Periodontics/OralMedicine

Ashish Kumar

Sujata Surendra Masamatti and Mandeep Singh Virdi

Periodontal Diseases in Children

and Adolescents: A Clinician’s
Perspective Part 2
Abstract: The general dental practitioner and paediatric dentist are in a unique position to identify and distinguish between a seemingly
innocuous condition that may be a normal physiological aberration or an early sign of severe destructive periodontal disease. Although
severe destructive periodontal conditions are uncommon in children, it is essential that children receive a periodontal screening as part of
their regular dental examination. Early diagnosis ensures a high likelihood of a successful therapeutic outcome, primarily by reduction of
aetiologic factors, remedial therapy and development of an effective maintenance protocol. This prevents the recurrence and progression
of disease and reduces the incidence of tooth loss. In the first article, we discussed the classification, plaque-induced and non plaque-
induced gingival diseases, localized and generalized forms of chronic as well as aggressive periodontitis. In this second article, we discuss
periodontitis as a manifestation of systemic disease, necrotizing periodontal diseases, periodontal screening and basic periodontal
examination, and treatment of periodontal diseases in children and adolescents.
Clinical Relevance: Incorporation of periodontal screening in regular dental examination by dentists can help in early diagnosis and
treatment of periodontal diseases. This could prevent further progression of disease and reduce the frequency of tooth loss.
Dent Update 2012; 39: 639–652

Periodontitis as a category includes diseases like deficiencies show evidence of severe

manifestation of systemic
diseases
Periodontitis as a manifestation
of systemic diseases is classified in Table 1.1
The ‘Not otherwise specified’
Ashish Kumar, MDS, Reader, Department
of Periodontics, Institute of Dental
Studies and Technologies, Modinagar,
Uttar Pradesh, Sujata Surendra
Masamatti, MDS, Reader, Department
of Periodontics, ITS – Centre for Dental
Studies and Research, Murad Nagar,
Ghaziabad, Uttar Pradesh and Mandeep
Singh Virdi, MDS, Professor and Head,
Department of Pedodontics and
Preventive Dentistry, PDM Dental College
and Research Institute, Bahadurgarh,
Haryana, India.
November 2012 DentalUpdate 639
osteoporosis and oestrogen deficiency,
which have been shown to affect the
periodontium, but data regarding their
effect requires confirmation. It was
emphasized in the consensus report that
other systemic conditions may be added
after the evidence is available.
Defects in neutrophil and
immune cell function associated with
these diseases may play an important role
in increased susceptibility to periodontitis
and other infections. Periodontitis as
a manifestation of systemic disease in
children is a rare disease that frequently
begins between the times of eruption of
the primary teeth up to the age of 5.2,3 In
the localized form, affected sites exhibit
rapid bone loss and minimal gingival
inflammation.2
Quantitative (agranulocytosis
or neutropenia) or qualitative
(chemotactic or phagocytic) leukocytic
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annihilation of the periodontal tissues.
Quantitative deficiencies are generally
accompanied by destruction of the
periodontium of all teeth, whereas
qualitative defects are often associated
with localized destruction affecting only
the periodontium of certain teeth.4
Neutropenia
Patients present with
diverse periodontal manifestations. In
the malignant form there is ulceration
and necrosis of the marginal gingiva.
Bleeding from gums is generally present
and attached gingiva may become
involved.5 In cyclic, chronic and familial
benign neutropenia, the lesions show
deep periodontal pockets and extensive,
generalized bone loss involving the
permanent dentition.6–8 Bone resorption
may be seen in the deciduous dentition.9,10
 Periodontics/OralMedicine
Associated with haematological
disorders:
 Acquired neutropenia;
 Leukaemias;
 Others.
Associated with genetic disorders:
 Familial and cyclic neutropenia;
 Down’s syndrome;
 Leukocyte adhesion deficiency
syndrome;
 Papillon-Lefèvre syndrome;
 Chediak-Higashi syndrome;
 Histocytosis syndromes;
 Glycogen storage disease;
 Infantile genetic agranulocytosis;
 Cohen’s syndrome;
 Ehlers-Danlos syndrome (Types IV
and VIII);
 Hypophosphatasia.
