Periodontal Diseases In Children Health And Social Care Essay
Periodontics is a vast subject by itself and a pediatric dentist is called upon to use the knowledge of the same while examining and planning the treatment of children and young adults. Contrasting forms of periodontal disease affect children and adolescents with varying prevalence, severity, and extent, leading to a diverse prognosis in these age groups. For an early diagnosis and treatment of periodontal conditions in young patients, it is essential to be able to identify and classify the disease correctly at the earliest applying the basic principles along with understanding of etiology and risk factors. A pediatric dentist is 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, however 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 etiologic 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.
Key Words: adolescents, aggressive, chronic, gingivitis periodontitis.
Clinical Relevance: Incorporation of periodontal screening in regular dental examination by pediatric dentist can help in early diagnosis and treatment of periodontal diseases. This would prevent further progression of disease and reduce the frequency of tooth loss.
Objective: The reader should understand the importance of periodontal screening, early diagnosis, proper treatment planning and effective maintenance plan to prevent the progression and recurrence of periodontal disease in children and adolescents.
Different forms of periodontal disease affect children and adolescents. The diseases affecting the periodontium can be limited to the gingival tissues or can be associated with destruction of the periodontal ligament and alveolar bone. There have been various attempts to classify periodontal diseases. Various classifications have been developed over a period of time.1-4
Based on the World Workshop in Clinical Periodontics in 1989,3 the American Academy of Periodontology proposed a classification of periodontitis as a) adult periodontitis b) early-onset periodontitis c) Periodontitis associated with systemic disease d) necrotizing ulcerative periodontitis and e) refractory periodontitis. Early-onset periodontitis was further classified into a) pre-pubertal periodontitis (localized and generalized) b) juvenile periodontitis c) rapidly progressive periodontitis.(Table 1)
Problems associated with the 1989 classification led to 1999 international workshop on the classification of periodontal diseases.4 A new classification system was proposed in 1999 and is presently the most accepted classification system of periodontal diseases. The periodontal diseases are classified as: 1) gingival diseases (plaque induced and non plaque induced) 2) chronic periodontitis (localized and generalized) 3) aggressive periodontitis (localized and generalized 4) periodontitis as a manifestation of systemic disease 5) necrotizing periodontal disease 6) abscesses of periodontium 7) periodontitis associated with endodontic lesions and 8) developmental and acquired deformities and conditions.(Table 1)
In the new classification4 “adult periodontitis” was changed to chronic periodontitis and juvenile periodontitis to aggressive periodontitis. These changes were made to eliminate the age-dependent criteria. Chronic periodontitis was considered less age-dependent description than adult periodontitis. The term ”early-onset periodontitis” was discarded as this form of disease can occur in children, adolescents and adults. ”Localized aggressive periodontitis” replaced the older expression ”localized juvenile periodontitis” or ”localized early-onset periodontitis”. ”Generalized aggressive periodontitis” replaced ”generalized juvenile periodontitis” or ”generalized early-onset periodontitis.”(Table 2)
Table 1
1989 Classification Of Periodontal Diseases
1999 Classification Of Periodontal Diseases
Gingival diseases
(Plaque induced and Non- Plaque Induced)
Adult periodontitis
Chronic periodontitis
(Localized and Generalized)
Early-onset periodontitis
Aggressive periodontitis
(Localized and Generalized).
Periodontitis associated with systemic disease
Periodontitis as a manifestation of systemic disease
Necrotizing ulcerative periodontitis
Necrotizing periodontal disease
Refractory periodontitis
Abscesses of periodontium
Periodontitis associated with endodontic lesions
Developmental and acquired deformities and conditions
The categories of refractory periodontitis and rapidly progressive periodontitis were eliminated because of their heterogeneity. Prepubertal periodontitis was also eliminated as it was not perceived to be a single entity. Many severe periodontitis cases in children are caused due to presence of a systemic disease/s.5,6 (Table 2).
