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Anderson DC, Springer TA. Leukocyte adhesion deficiency: an inherited defect in the Mac-1, LFA-1 and p150, 95 glycoproteins. Ann Rev Med. 1987; 38:175-194
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Anderson DC, Schmalsteig FC, Finegold MJ The severe and moderate phenotypes of heritable Mac-1, LFA-1 deficiency: their quantitative definition and relation to leukocyte dysfunction and clinical features. J Infect Dis. 1985; 152:668-689
Page RC, Beatty P, Waldrop TC. Molecular basis for the functional abnormality in neutrophils from patients with generalized prepubertal periodontitis. J Periodont Res. 1987; 22:182-183
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Stevens HP, Kelsell DP, Bryant SP Linkage of an American pedigree with palmoplantar keratoderma and malignancy (palmoplantar ectodermal dysplasia type III) to 17q24. Literature survey and proposed updated classification of the keratodermas. Arch Dermatol. 1996; 132:640-651
Bach JN, Levan NE. Papillon-Lefèvre syndrome. Arch Dermatol. 1968; 97:154-158
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Hart TC, Hart PS, Bowden DW, Michalec MD, Callison SA, Walker SJ, Zhang Y, Firatli E. Mutations of the cathepsin C gene are responsible for Papillon-Lefèvre syndrome. J Med Genet. 1999; 36:881-887
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Hamilton RE, Giansanti JS. Chediak-Higashi syndrome. Report of a case and review of the literature. Oral Surg Oral Med Oral Pathol. 1974; 37:754-761
Hartsfield JK, Kousseff BG. Phenotypic overlap of Ehlers-Danlos syndrome types IV and VIII. Am J Med Genet. 1990; 37:465-470
Linch DC, Acton CHC. Ehlers-Danlos syndrome presenting with juvenile destructive periodontitis. Br Dent J. 1979; 147:95-96
Stewart RE, Hollister DW, Rimoin DL. A new variant of Ehlers-Danlos syndrome: an autosomal dominant disorder of fragile skin, abnormal scarring and generalized periodontitis. Birth Defects. 1977; 13:85-93
Reibel A, Manière M-C, Clauss F Orodental phenotype and genotype findings in all subtypes of Hypophosphatasia. Orphanet J Rare Dis. 2009; 4
Whyte MP. Hypophosphatasia and the role of alkaline phosphatase in skeletal mineralization. Endocr Rev. 1994; 15:439-461
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Mornet E. Hypophosphatasia. Orphanet J Rare Dis. 2007; 2
Whyte MP, Teitelbaum SL, Murphy WA, Bergfeld MA, Avioli LV. Adult hypophosphatasia. Clinical, laboratory, and genetic investigation of a large kindred with review of the literature. Medicine. 1979; 58:329-347
Herasse M, Spentchian M, Taillandier A Molecular study of three cases of Odontohypophosphatasia resulting from heterozygosity for mutations in the tissue non-specific alkaline phosphatase gene. J Med Genet. 2003; 40:605-609
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Lang N, Soskolne WA, Greenstein G Consensus report: Necrotizing periodontal diseases. Ann Periodontol. 1999; 4
Rowland RW. Necrotizing ulcerative gingivitis. Ann Periodontol. 1999; 4:65-73
John Novak M. Necrotizing ulcerative periodontitis. Ann Periodontol. 1999; 4:74-77
Smith BW, Dennison DK, Newland JR. Acquired HIV deficiency syndrome: implications for the practising dentist. Va Dent J. 1987; 63:38-42
Taiwo JO. Severity of necrotizing ulcerative gingivitis in Nigerian children. Periodontal Clin Investig. 1995; 17:24-27
Contreras A, Falkler WA, Enwonwu CO Human Herpesviridae in acute necrotizing ulcerative gingivitis in children in Nigeria. Oral Microbiol Immunol. 1997; 12:259-265
Chicago: American Academy of Periodontology; 1992
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A simplified periodontal examination for dental practices based on the Community Periodontal Index of Treatment Needs.Paris: FDI; 1986
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Clerehugh V, Tugnait A. Clinical examination and local risk factors for periodontal diseases. In: Clerehugh V, Tugnait A, Chapple ILC. London: Quintessence Publishing Co Ltd; 2004
Position paper: Guidelines for periodontal therapy. J Periodontol. 2001; 72:1624-1628
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Treatment of plaque-induced gingivitis, chronic periodontitis, and other clinical conditions. J Periodontol. 2001; 72:1790-1800
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Consensus Report: Periodontal regeneration around natural teeth. Ann Periodontol. 1996; 1:667-670
Consensus Report: Mucogingival therapy. Ann Periodontol. 1996; 1::702-706
Bowers GM, Chadroff B, Carnevale R Histologic evaluation of new human attachment apparatus formation in humans, Part I. J Periodontol. 1989; 60:664-674
Bowers GM, Chadroff B, Carnevale R Histologic evaluation of new human attachment apparatus formation in humans, Part II. J Periodontol. 1989; 60:675-682
Bowers GM, Chadroff B, Carnevale R Histologic evaluation of new human attachment apparatus formation in humans, Part III. J Periodontol. 1989; 60:683-693
McClain PH, Schallhorn RG. Long-term assessment of combined osseous composite grafting, root conditioning, and guided tissue regeneration. Int J Periodont Restor Dent. 1993; 13:9-27
Cortellini P, Pini Prato G, Tonetti MS. Periodontal regeneration of human intrabony defects with bioresorbable membranes. A controlled clinical trial. J Periodontol. 67:217-223