Not otherwise specified
Table 1. Periodontitis as a manifestation of
systemic diseases.
Leukaemia
Periodontal lesions have been
frequently observed in patients with
leukaemia, particularly those with an acute
form. Generalized gingival enlargement
was apparent in 36% of the individuals with
acute, and in 10% of those with chronic,
forms.11 Gingival swelling due to infiltration
by leukaemic cells is a feature of acute
monocytic leukaemia.12 Gingival bleeding is
also a common sign of the disease in both
acute and chronic leukaemia and may relate
to the associated thrombocytopenia.13
Down’s syndrome
Patients with Down’s syndrome
show a generalized early periodontitis,
which commences in the deciduous
dentition14,15 and continues into the adult
dentition. The prevalence and severity of
periodontal disease in individuals with
Down’s syndrome is high in comparison to
their siblings16 or other mentally disabled
people.15 Several studies have reported
increased prevalence and severity of
640 DentalUpdate November 2012
periodontal disease in children of older age
groups.14,15 The periodontal destruction is
most commonly seen around the incisor
and molar teeth.14 The short roots of the
mandibular incisors,17 and the bone loss in
the mandibular anterior region, can lead to
the premature loss of these teeth.15
Leukocyte adhesion deficiency
syndrome
Defects in numbers of cell-
cell adhesion receptors on the neutrophil
surface may lead to increased inclination
to periodontitis and other infectious
diseases in conditions such as leukocyte
adhesion deficiency syndrome.18 Young
patients with leukocyte adhesion deficiency
syndrome present with severe inflammatory
periodontal disease.19–21 Leukocyte adhesion
deficiency syndrome is a rare autosomal
recessive disease. The disease is generally
fatal and children with deficiencies in
expression of the leukocyte function
associated family of adhesions suffer from
severe periodontal infections.18
Papillon-Lefèvre syndrome
The palmoplantar keratodermas
are a heterogeneous group of more than
40 keratinization disorders characterized by
erythema and hyperkeratosis of the palms
and soles.22,23 A prevalence of 1–4 cases
per million people has been reported.24
Papillon-Lefèvre syndrome is an uncommon
autosomal recessive type-IV palmoplantar
ectodermal dysplasia.25
Papillon-Lefèvre syndrome
is a rare genodermatosis inherited as an
autosomal recessive trait, affecting children
between the ages of 1–4 years.26,27 Males and
females are equally affected.23 The disorder
is characterized by diffuse palmoplantar
keratoderma and premature loss of both
deciduous and permanent teeth. The
palmoplantar keratoderma starts between
the ages of 1 and 4 years.26 The sharply
demarcated erythematous keratotic plaques
involve the surface of the palms and soles,
occasionally extending on to the dorsal
surfaces of the hands and feet.24 Elbows and
knees may also get involved.27 Often, there
is associated hyperhidrosis of the palms and
soles resulting in a foul-smelling odour.24
Another key feature of Papillon-
Lefèvre syndrome is severe periodontitis,
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which starts at age 3 or 4 years.27 The
development and eruption of the deciduous
teeth proceed normally, but their eruption
is accompanied by gingival inflammation
and ensuing rapid destruction of the
periodontium. The resulting periodontitis
characteristically is unresponsive to
conventional periodontal treatment and
the primary dentition is usually exfoliated
prematurely by the age of 4 years. After
exfoliation, the inflammation subsides
and the gingiva appears healthy. With
the eruption of the permanent dentition,
gingivitis and periodontitis initiates again
and there is premature exfoliation of the
permanent teeth.28,29 Teeth are normally
lost in the order of eruption.29 The degree
of dermatologic involvement may not
be related to the level of periodontal
infection.30 A multidisciplinary approach
is important for the care of patients with
Papillon-Lefèvre syndrome. A dermatologist
and oral medicine specialist, along with a
periodontist, should be involved in treating
such cases. Involvement of other specialists
may be required and depends upon the
systemic and dental conditions of
the patient.
Chediak-Higashi syndrome
Chediak-Higashi syndrome is
an autosomal recessive disease associated
with severe periodontitis.31,32 The people
suffering from this disease are extremely
susceptible to bacterial infections;
neutrophil chemotaxis and bactericidal
functions are abnormal in these patients.