Various studies show that gingivitis is prevalent in children and adolescents.7-11 Studies have indicated that attachment loss and supporting bone loss is infrequent in the young but that the incidence increases in adolescents aged 12 to 17 when compared to children aged 5 to 11.11-13 A study conducted on schoolchildren demonstrated that the prevalence and extent of gingivitis increased with age.14 Gingivitis starts in the deciduous dentition and reaching a peak at puberty. Gingivitis reduced during adolescence and followed by a gradual rise throughout adult life.15 The increase in gingivitis levels may be ascribed to the increase in sites at risk, plaque accumulation and inflammatory changes related with tooth eruption and the influence of hormonal factors in puberty. The decline in gingivitis in adolescence may be due to improved social awareness and enhanced oral hygiene.16
Table 2
Changes introduced in 1999 classification in comparison to 1989 Classification Of Periodontal Diseases
A category of Gingival diseases (Plaque induced and Non- Plaque Induced) was introduced. Gingival diseases were not represented in 1989 classification.
The term Adult periodontitis changed to Chronic periodontitis to eliminate the age-dependent criteria.
The term Early-onset periodontitis was replaced by Aggressive Periodontitis to eliminate the age-dependent criteria.
Localized juvenile periodontitis or localized early-onset periodontitis was replaced by Localized aggressive periodontitis.
Generalized juvenile periodontitis or generalized early-onset periodontitis was replaced by Generalized aggressive periodontitis.
Refractory periodontitis and rapidly progressive periodontitis eliminated because of their heterogeneity
Prepubertal periodontitis was also eliminated as severe periodontitis cases in children are caused due to presence of a systemic disease/s.
Prevalence of periodontitis in the deciduous dentition is difficult to estimate because of scarcity of data. Exfoliation and eruption can lead to undependable information. A low prevalence of marginal bone loss in the deciduous dentition is found in children of European origin in comparison to Asian children.17,18 The prevalence of early onset periodontitis in blacks was 2.1% 19- 2.6%.20 The prevalence rate for whites was 0.17%.20 In a survey in the United States, no significant difference was found in prevalence rates between males and females.20 Black males and white females were approximately three times more likely to have localized early-onset periodontitis than black females and white males respectively.20
Periodontitis in the deciduous dentition is generally clinically insignificant, severe generalized periodontitis may be found in young children with rare systemic diseases, such as Papillon-Lefevre syndrome, cyclic neutropenia, agranulocytosis, Down’s syndrome, hypophosphatasia and leukocyte adhesion deficiency.21
Periodontal diseases that can affect young individuals include: 1) dental plaque-induced gingival diseases; 2) chronic periodontitis; 3) aggressive periodontitis; 4) periodontitis as a manifestation of systemic diseases; and 5) necrotizing periodontal diseases.22 However few other diseases like primary herpetic gingivostomatitis may also affect children.(Table 3)
Table 3
Periodontal diseases affecting children and adolescents
Dental plaque-induced gingival diseases
Chronic periodontitis
Aggressive periodontitis
Periodontitis as a manifestation of systemic diseases
Necrotizing periodontal diseases
Dental plaque-induced gingival diseases:
Definition: Plaque-induced gingivitis is defined as inflammation of the gingiva in the absence of clinical attachment loss.23
Gingivitis associated with dental plaque only: Chronic marginal gingivitis is the most prevalent type of gingival change in childhood. Dental plaque causes inflammation within the gingival tissues which manifests as clinical signs of gingivitis.
The gingival diseases associated with plaque, endogenous hormonal fluctuations, drugs, systemic diseases, and malnutrition have numerous universal characteristics. The universal features of these gingival diseases include clinical signs of inflammation, signs and symptoms that are restricted to the gingiva, reversibility of the diseases by removing the etiology, the presence of bacterial plaque to initiate and intensify the severity of the lesion, and a potential role as a precursor to attachment loss.24 (Table 4).
Table 4
Universal features of gingival diseases
Clinical signs of inflammation
Signs and symptoms that are restricted to the gingiva,
Reversibility of the diseases by removing the etiology.
Presence of bacterial plaque to initiate and intensify the severity of the lesion.
A potential role as a precursor to attachment loss
The features of plaque-induced gingivitis24 are 1) plaque present at gingival margin; 2) disease begins at the gingival margin; 3) change in gingival color;25,26 4) change in gingival contour;25,26 5) sulcular temperature change;27 6) increased gingival exudate;28 7) bleeding upon probing;25 8) absence of attachment loss; 9) absence of bone loss; 10) histological changes including an inflammatory lesion; 11) reversible with plaque removal. Subgingival levels of Actinomyces sp., Capnocytophaga sp., Leptotrichia sp., and Selenomonas sp. have been found to be increased in experimental gingivitis in children when compared to gingivitis in adults.29
Gingival Diseases Modified by Systemic Factors Associated with the Endocrine System: Hormonal changes affect the periodontal diseases, although bacterial plaque is essential to initiate gingival disease.
