Showing papers in "Annals of Periodontology in 1999"
TL;DR: How the new classification for periodontal diseases and conditions presented in this volume differs from the classification system developed at the 1989 World Workshop in Clinical Periodontics is summarized.
Abstract: Classification systems are necessary in order to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. The last time scientists and clinicians in the field of periodontology and related areas agreed upon a classi- fication system for periodontal diseases was in 1989 at the World Workshop in Clinical Periodontics.1 Subsequently, a simpler classification was agreed upon at the 1st European Workshop in Periodontology.2 These classification systems have been widely used by clinicians and research scientists throughout the world. Unfortunately, the 1989 classification had many shortcomings including: 1) considerable overlap in disease categories, 2) absence of a gingival disease component, 3) inappropriate emphasis on age of onset of disease and rates of progression, and 4) inadequate or unclear classification criteria. The 1993 Europea...
4,653 citations
TL;DR: The group agreed that there are enough specific features, which are sufficiently discriminating, to allow for the subclassification of Aggressive Periodontitis into localized and generalized forms.
Abstract: Not all characteristics must be present to assign a diagnosis or classify the disease. The diagnosis may be based on clinical, radiographic, and historical data. Although helpful, laboratory testing may not be essential for assigning a diagnosis. The group agreed that there are enough specific features, which are sufficiently discriminating, to allow for the subclassification of Aggressive Periodontitis into localized and generalized forms. In addition to the features common to all forms of Aggressive Periodontitis, the following specific features were identified:
357 citations
TL;DR: The purpose of this review is to discuss the criteria generally utilized to classify EOP, provide the rationale to designate EOP as a distinct disease entity, and to review the evidence justifying a subclassification into particular subgroups of EOP.
Abstract: In 1993, the 1st European Workshop on Periodontology explicitly recognized that there was insufficient knowledge to differentiate truly different forms of periodontal disease from differences in the presentation/severity of the same disease. In spite of recent progress in our understanding of periodontal diseases, the issue is far from having been resolved. Classification of periodontal diseases, therefore, remains based upon the definition of specific clinical syndromes. Early-onset periodontitis (EOP) is one such syndrome and comprises a group of pathological conditions leading to loss of periodontal tissues early in life. The notion that classifies periodontitis syndromes as "early-onset" or "adult" is primarily epidemiological in nature and is based on the observation that periodontitis is rather infrequent in children and young adults. Nevertheless, considerable epidemiological evidence indicates that periodontitis does affect children and young adults to a level of severity that may lead to premature exfoliation of primary and/or permanent teeth. Clinical presentation of periodontitis early in the life of an individual is thought to indicate that the etiologic agents have been able to cause considerable tissue damage over a relatively short period of time. It also implies either infection with highly virulent bacteria and/or a highly susceptible subject. The purpose of this review is to discuss the criteria generally utilized to classify EOP, provide the rationale to designate EOP as a distinct disease entity, and to review the evidence justifying a subclassification into particular subgroups of EOP.
326 citations
TL;DR: The classification of gingival disease in this review relied upon experimental and/or epidemiological human studies that accurately and reliably assessed an underlying functional derangement that was localized to the gingiva and was reported in a peer-reviewed journal.
Abstract: Gingival diseases are a diverse family of complex and distinct pathological entities found within the gingiva that are the result of a variety of etiologies. There are several clinical characteristics common to all gingival diseases and these features include clinical signs of inflammation, signs and symptoms that are con- fined to the gingiva, reversibility of the disease by removing the etiology, the presence of bacterial laden plaque to initiate and/or exacerbate the severity of the disease and a possible role as a precursor for attachment loss around teeth. Defining and classifying gingival diseases has not been an easy task. The tools and methods to identify gingival diseases have varied depending on the criteria used by epidemiologists, researchers, or the practicing clinician. The classification of gingival disease in this review relied upon experimental and/or epidemiological human studies that accurately and reliably assessed an underlying functional derangement that was localized to the gingiva ...
295 citations
TL;DR: The group concluded that recurrentperiodontitis represents a return of periodontitis and is not a separate disease entity.