Generalized, severe gingivitis, extensive loss
of alveolar bone and premature loss of teeth
are features commonly seen.33
Histiocytosis syndromes
Histiocytosis is a general name
for a group of syndromes that involve
an abnormal increase in the number of
immune cells called histocytes.34 This group
of diseases may affect infants, children and
adults.
There are three major classes of
histiocytoses:34
 Langerhans cell histiocytosis, which is also
called histiocytosis X;
 Malignant histiocytosis syndrome (now
known as T-cell lymphoma);
 Non-Langerhans cell histiocytosis (also

known as haemophagocytic syndrome).
Langerhans cell histiocytosis
is of importance to dentists because
oral soft tissue and bony lesions are
common and may be an initial indication
of disease.35 Symptoms can vary between
children and adults, although there can
be some overlap. Tumours in weight-
bearing bones, such as the legs or spine,
may cause the bones to fracture without
apparent reason. Symptoms in children
may include:
 Abdominal pain;
 Bone pain (possibly);
 Delayed puberty;
 Dizziness;
 Ear drainage that continues long-term;
 Protruding eyes that appear to
protrude more and more;
 Irritability;
 Fever;
 Frequent urination;
 Headache;
 Jaundice;
 Limping;
 Mental deterioration;
 Rash (petechiae or purpura);
 Seizures; and
 Thirst, vomiting and weight loss.34
Children over 5 years old
often have only bone involvement. Oral
soft tissue invasion by Langerhans cells
can present as gingival inflammation and
ulceration. The periodontal lesions may
clinically resemble necrotizing ulcerative
periodontitis lesions. The lesions are
punched-out necrotic ulcers with
considerable granulation tissue, tissue
necrosis and marked bone loss.36
Manifestations in the jaws
are seen in 10–20% of all cases. Swelling,
tenderness, pain and loosening of teeth
are frequent symptoms. The primary
teeth may be lost prematurely. The
jaw lesions often appear as punched-
out radiolucencies but ill-defined
radiolucencies are also seen, sometimes
mimicking periodontal disease.
Tests in children may also
include:
 Biopsy of skin to check for the presence
of Langerhans cells;
 Bone marrow biopsy to check for the
presence of Langerhans cells;
 Complete blood count;
 Skeletal x-rays (x-rays of all bones) to
find out how many bones are affected.34
November 2012 DentalUpdate 641
Biopsy of the granulation
tissue can also help in diagnosing the
condition.36
Glycogen storage disease
This is an autosomal recessive
condition associated with defective
carbohydrate metabolism. Clinical features
include reduced neutrophil numbers,
impaired neutrophil function and
periodontal disease.37,38
Infantile genetic
agranulocytosis
This disease presents with
severe neutropenia and has been linked
with periodontitis similar to the early-
onset form. This is a rare autosomal
recessive disorder.39,40
Cohen’s syndrome
This is also an autosomal
recessive condition characterized by
frequent and extensive alveolar bone
loss.38 The patients also suffer from non-
progressive mental and motor retardation,
obesity and neutropenia.41
Ehlers-Danlos syndrome
Ehlers-Danlos syndrome is an
autosomal dominant disorder, is classified
into 10 types and is characterized by
defective collagen synthesis. Symptoms of
EDS include:
 Double-jointedness;
 Easily damaged, bruised and stretchy
skin;
 Easy scarring and poor wound healing;
 Flat feet;
 Increased joint mobility, joints popping,
early arthritis;
 Joint dislocation;
 Joint pain;
 Very soft and velvety skin;
 Vision problems.42
Types IV and VIII have an
increased susceptibility to periodontitis.43
Type VIII is linked with fragile oral mucosa
and blood vessels. It is also associated
with severe generalized periodontitis with
manifestation of generalized aggressive
periodontitis,44 causing premature loss of
permanent teeth.45
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Periodontics/OralMedicine
Tests performed to diagnose EDS
include:
 Collagen typing (performed on a skin
biopsy sample);
 Collagen gene mutation testing;
 Echocardiogram;
 Lysyl hydroxylase or oxidase activity.42
Hypophosphatasia
Hypophosphatasia is an
inherited disorder characterized by
defective bone and tooth mineralization.