Puberty-Associated Gingivitis: The rise in steroid hormone levels during puberty in both sexes has a transitory effect on gingivitis.30 There is an increase in gingival inflammation in circumpubertal age individuals of both sexes without a simultaneous increase in plaque levels.31-33 The predilection to develop candid signs of gingival inflammation in the presence of relatively small amounts of plaque during the circumpubertal period differentiates the disease. The incidence and severity of gingivitis in adolescents are also influenced by dental caries, mouth breathing, crowding of the teeth, and tooth eruption.34
Diabetes Mellitus-Associated Gingivitis: Diabetes mellitus-associated gingivitis is found in children with poorly controlled Type 1 diabetes mellitus (insulin-dependent diabetes mellitus or juvenile onset).35,36 The features of gingivitis associated with diabetes mellitus are similar to plaque-induced gingivitis. The level of diabetic management is an significant characteristic than plaque control in the severity of the gingival inflammation.35,36
Gingivitis is frequently associated with tooth eruption. Tooth eruption by itself does not cause gingivitis. The inflammation results from plaque accumulation around erupting teeth. Partially exfoliated, loose deciduous teeth often cause gingivitis due to plaque accumulation. The incidence and severity of gingivitis is more around malpositioned teeth because of their increased tendency to accumulate plaque.37
Periodontitis:
Periodontitis irrespective of the specific classification show irreversible loss of connective tissue attachment and apical migration of the junctional epithelium and true pocket formation. The correct diagnosis of the different types of periodontitis is important as the management of periodontitis depends on the correct diagnosis.
Incipient and incidental attachment loss – A precursor to periodontitis:
The terms “incipient” attachment loss38,39 and incidental attachment loss38,39 have been used to describe loss of support in adolescents. A loss of attachment >1 mm and early alveolar bone loss are prevalent and can affect a sizable proportion of adolescents.40-41 The term “incipient” is used to describe the initial stage of adult type periodontitis (chronic periodontitis) and a working definition is the presence of loss of attachment >2 mm that is not related to gingival recession.39
The term “incidental” attachment loss was used by Löe & Brown in relation to early-onset (aggressive) periodontitis in adolescents.20 It was suggested that it may correspond to an initial phase of an early-onset ”juvenile” periodontitis or even be incidental to other factors. There is prevalence of attachment loss in adolescents that does not fit the categorization of localized early-onset periodontitis and/or generalized early onset periodontitis.38,42
The category of incidental attachment loss includes individuals who do not fit the criteria for diagnosis of either localized early-onset periodontitis or generalized early-onset periodontitis, but show ≥4 mm of attachment loss on one or more teeth.39 An epidemiological survey of early-onset periodontitis in 14 to 17 years old adolescents used attachment loss of ≥3 mm as the cut-off for diagnosis and found that 71% of the incidental early-onset periodontitis group had one site affected and 97% had three or less affected sites.42 The definition of incidental attachment loss can be used to classify individuals with few sites affected by abnormal attachment loss, not associated with local causes such as proximal caries or overhanging restorations.
Chronic periodontitis:
Definition: Chronic periodontitis is defined as inflammation of the gingiva extending into the adjacent attachment apparatus. The disease is characterized by loss of clinical attachment due to destruction of the periodontal ligament and loss of the adjacent supporting bone.43
Clinical Features:44(Table 5)
1. Chronic periodontitis is the most common form of periodontal disease in adults but can be found in children and adolescents affecting both the primary and secondary dentitions.
2. The amount of periodontal destruction is proportionate to local factors.
3. The composition of microbial plaque is complex and varies to a great extent within and between patients and subgingival calculus is a frequent finding.
4. Chronic periodontitis can be classified on the basis of extent of disease as localized when fewer than 30% of sites are affected, and generalized when this level is exceeded.
5. Chronic periodontitis can also be classified on the basis of the severity of the periodontal destruction. Disease is mild (1 to 2 mm clinical attachment loss), moderate (3 to 4 mm clinical attachment loss), or severe (≥5 mm clinical attachment loss)
6. Although chronic periodontitis is initiated by microbial plaque, factors such as systemic risk factors including smoking, stress, diabetes, HIV and host factors influence the pathogenesis and progression of the disease.