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Periodontal diseases in children and adolescents: a clinician's perspective part 2 Ashish Kumar Sujata Surendra Masamatti Mandeep Singh Virdi Dental Update 2024 39:9, 707-709.
Authors
AshishKumar
MDS
Senior Lecturer, Department of Periodontology, PDM Dental College and Research Institute, Sarai Aurangabad, Bahadurgarh, Haryana
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.
Article
Periodontitis as a manifestation of systemic diseases
Periodontitis as a manifestation of systemic diseases is classified in Table 1.1
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
The ‘Not otherwise specified’ category includes diseases like 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 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.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
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 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, 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.
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;
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
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;
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
Tests performed to diagnose EDS include:
Collagen typing (performed on a skin biopsy sample);
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:
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
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:
Necrotizing ulcerative gingivitis; and
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 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 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 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
The probe's coloured band is still completely visible
Bleeding on probing may be present and supragingival or subgingival calculus and/or defective margins found
Treatment: plaque and calculus removal; correction of plaque-retentive margins of restorations; 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 treatmentIf two or more sextants score Code 3, a comprehensive full-mouth examination and charting is indicated
Code 4
The coloured band completely disappears in the pocket (depth >5.5 mm)
Comprehensive full-mouth periodontal examination, charting, and 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)
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.
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:
Probing pocket depths;
Clinical attachment levels;
Bleeding on probing;
Mobility;
Furcation involvement;
Suppuration;
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 assessment
The British Society of Periodontology recommends following complexity codes in its document on ‘Referral Policy and Parameters of Care’ on 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 simplistic manner with the addition of a list of modifying factors that are relevant to periodontal treatment and an outline of medical history that significantly affects clinical management. It is strictly a complexity assessment and does not address either the motivational aspects of treatment or a prioritization of treatment.
Modifying factors that are relevant to periodontal treatment67
A modifying factor can only increase complexity by one increment. Multiple factors are not cumulative:
Medical history that significantly affects clinical management;
Special needs for the acceptance or provision of dental treatment;
Mandibular dysfunction;
Atypical facial pain;
Undiagnosed facial pain;
Presence of a retching tendency;
Limited operating access;
Concurrent mucogingival disease.
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 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.
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.
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 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 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 aggressive periodontitis in the permanent dentition.2,8,86,87 Successful resolution of localized lesions occurs with this treatment modality.2,3 The extent of success has been limited in treatment of generalized periodontitis present as a manifestation of systemic diseases.2,3 Extraction of affected teeth has been the line of treatment in many cases.2,3
Treatment of necrotizing periodontal diseases
Treatment should aim at irrigation and debridement of the necrotic areas and tooth surfaces. Oral hygiene instructions should be reinforced.88 The use of oral rinses, pain control and management of systemic manifestations, including appropriate antibiotic therapy, may be required. The patient should be advised about the importance of proper nutrition, oral care, appropriate fluid intake and smoking cessation.88 A comprehensive periodontal assessment should follow resolution of the acute condition. Mechanical debridement, oral hygiene instruction, and careful follow-up results in improvement of the condition.89,90 Antibiotics like metronidazole and penicillin have been used as an adjunct in the febrile patients.91
Summary
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, co-operation 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.