Hypophosphatasia is due to mutations in
the liver/bone/kidney alkaline phosphatase
gene encoding the tissue non-specific
alkaline phosphatase.46,47 Clinical
manifestations are varied and range from
isolated premature loss of primary teeth to
stillbirth.47,48
Six clinical forms of
hypophosphatasia are known, depending
upon the age of onset:
 Lethal perinatal;
 Prenatal (benign);
 Infantile;
 Childhood;
 Adult;
 Odontohypophosphatasia.49
Infantile hypophosphatasia
The clinical signs may start
during the first six months. The clinical signs
include hypercalcaemia, rachitic deformities
of the chest, premature craniosynostosis,
widespread demineralization and rachitic
changes in the metaphyses are classical
features. Short stature in adulthood and
premature shedding of deciduous teeth are
also common.46
Childhood hypophosphatasia
Clinical signs appear after six
months of age. Skeletal deformities, a delay
in walking, waddling, history of fractures,
bone pain and a short stature are common
features. Premature loss of primary teeth is a
trigger sign predicting the diagnosis.47
Adult hypophosphatasia
This generally develops during
middle age. The primary complaint may
be foot pain due to stress fractures of the
metatarsals. Many of the patients present
premature loss of permanent teeth.50
 Periodontics/OralMedicine
Odontohypophosphatasia
This is a form of the disease
with only dental manifestations. The
manifestations include spontaneous
exfoliation of deciduous teeth, enlarged
pulp chambers and root canals, not
associated with abnormalities of the
skeleton.49,51,52 Odontohypophosphatasia
should be considered in any patient with a
history of early unexplained loss of teeth.46
Oral findings, such as premature
loss of anterior primary teeth without root
resorption and reduced alveolar bone
height, may represent the main clinical
manifestations and premature exfoliation
of primary teeth can lead to a possible
diagnosis.
In addition to clinical and
radiological examinations, laboratory assays
are performed in the case of suspicion of
hypophosphatasia and total serum alkaline
phosphatase activity is markedly reduced.
Molecular biology alone can establish the
diagnosis.
Necrotizing periodontal
diseases
Necrotizing periodontal diseases
are classified as:
(a) Necrotizing ulcerative gingivitis; and
(b) Necrotizing ulcerative periodontitis.
The working definitions and
clinical features proposed are as follows.
Necrotizing ulcerative gingivitis
This is an infection characterized
by gingival necrosis presenting as ‘punched-
out’ papillae, gingival bleeding, and
pain. Fetid odour and pseudomembrane
formation may be secondary diagnostic
criteria. The predisposing factors include:
emotional stress, poor diet, cigarette
smoking and HIV infection.53
Necrotizing ulcerative periodontitis
This is an infection characterized
by necrosis of gingival tissue, periodontal
ligament and alveolar bone. The lesions are
most commonly observed in individuals
with systemic conditions including, but not
limited to, HIV infection, severe malnutrition
and immunosuppression.53
The two most significant
findings used in the diagnosis of necrotizing
periodontal diseases are the presence of
642 DentalUpdate November 2012
interproximal necrosis and ulceration and
the rapid onset of gingival pain. Absence
of any of the three criteria: the presence of
interproximal necrosis, the rapid onset of
gingival pain and bleeding from the gingiva,
means that a diagnosis of necrotizing
ulcerative gingivitis cannot be made.
Necrotizing ulcerative gingivitis is
diagnosed at the onset of specific clinical
signs and symptoms.54 Necrotizing
ulcerative gingivitis primarily affects
the interdental and marginal soft tissue.
Periodontitis present before the onset
of necrotizing ulcerative gingivitis can
make the diagnosis difficult. Gingival
bleeding associated with necrotizing
ulcerative gingivitis is the least distinctive
of the clinical signs since it is also present
in other periodontal diseases. Gingival
bleeding in necrotizing ulcerative gingivitis
occurs with little or no provocation. Pain
is the distinctive feature of necrotizing
ulcerative gingivitis and can be intense.
Typical gingivitis and periodontitis are
not associated with severe gingival pain.