7. Progression can only be confirmed by repeated clinical examinations and is considered likely to occur in diseased sites that are left untreated. It usually has slow to moderate rates of progression, but may have periods of rapid progression.
Table 5
Clinical Features of Chronic periodontitis
Most common form of periodontal disease in adults but children and adolescents also affected.
The amount of periodontal destruction is proportionate to local factors.
The composition of microbial plaque is complex and variable.
Slow to moderate rates of progression with periods of rapid progression.
Initiated by plaque but modified by systemic factors such as smoking, stress, diabetes, HIV and host factors.
Extent of disease: Localized : < 30% of sites involved; Generalized: >30% of sites involved.
Severity of disease: Mild: 1-2mm of clinical attachment loss; Moderate: 3-4 mm of clinical attachment loss; Severe: ≥5mm of clinical attachment loss.
Aggressive periodontitis:
Definition: Aggressive periodontitis encompasses distinct types of periodontitis that affect people who, in most cases, otherwise appear healthy. It tends to have a familial aggregation and there is a rapid rate of disease progression. Aggressive periodontitis occurs in localized and generalized forms.45
Aggressive periodontitis can be classified as localized aggressive periodontitis and generalized aggressive periodontitis.
Clinical Features:46 (Table 6)
Primary features:
Non-contributory medical history
Rapid attachment loss and bone destruction
Familial aggregation of disease
Secondary features that are generally present but may not be present in all cases:
1) Amount of microbial deposits inconsistent with the severity of periodontal destruction.
2) Elevated proportions of Actinobacillus actinomycetemcomitans.
3) Phagocytic abnormalities
4) Hyper-responsive macrophage phenotype, including elevated production of PGE2 and interleukin-1β in response to bacterial endotoxins.
5) Progression of attachment loss and bone loss may be self-arresting.
The diagnosis may be made on historical, radiographic and clinical data. In addition to primary and secondary features common to all aggressive periodontitis patients, following features can be identified:
Localized aggressive periodontitis:
1) Circumpubertal onset; 2) Localized first molar/incisor show interproximal attachment loss on at least two permanent teeth, one of which is a first molar, and involving no more than two teeth other than first molars and incisors; 3) Robust serum antibody response.
Generalized aggressive periodontitis:
1) Usually affecting persons under 30 years of age but patients may be older; 2) Generalized interproximal attachment loss affecting at least three permanent teeth, other than first molars and incisors; 3) Pronounced episodic nature of destruction of attachment and alveolar bone. 4) Poor serum antibody response.
Chronic and aggressive periodontitis have numerous common clinical features, but the common features are not necessarily alike in both forms of the disease. It is well recognized that both chronic and aggressive periodontitis are complex infections that occur in susceptible hosts and are caused by biofilms.47-49 In addition, host immune response to the biofilms is largely responsible for periodontal destruction.50,51 Successful management of both forms of periodontitis includes reduction of bacterial load.52 The untreated disease invariably leads to loss of tooth.
Table 6
Clinical Features of Aggressive periodontitis
Primary features:
Non-contributory medical history.
Rapid attachment loss and bone destruction
Familial aggregation of disease.
Secondary features: generally present but not universal:
Amount of microbial deposits inconsistent with the severity of periodontal destruction.
Elevated proportions of Actinobacillus actinomycetemcomitans.
Phagocytic abnormalities
Hyper-responsive macrophage phenotype, including elevated production of PGE2 and interleukin-1β.
Progression of attachment loss and bone loss may be self-arresting.
Localized aggressive periodontitis:
Circumpubertal onset
Localized first molar/incisor involvement with interproximal attachment loss on at least two permanent teeth, one of which is a first molar, and involving no more than two teeth other than first molars and incisors.
Robust serum antibody response.
Generalized aggressive periodontitis:
Usually affecting persons under 30 years of age but patients may be older;
Generalized interproximal attachment loss affecting at least three permanent teeth, other than first molars and incisors;
Pronounced episodic nature of destruction of attachment and alveolar bone.
Poor serum antibody response.
Similarities and differences in clinical features of chronic and aggressive periodontitis:
One of the shared clinical characteristics of chronic and aggressive periodontitis is that affected individuals have no known medical or general health conditions that might contribute to development of their periodontitis. If an individual has a systemic disease that modifies the initiation and clinical course of periodontal infections, the resulting periodontitis should be classified as periodontitis as a manifestation of systemic disease.4
Chronic and aggressive forms of periodontitis have a number of significant clinical differences including: (i) age of onset; (ii) rates of progression; (iii) patterns of destruction; (iv) clinical signs of inflammation and (v) amount of plaque and calculus. The clinical differences are the primary basis for classifying individuals into one of the categories of periodontitis.
