranes.
Classification of oral candidiasis
1) Acute pseudomembranous candidiasis (thrush)
2) Acute atrophic candidiasis,
3) Chronic hyperplastic candidiasis,
4) Chronic atrophic candidiasis.
Acute pseudomembranous candidiasis (thrush)
Pathogens: Candida albicans. It’s a harmless commensal organism, but if there
is a disturbance in the oral flora or a decrease in the immune defenses, it becomes
opportunistic pathogen.
Transmission: Vagina or infection from breast or feeding utensil
Risk Factors:
Low level of Antifungals substance
Deficiency of myeloperoxidase (脊髓过氧化物酶)
Low secretion of saliva
Clinical features
Age：Neonates and infants within 6 months
Oral lesion:
White patches oral mucosa, tongue
Lesions develop into confluent plaques that resemble milk curds and can
be wiped off to reveal a raw erythematous and sometimes bleeding
base.
Systemic reaction
Diagnosis
Clinical diagnosis：Clinical features
Fungal infection：Smear
Candida albicans：Culture
Treatment
Medication
1）1%~2% NaHCO2 once 2~3h
2）0.05% Gentian violet(龙胆紫)， three times daily
3）10 万 U Nystatin(制霉菌素)/ml，once 2~3h
4）Obstinate cases,100mg Amphotericin(两性霉素)/ml，4 times daily
5）Severe cases， clotrimazole(克霉唑)
Assistant management
Oral hygiene
Sterilization
2 Traumatic Ulcers
Due to trauma to the tissue
• Toothbrush abrasion
• Tortilla chip
• Bite
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External trauma-physical violence
Any location
Yellow ulcerated tissue with surrounding erythematous halo
Painful
*Riga-Feda disease
Cause
A Early eruption of primary incisors
B Sharpness of primary incisors
C Ankyloglossia
Clinical features
A Site:
B Shape:φ
C Progress:
Treatment
• Local management
• Removal of factors
• Change feeding method
• Excise of Ankyloglossia
* Bednar’s ulcer
Cause
Clinical features
Treatment
* Aphthous Ulcers
Be often found in children
One or more small ulcers
The majority of aphthous ulcers in children are of the minor variety
Heal within 10-14 days
Treatment is often unnecessary
In severe cases: topical steroids
Older children: antiseptic rinses to prevent secondary infection
3 White leisions
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Geographic tongue
Normally symptomless
Some discomfort with spicy foods
Areas of the tongue appear shiny and red due to loss of filiform papillae
These red patches are surrounded by white margins
These areas disappear before reappearing in other region of the tongue
Begin
Require no treatment
4 Cysts
5 Tumors