Periodontal conditions like abscesses and
herpetic infections are painful but can
be easily distinguished from necrotizing
ulcerative gingivitis.55
Necrotizing ulcerative
periodontitis suggests that the pathologic
process is similar to that observed in
periodontitis, with the addition of tissue
necrosis. Necrotizing periodontal disease
has been separately classified from gingivitis
and periodontitis, as tissue necrosis is
the common distinctive clinical feature
of necrotizing ulcerative gingivitis and
necrotizing ulcerative periodontitis.56
Necrotizing periodontal diseases
(NPDs) are present with higher frequency
(2–5%) in children and adolescents from
developing areas of Africa, Asia and South
America compared to North American and
European children (<1%).57–59
Examination of the patient
The patient’s history, along
with the examination, helps in diagnosis of
the periodontal diseases. The examination
should include the chief complaint, history
of present complaint, past dental and
medical history. The child or adolescent’s
guardian can facilitate in collecting the
information. The treatment planning of the
child with a compromised medical status
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may involve consultation with the child’s
paediatrician.
Periodontal screening
Examination of the periodontal
tissues in the younger patient should be
a routine part of the dental examination.
Periodontal screening in children and
adolescents provides a simple process of
identifying periodontal problems. It gives
the dental practitioner an indication of
whether the child/adolescent requires
treatment or further assessment.
Periodontal screening and
recording introduced by the American
Dental Association60 has been found to
be a sensitive, easy, quick method of
screening patients for periodontal diseases
that summarizes essential information.61
Periodontal screening and recording,
when compared to full-mouth probing
with a graduated periodontal probe in
children and adolescents, was found to be
better accepted, faster, and no differences
were found in diagnosis and clinical
management.62
After the eruption of the incisors
and first permanent molars in children,
the basic periodontal examination can be
used for screening the index teeth UR6,
UR1, UL6, LL6, LL1 and LR6 (International
Dental Federation notation). The WHO
621 (Figure 1) probe with the 0.5 mm
spherical ball on the tip and shaded band
at 3.5–5.5 mm is used to detect normal
sulcus and periodontal pockets.63 Usage of
codes up to 2 is recommended until the
age of 11 years because of the probability
of pseudopockets associated with newly
erupting teeth.64 Presence of a deep
pocket in which the 3.5–5.5 mm black
band disappears would necessitate further
periodontal investigation.
The 0.5 mm ball end on this
probe can be used to detect subgingival
calculus. In 12–19 year-olds, the full
range of scores can be used on the index
teeth so that periodontal pockets can be
detected as early as possible.64 It is crucial
to assess the base of the pocket. In true
pocket, the base of the pocket is apical to
the cemento-enamel junction. If pockets
are detected, then full-mouth monitoring
should be undertaken. Screening of six
index teeth is swift, easy and acceptable to
young patients. Periodontal screening of

Figure 1. WHO 621-clinical probe.
new patients and 4- or 6-monthly recalls in
children and adolescents is recommended
so that periodontal problems can be
detected early and treated properly.65 This
basic periodontal examination screening
system typically takes less than 1 or 2
minutes in children and adolescents.65
Basic Periodontal Examination
(BPE) scoring criteria (Table 2)
Index Teeth used: UR6, UR1,
UL6, LL6, LL1 and LR6. In children, the WHO
probe is walked around the index teeth,
covering six sites per tooth, whereas in
young adults all the teeth in each sextant
are probed.
In the age group of 7–11 years,
codes 0–2 are used and the worst finding
is recorded on each index tooth or in each
sextant.
Frequency of recording BPE66
BPE is recorded for all new
patients and patients requiring advanced
restorative or orthodontic treatment.
Score 0: Screen again within one year.
Score 1 or 2: Treat and screen within one
November 2012 DentalUpdate 645
Periodontics/OralMedicine
its official website.67
Based on the Basic Periodontal
Examination Code:
Complexity 1: BPE Score 1–3.
Complexity 2: BPE Score of 4 in any
sextant.
Surgery involving the
periodontal tissues.
Complexity 3: Surgical procedures
associated with osseo-integrated implants.
Surgical procedures involving
periodontal tissue augmentation and/or
bone removal.
BPE score of 4 in any sextant and
including one or more of the following
factors:
 Patients under the age of 35 = Complexity
3;
 Smoking 10+ cigarettes daily;
 A concurrent medical factor that is
affecting the periodontal tissues;
 Root morphology that adversely affects
prognosis;
 Rapid periodontal breakdown >2 mm
attachment loss in any one year.