A diagnosis is a summary statement of the clinician’s best estimate regarding the disease or condition detected in a given patient. It is derived from a thorough analysis of all information collected during a review of relevant data from medical â„ dental histories, the results of diagnostic tests, and findings from a careful clinical examination.53,54 A diagnosis should be a short and concise statement that gives an idea of disease present in a specific patient. It provides a foundation about appropriate treatment approaches. The diagnosis may not precisely be according to the classification system. The exact definition of case is not a main issue in the management of specific patients in clinical practice, as the diagnosis is tailor-made for the individual.55 The clinical distinction between chronic and aggressive periodontitis may be difficult sometimes. This distinction becomes insignificant from a treatment viewpoint as anti-infective therapies are successful for both forms of the disease.55
Periodontitis as a manifestation of systemic diseases:
Systemic diseases that predispose patients to highly destructive disease of the primary teeth, the diagnosis is periodontitis as a manifestation of systemic disease. This group is classified as:56(Table 7)
Associated with hematological disorders: 1) Acquired neutropenia; 2) Leukemias; 3) Others.
Associated with genetic disorders: 1) Familial and cyclic neutropenia; 2) Down’s syndrome; 3) Leukocyte adherence deficiency syndrome; 4) Papillon-Lefèvre syndrome; 5) Chediak-Higashi syndrome; 6) Histocytosis syndromes; 7) Glycogen storage disease; 8) Infantile genetic agranulocytosis; 9) Cohen syndrome; 10) Ehlers-Danlos syndrome (Types IV and VIII); 11) hypophosphatasia.
Not Otherwise specified.
Not otherwise specified includes diseases like osteoporosis and estrogen deficiency which have shown to affect 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 time of eruption of the primary teeth up to the age of 5.57,58 In the localized form, affected sites exhibit rapid bone loss and minimal gingival inflammation.57
Quantitative (agranulocytosis or neutropenia) or qualitative (chemotactic or phagocytic) leukocytic deficiencies show evidence of severe 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.59
Neutropenia. Patients present with a 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 get involved.60 In cyclic, chronic, and familial benign neutropenia the lesions show deep periodontal pockets and extensive, generalized bone loss involving the permanent dentition.61-63 Bone resorption may be seen in the deciduous dentition.64,65
Leukemia. Periodontal lesions have been frequently observed in patients with leukemia, 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.66 Gingival swelling due to infiltration by leukemic cells is a feature of acute monocytic leukemic.67 Gingival bleeding is also a common sign of the disease in both acute and chronic leukemia and may relate to the associated thrombocytopenia.68
Down’s Syndrome. Patients with Down syndrome show a generalized early periodontitis, which commences in the deciduous dentition69,70 and continues into the adult dentition. The prevalence and severity of periodontal disease in individuals with Down syndrome is exceedingly high in comparison to their siblings71 or other mentally subnormal persons.70 Several studies have reported increased prevalence and severity of periodontal disease in children of older age groups.69,70 The periodontal destruction is most commonly seen around the incisor and molar teeth.69 The short roots of the mandibular incisors72 and the bone loss in the mandibular anterior region, can lead to the premature loss of these teeth.70
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.73 Young patients with leukocyte adhesion deficiency syndrome present with severe inflammatory periodontal disease.74-76 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 adhesins suffer from severe periodontal infections.73
Papillon-Lefèvre Syndrome. Papillon-Lefèvre syndrome is a disease with autosomal recessive inheritance.77 The disease shows signs of diffuse palmar-plantar keratosis with a severe generalized periodontitis, usually seen before puberty with early loss of deciduous and permanent teeth.78-80 A frequency of 1 in 4 million in the general population has been reported.80 25% have been reported to have an increased susceptibility to infection, and 33% have a history of consanguinity.79 Teeth are normally lost in the order of eruption.79 Haim Munk syndrome is also characterized by presence of palmoplantar hyperkeratosis and severe early-onset periodontitis. Genetic studies of the diseases exhibiting palmoplantar keratosis and early-onset periodontitis suggested that the gene defect in Haim Munk syndrome is not genetically linked to the more common forms of palmoplantar keratosis.81 It has been reported that there is a high degree of consanguinity in these families and that they are most likely part of the similar syndrome.82
Chediak-Higashi Syndrome. Chediak-Higashi syndrome is as an autosomal recessive disease associated with severe periodontitis.83,84 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.85
Histiocytosis Syndromes. This group of diseases includes may affect infants, children, and adults. 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. Biopsy of the granulation tissue can help in diagnosing the condition.86 Skeletal surveys and chest radiographs will assist in determining the extent of the disease.
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.87,88
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.89,90
Cohen’s syndrome. This is also an autosomal recessive condition is characterized frequent and extensive alveolar bone loss.88 The patients also suffer from non-progressive mental and motor retardation, obesity, dysmorphia, and neutropenia.91
Ehlers-Danlos Syndrome. The Ehlers-Danlos syndrome is autosomal dominant disorder. Ehlers-Danlos syndrome is classified into 10 types and is characterized by defective collagen synthesis. Types IV and VIII have an increased susceptibility to periodontitis.92 Type VIII is linked with fragile oral mucosa and blood vessels. It is also associated with severe generalized periodontitis with manifestation of generalized early-onset periodontitis.93 Ehlers-Danlos syndrome type VIII has clinical similarity to the early-onset form, causing premature loss of permanent teeth.94
Hypophosphatasia. Patients present with decreased serum alkaline phosphatase levels. There is severe loss of alveolar bone and premature loss of the deciduous teeth.95-97 Premature loss of deciduous dentition primarily involves anterior region.97
Table 7
Periodontitis as a manifestation of systemic diseases
Associated with hematological disorders:
Acquired neutropenia;
Leukemias;
Others.
Associated with genetic disorders:
Familial and cyclic neutropenia;
Down’s syndrome;
Leukocyte adherence deficiency syndrome;
Papillon-Lefèvre syndrome;
Chediak-Higashi syndrome;
Histocytosis syndromes;
Glycogen storage disease;
Infantile genetic agranulocytosis;
Cohen syndrome;
Ehlers-Danlos syndrome (Types IV and VIII);
Hypophosphatasia.
Not Otherwise specified
Necrotizing periodontal diseases:
Necrotizing periodontal diseases are classified as a) Necrotizing ulcerative gingivitis; b) necrotizing ulcerative periodontitis. The working definitions and clinical features proposed are:
Necrotizing ulcerative gingivitis: This is an infection characterized by gingival necrosis presenting as “punched out” papillae, gingival bleeding, and pain. Fetid odor and pseudomembrane formation may be secondary diagnostic criteria. The predisposing factors include: emotional stress, poor diet, cigarette smoking and HIV infection.98
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.98
The two most significant findings used in the diagnosis of necrotizing periodontal diseases are the presence of interproximal necrosis and ulceration and the rapid onset of gingival pain.(Table 8) Absence of any of the three criteria (interproximal necrosis, bleeding, and pain), a diagnosis of necrotizing ulcerative gingivitis cannot be made. Necrotizing ulcerative gingivitis is diagnosed at the onset of specific clinical signs and symptoms.99 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 less 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. There is intense pain in necrotizing ulcerative gingivitis results. 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.100
Necrotizing ulcerative periodontitis suggests that the pathologic process is similar to that observed in periodontitis, with the addition of tissue necrosis. Necrotizing periodontal diseases 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.101
Necrotizing periodontal diseases (NPD) is present with higher frequency (2% to 5%) in children and adolescents from developing areas of Africa, Asia, and South America compared to North American and European children (less than 1%).102-104
Table 8
Necrotizing periodontal diseases
Significant findings used in the diagnosis of necrotizing periodontal diseases
The presence of interproximal necrosis and ulceration.
Rapid onset of gingival pain.
Bleeding from gingiva.
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 compromised medical status child may involve consultation with the child’s pediatrician.
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 whether the child/adolescent requires treatment or further assessment.
Periodontal screening and recording introduced by American Dental Association105 has been found to be sensitive, easy, quick method of screening patients for periodontal diseases that summarizes essential information.106 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.107
After the eruption of the incisors and first permanent molars in children, the basic periodontal examination can be used for screening the index teeth 16, 11, 26, 36, 31 and 46 (International Dental Federation notation). The WHO 621 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.108 Usage of codes up to 2 is recommended till the age of 11 years because of the probability of pseudopockets associated with newly erupting teeth.109 Presence of deep pocket in which the 3.5- to 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- to 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.109 It is crucial to assess the base of the pocket. In true pocket the base of the pocket is apical to the cementoenamel 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 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.110 This basic periodontal examination screening system typically takes less than 1 or 2 minutes in children and adolescents.110
Basic Periodontal Examination (BPE) scoring criteria (Table 9):
Index Teeth used: 16, 11, 26, 36, 31, 46. 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.