Periodontal treatment
assessment sets complexity codes in a
year.
simplistic manner with the addition of a
Score 3: If score 3 is recorded in one or more
list of modifying factors that are relevant
sextants, treat and review. If still code 3,
to periodontal treatment and an outline
record full periodontal indices in affected
of medical history that significantly
sextants.
affects clinical management. It is strictly
Score 4 or *: Record full periodontal indices
a complexity assessment and does not
and consider referral.
address either the motivational aspects of
A detailed periodontal
treatment or a prioritization of treatment.
examination should include indices to
record:
 Probing pocket depths;
 Clinical attachment levels; Modifying factors that are
 Bleeding on probing; relevant to periodontal
 Mobility; treatment67
 Furcation involvement; A modifying factor can only
 Suppuration; increase complexity by one increment.
 Recession. Multiple factors are not cumulative:
Radiographs can also be  Co-ordinated medical (eg renal:
considered if BPE score is 3, 4 or * to assess cardiac) and/or dental (eg oral surgery:
bone levels. The diagnosis of periodontal orthodontic) multidisciplinary care;
problems is reached after deliberation of  Medical history that significantly affects
the findings of the history and examination. clinical management;
 Special needs for the acceptance or
provision of dental treatment;
Periodontal treatment  Mandibular dysfunction;
assessment  Atypical facial pain;
The British Society of  Undiagnosed facial pain;
Periodontology recommends following  Presence of a retching tendency;
complexity codes in its document on  Limited operating access;
‘Referral Policy and Parameters of Care’ on  Concurrent mucogingival disease.
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 Periodontics/OralMedicine

Basic Periodontal Examination

Basic Periodontal Examination used after the eruption of the incisors and first permanent molars.
WHO 621 probe with the 0.5 mm spherical ball on the tip and shaded band at 3.5−5.5 mm is used.
The index teeth used for screening in children: Six sites per tooth UR6 UR1 UL6
In young adults: all teeth in each sextant are probed. LR6 LL1 LL6
Scores used:
1) Codes up to 2 recommended in the age group of 7−11;
2) Full range of scores used in the age group of 12−19.
Worst finding recorded on each index tooth or in each sextant.
If pockets are detected, then full-mouth monitoring should be undertaken.
Scoring Criteria
Code 0 In deepest sulcus of sextant, probe’s Gingival tissue healthy, does not Treatment: preventive care
coloured band remains completely visible bleed on gentle probing. No required
calculus or defective margins found
Code 1 In deepest sulcus of sextant, probe’s No calculus or defective margins Treatment: subgingival plaque
coloured band remains completely visible found, but some bleeding after removal; appropriate oral hygiene
gentle probing detected instructions
Code 2 The probe’s coloured band is still Bleeding on probing may be present Treatment: plaque and calculus
completely visible and supragingival or subgingival removal; correction of plaque-
calculus and/or defective margins retentive margins of restorations;
found oral hygiene instruction
Code 3 The coloured band is partially submerged Need for a comprehensive periodontal examination and charting of the
affected sextant to determine the necessary treatment
If two or more sextants score Code 3, a comprehensive full-mouth
examination and charting is indicated
Code 4 The coloured band completely disappears Comprehensive full-mouth periodontal examination, charting, and
in the pocket (depth >5.5 mm) treatment planning are needed
Code * To mark the presence of following abnormalities an asterisk (*) is entered in addition to code number: furcation
involvement, tooth mobility, mucogingival problem, or gingival recession extending to the coloured band of the probe
(≥3.5 mm)

Table 2. Basic Periodontal Examination (BPE) scoring criteria.

Medical history that
significantly affects clinical
management67
 Patients requiring IM or IV medication as a
component of clinical management;
 Patients with a history of head/neck
radiotherapy;
 Patients who are significantly
immunocompromised or
immunosuppressed;
 Patients with a significant bleeding
dyscrasia/disorder;
 Patients with a potential drug interaction.