Code 0: In the deepest sulcus of the sextant, the probe’s colored band remains completely visible. Gingival tissue is healthy and does not bleed on gentle probing. No calculus or defective margins are found. These patients require only appropriate preventive care.
Code 1: The colored band of the probe remains completely visible in the deepest sulcus of the sextant; no calculus or defective margins are found, but some bleeding after gentle probing is detected. Treatment for these patients consists of subgingival plaque removal and appropriate oral hygiene instructions.
Code 2: The probe’s colored band is still completely visible, but there is bleeding on probing, and supragingival or subgingival calculus and/or defective margins are found. Treatment should include plaque and calculus removal, correction of plaque-retentive margins of restorations, and oral hygiene instruction.
Code 3: The colored band is partially submerged. This indicates the need for a comprehensive periodontal examination and charting of the affected sextant to determine the necessary treatment plan. If two or more sextants score Code 3, a comprehensive full-mouth examination and charting is indicated.
Table 9
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:
16
11
26
46
31
36
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
Probe’s colored band remains completely visible
Gingival tissue healthy
Preventive care required
Code 1
Probe’s colored band remains completely visible in the deepest sulcus of the sextant
Bleeding after probing detected
Subgingival plaque removal;
Appropriate oral hygiene instructions
Code 2
The probe’s colored band is still completely visible.
Bleeding on probing and supragingival or subgingival calculus and/or defective margins found
Plaque and calculus removal;
Correction of plaque-retentive margins of restorations;
Oral hygiene instruction.
Code 3
The colored 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 colored band completely disappears in the pocket
Comprehensive full-mouth periodontal examination, charting, and treatment planning are needed.
Code *
To mark the presence of following abnormalities an asterisk (*) is entered: furcation involvement, tooth mobility, mucogingival problem, or gingival recession extending to the colored band of the probe (3.5 mm or greater).
Code 4: The colored band completely disappears in the pocket, indicating a depth greater than 5.5 mm. In this case a comprehensive full-mouth periodontal examination, charting, and treatment planning are needed.
Code *: When any of the following abnormalities are seen, an asterisk (*) is entered, in addition to the code number: furcation involvement, tooth mobility, mucogingival problem, or gingival recession extending to the colored band of the probe (3.5 mm or greater).
Frequency of recording BPE111: 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 year.
Score 3: If score 3 is recorded in one or more sextants, treat and review. If still code 3, record full periodontal indices in affected sextants.
Score 4 or *: Record full periodontal indices and consider referral.
A detailed periodontal examination should include indices to record: a) probing pocket depths; b) clinical attachment levels; c) bleeding on probing; d) mobility; e) furcation involvement; f) supparation; g) recession. Radiographs can also be considered if BPE score is 3, 4 or * to assess bone levels. The diagnosis of periodontal problems is reached after deliberation of the findings of the history and examination.
Periodontal treatment in children and adolescents:
The periodontal therapy aims to preserve the natural dentition and periodontium and to improve comfort, esthetics, 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.112
Periodontal treatment is undertaken in three phases: i) initial cause-related therapy to eliminate or control plaque; ii) Additional therapeutic measures; and iii) supportive (maintenance) therapy to prevent disease recurrence and progression with follow-up recalls arranged at a time interval appropriate to the diagnosis.113(Table 10)
Initial cause-related therapy includes:
Patient education, personal oral hygiene instructions, control of risk factors (eg, smoking, medical status).
Scaling and root planning to remove plaque and calculus.
Eliminate plaque retentive factors- caries treatment, endodontic treatment, extractions, temporary prosthetic reconstruction.
Post-treatment evaluation with review and reinforcement of personal daily oral hygiene.
Additional therapeutic measures:
The amount of corrective therapy required can be determined only by the level of improvement after causative therapy is evaluated. The patient’s cooperation towards treatment determines the corrective treatment. Entirely cooperative patients should be the candidates for treatment procedures to improve oral esthetics and function permanently. Additional treatments indicated for cooperative patients include:112
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 esthetics.