Referral policy of British
Society of Periodontology67
Referral of patients with
periodontal problems, to either specialist
practitioners or hospital consultants,
depends on several factors:
 The GDP’s knowledge and ability to treat
patients, which will vary considerably;
 The patient’s desire to see a specialist or
undergo specialist treatment;
 The age and general health status of the
patient;
 The complexity of treatment required.
According to the British Society
of Periodontology, it is difficult to be
absolute in determining referral policy
guidelines. The interpretations of Basic
Periodontal Examination and the level of
complexity help in deciding the referral
guidelines.67
Complexity 1: cases may be treated in
general practice.
Complexity 2: cases either referred or
treated by the GDP.
Complexity 3: cases mostly referred.
Although, depending on the treatment

646 DentalUpdate November 2012

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requirements, simple periodontal treatment
may have to be delivered by specialists
as part of a more complex integrated
treatment strategy in order to maintain the
integrity of the restored dentition. Also,
Complexity 3 category may not necessarily
require care from a specialist.
Periodontal treatment in
children and adolescents
The periodontal therapy aims
to preserve the natural dentition and
periodontium and to improve comfort,
aesthetics and function. The clinical signs
of a healthy periodontium comprise the
absence of redness, swelling, suppuration
and bleeding on probing; maintenance of
a functional periodontal attachment level;
minimal or no recession in the absence of
inter-proximal bone loss.68
Periodontal treatment may be
undertaken in three phases:
 Initial cause-related therapy to eliminate
or control plaque;
 Additional therapeutic measures; and
 Supportive (maintenance) therapy to
prevent disease recurrence and progression
with follow-up recalls arranged at a time
interval appropriate to the diagnosis.69
Initial cause-related therapy includes the
following
 Patient education, personal oral hygiene
instructions, control of risk factors (eg
smoking, medical status).
 Scaling and root planing to remove
plaque and calculus.
 Eliminate plaque retentive factors –
caries treatment, endodontic treatment,
extractions and temporary prosthetic
reconstruction.
 Post-treatment evaluation with review
and reinforcement of personal daily oral
hygiene.
Additional therapeutic measures
Only the level of improvement
can determine the amount of corrective
therapy required after causative therapy
is evaluated. The patient’s co-operation
towards treatment determines the
corrective treatment. Entirely co-operative
patients should be the candidates for
treatment procedures to improve oral
aesthetics and function permanently.
November 2012 DentalUpdate 649
Additional treatments indicated for
co-operative patients include:68
 Use of chemotherapeutic agents to
reduce or eliminate pathogens; or as host
response modulation through local or
systemic delivery of chemotherapeutic
agents.
 Resective periodontal procedures to
reduce or eradicate periodontal pockets
and create a satisfactory gingival form
to aid in effective oral hygiene and
periodontal maintenance treatment.
The procedures include gingivectomy,
gingivoplasty, ostectomy and osteoplasty,
root resection, tooth hemisection and
mucogingival soft tissue procedures.
 Management of endodontic-periodontic
lesion by combination of various
procedures.
 Periodontal regenerative procedures
are used for osseous and recession defects
to regenerate lost tissue by bone grafts,
soft tissue grafts, or using guided tissue
regeneration.
 Periodontal plastic surgery for gingival
augmentation, recession treatment and
improvement of aesthetics.
 Occlusal therapy to reduce occlusal
trauma.
 Preprosthetic periodontal procedures
to aid restorative or prosthetic treatment
plans.
 Procedures to assist orthodontic
treatment, eg tooth exposure, frenectomy.
 Replacement of teeth by dental
implants.
Supportive periodontal therapy
The aim of this treatment is
the prevention of disease recurrence and
includes:68
 Update of medical and dental histories.
 Evaluation of extra- and intra-oral,
periodontal and peri-implant soft tissues as
well as dental hard tissues.
 Assessment of the oral hygiene status
with re-instruction when indicated.
 Scaling and root planing. Local or
systemic chemotherapeutic agents may be
used as adjunctive treatment.
 Eradication of risk and aetiologic factors
with appropriate treatment.
 Detection and treatment of new,
recurrent, or refractory areas of periodontal
disease.
 Developing of a personalized
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Periodontics/OralMedicine
periodontal maintenance protocol for the
patient.
Treatment of plaque-induced gingivitis
Treatment of chronic gingivitis is
aimed at reduction of oral bacteria, plaque
and calculus and other local contributing
factors below a level capable of initiating
clinical inflammation. Patients with chronic
gingivitis respond to a therapeutic regimen
consisting of improved personal plaque
control alone or to thorough removal of
bacterial deposits by supragingival scaling.70
Treatment of gingival enlargement
Gingival enlargement may be
caused by chronic gingival inflammation,
or exaggerated in patients with genetic
factors or drug induced. Consultation with
the patient’s physician about possible use
of a substitute drug that does not induce
gingival overgrowth should be an option.70
Tissue topography can be recontoured
surgically by procedures like gingivoplasty,
gingivectomy or periodontal flap surgeries
to create a favourable oral environment.
Treatment of chronic periodontitis
The primary aim of the
treatment of chronic periodontitis is
resolution of inflammation and arrest
disease progression. Reduction of aetiologic
factors allows repair of the area affected by
periodontal destruction. Scaling and root
planing and adjunct antimicrobial therapy
may be used for management of chronic
periodontitis.70 A surgical treatment of
periodontitis:
 Provides better access for removal of
aetiologic factors;
 Reduces deep probing depths; and
 Regenerates or reconstructs lost
periodontal tissues.71–73
Regenerative therapies with
bone grafting74–76 and guided tissue
regeneration (GTR) techniques, with or
without bone replacement grafts,77,78
may be successful at selected sites with
advanced bone loss.
Treatment of aggressive periodontitis
Monitoring compliance with oral
hygiene procedures is important in treating
periodontitis patients. An important factor
in treating aggressive periodontitis patients
is consultation with other dental specialists
 Periodontics/OralMedicine
to evaluate the restorative importance of
certain teeth before starting periodontal
therapy.79 The family history of periodontal
problems should be considered.
Antibiotics as an adjunct
therapy is of paramount importance in
patients with generalized aggressive
periodontitis. Antibiotic therapy helps in
improving the magnitude of improvement
at individual sites80 and also reduces the
number of sites with probing depths >6
mm.81 The combination of metronidazole
plus amoxicillin (500 mg each) three times
daily is the most commonly used antibiotic
regimen.79 The antibiotic therapy should
be initiated 24 h before starting scaling
and root planing, and that root planing
is performed during the time period of
the antibiotic prescription.79 If surgical
treatment is undertaken in the patient with
aggressive disease, a biopsy of associated
granulation tissues to rule out certain
pathological entities such as Langerhans cell
histiocytosis is recommended.79
Although the consensus
report of the sixth European Workshop on
Periodontology 2008 stated that there is no
direct evidence to recommend a specific
protocol for the use of adjunctive systemic
antimicrobials with non-surgical mechanical
debridement, it has been suggested that
antibiotic intake should start on the day
of debridement completion; debridement
should be completed within a short time
(preferably <1 week) and with an adequate
quality, because these may help to improve
the results.82
The response to conventional
mechanical therapy or antibiotics may
not be on expected lines.83,84 Alternative
antibiotics may be required, based upon the
character of the pathogenic flora. In patients
who have failed to respond to regular
periodontal therapy, laboratory tests of
plaque samples may recognize periodontal
pathogens that are resistant to regular
antibiotics normally used in periodontitis.85
Treatment of periodontitis as a manifestation
of systemic disease
Treatment includes non-surgical
or surgical mechanical debridement and
antimicrobial therapy. The management of
periodontitis as a manifestation of systemic
disease in children is comparable to the
management of localized and generalized
650 DentalUpdate November 2012
aggressive periodontitis in the permanent Prepubertal periodontitis. I. Definition of
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teeth has been the line of treatment in 4. Wilton JM, Griffiths GS, Curtis MA et
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irrigation and debridement of the necrotic
5. Awbrey JJ, Hibbard ED. Abbreviated
areas and tooth surfaces. Oral hygiene
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instructions should be reinforced.88
Oral Surg Oral Med Oral Pathol 1973; 35:
The use of oral rinses, pain control and
526–530.
management of systemic manifestations,
6. Levine S. Chronic familial neutropenia,
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proper nutrition, oral care, appropriate
7. Smith JF. Cyclic neutropenia. Oral Surg
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