Occlusal therapy to reduce occlusal trauma.
Preprosthetic periodontal procedures to aid restorative or prosthetic treatment plans.
Procedures to assist orthodontic treatment e.g. tooth exposure, frenectomy.
Replacement of teeth by dental implants.
Supportive periodontal therapy:112
The aim of this treatment is the prevention of disease recurrence.
Update of medical and dental histories.
Evaluation of extra- and intraoral, periodontal and peri-implant soft tissues as well as dental hard tissues.
Assessment of the oral hygiene status with reinstruction when indicated.
Scaling and root planning. Local or systemic chemotherapeutic agents may be used as adjunctive treatment.
Eradication of risk and etiologic factors with appropriate treatment.
Detection and treatment of new, recurrent, or refractory areas of periodontal disease.
Developing of a personalized periodontal maintenance protocol for the patient.
Table 10
Periodontal treatment in children and adolescents
Phases of periodontal treatment:
Initial cause-related therapy to eliminate or control plaque:
Patient education, personal oral hygiene instructions, control of risk factors (eg, smoking, medical status).
Scaling and root planning to remove plaque and calculus.
Eliminate plaque retentive factors- caries treatment, endodontic treatment, extractions, temporary prosthetic reconstruction.
Post-treatment evaluation with review and reinforcement of personal daily oral hygiene.
Additional/corrective therapeutic measures:
If redness, swelling, suppuration, and bleeding on probing persists:
Use of chemotherapeutic agents. Periodontal surgical therapy (resective/regenerative). Periodontal plastic surgical procedures. Occlusal therapy. Definitive restorative work.
Supportive periodontal therapy:
Update of medical and dental histories.
Evaluation of extra- and intraoral, periodontal and peri-implant soft tissues as well as dental hard tissues.
Assessment of the oral hygiene status with reinstruction when indicated.
Scaling and root planning and use of local or systemic chemotherapeutic agents if required.
Eradication of risk and etiologic factors with appropriate treatment.
Detection and treatment of new, recurrent, or refractory areas of periodontal disease.
Developing of a personalized 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 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.114 Topical antibacterial agents may be used as an adjunct therapy for the control of gingivitis. The agents accepted by American Dental Association are the products containing (i) thymol, menthol, eucalyptol, and methyl salicylate; (ii) chlorhexidine digluconate and (iii) triclosan.114
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.114 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 etiologic 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.114 A surgical treatment of periodontitis 1) provides better access for removal of etiologic factors; 2) reduce deep probing depths; and 3) regenerate or reconstruct lost periodontal tissues.115-117 Regenerative therapies with bone grafting118-120 and guided tissue regeneration (GTR) techniques, with or without bone replacement grafts,121-22 may be successful at selected sites with advanced bone loss.
Treatment of aggressive periodontitis: The most commonly recommended treatment modality for localized aggressive periodontitis is a combination of surgical or non-surgical root debridement in conjunction with antimicrobial therapy.123-24 The most commonly used antibiotics that are successful in controlling infection are the tetracyclines, or tetracyclines used in combination with metronidazole.125 Metronidazole has been used along with amoxicillin.126 The response to conventional mechanical therapy or antibiotics may not be on expected lines.127,128 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.125
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 aggressive periodontitis in the permanent dentition.57,63,129,130 Successful resolution of localized lesions occurs with this treatment modality.57,58 The extent of success has been limited in treatment of generalized periodontitis present as a manifestation of systemic diseases.57,58 Extraction of affected teeth has been the line of treatment in many cases.57,58
Treatment of necrotizing periodontal diseases: Mechanical debridement, oral hygiene instruction, and careful follow-up results in improvement of the condition.131,132 Symptoms reduce after debridement with ultrasonics.133 Antibiotics like metronidazole and penicillin have been used as adjunct in the febrile patients.134
Summary:
Children and adolescents experience several periodontal diseases with plaque being the key contributing agent. Local and systemic risks factors can modify the response of periodontal tissues. Periodontal screening should be an integral part of the dental examination of children and adolescents. Most of the periodontal diseases respond well to appropriate periodontal therapy. Early diagnosis ensures the greatest likelihood for successful treatment. Periodontal management should follow the vital principles of initial cause related, corrective and supportive therapy. Age, cooperation and motivation of the child or adolescent must be taken into consideration in periodontal treatment. A personalized periodontal maintenance schedule should be suggested to the patient for long-term control of the disease.
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