Abstract: It may affect a variable number of teeth and it has variable rates of progression. Chronic periodontitis is initiated and sustained by bacterial plaque, but host defense mechanisms play an integral role in its pathogenesis. The progressive nature of the disease can only be confirmed by repeated examinations. It is reasonable to assume that the disease will progress further if treatment is not provided. Chronic periodontitis can be further characterized by extent and severity. Extent is the number of sites involved and can be described as localized or generalized. As a general guide, extent can be characterized as localized if ≤30% of the sites are affected and generalized if >30% of the sites are affected. Severity can be described for the entire dentition or for individual teeth and sites. As a general guide, severity can be categorized on the basis of the amount of clinical attachment loss (CAL) as follows: Slight = 1 to 2 mm CAL, Moderate = 3 to 4 mm CAL, and Severe = ≥5 mm CAL. The group acknowledged that in clinical practice, there are recurrent and refractory (non-responsive) cases of periodontitis. However, the group did not believe that there is enough evidence to place these cases in their own disease categories since any type of periodontitis can recur and a small percentage of cases can be non-responsive to therapy. The group concluded that recurrent periodontitis represents a return of periodontitis and is not a separate disease entity. For a variety of identifiable and non-identifiable reasons, not all cases of periodontitis have a successful treatment outcome. Such cases can be referred to as refractory periodontitis but do not necessarily constitute a separate disease entity. More research is needed to identify the reasons for the failure to respond to treatment. Since conditions or factors that modify the gingiva in gingivitis (see Gingival Diseases, pages 7-31) also modify the gingiva in periodontitis, they were not considered in this section of the classification.
263 citations
TL;DR: The categorization of the systemic modifying factors causing periodontitis and the evidence to support the role of these factors are the focus of this review.
Abstract: Microbial dental plaque is the initiator of periodontal disease but whether it affects a particular subject, what form the disease takes, and how it progresses, are all dependent on the host defenses to this challenge. Systemic factors modify all forms periodontitis principally through their effects on the normal immune and inflammatory defenses. Some good examples of this effect exist such as when there is a reduction in number or function of polymorphonuclear leukocytes (PMNs) that may result in an increased rate and severity of periodontal destruction. Many other systemic factors are much less clear cut and are difficult to causally link to periodontitis. In many cases the literature is insufficient to make definite statements on links between systemic factors and periodontitis. It is also at times difficult to be precise regarding the causative agent in systemic exposures such as smoking and even prescribed drug therapy. The possible role of systemic diseases and systemic exposures in initiating or modifying the progress of periodontal disease is clearly a complex issue. It is however generally agreed that several conditions may give rise to an increased prevalence, incidence, or severity of gingivitis and periodontitis. The categorization of the systemic modifying factors causing periodontitis and the evidence to support the role of these factors are the focus of this review. An attempt has been made to consider the conditions under broad headings, but it will be clear that many conditions fall within more than one category and that for several conditions only case reports exist whereas in other areas an extensive literature is present.
135 citations
TL;DR: An altered ability to cope with psychological stress, immunosuppression, and tobacco use are found to be strongly associated with the onset of necrotizing ulcerative gingivitis.
Abstract: Necrotizing periodontal diseases are unique in their clinical presentation and course. Data suggest that the etiology and pathogenesis of necrotizing periodontal diseases may also be distinctive from other periodontal diseases. Necrotizing ulcerative gingivitis (NUG) is a type of necrotizing periodontal disease in which the necrosis is limited to the gingival tissues. Three specific clinical characteristics must be present to diagnose NUG, pain (usually of rapid onset) interdental necrosis, and bleeding. Epidemiological and prospective clinical studies have found an altered ability to cope with psychological stress, immunosuppression, and tobacco use to be strongly associated with the onset of NUG.
100 citations
TL;DR: Gingival inflammation may result from toxic reactions, foreign body reactions, or mechanical and thermal trauma, and can be caused by allergic reactions to dental restorative materials, toothpastes, mouthwashes, and foods.
Abstract: The origin of gingival inflammation is occasionally different from that of routine plaque-associated gingivitis, and such non-plaqueassociated types of gingivitis often present characteristic clinical features. Examples of such forms of gingivitis are specific bacterial, viral, and fungal infections. Specific bacterial infections of gingiva may be due to Neisseria gonorrhea, Treponema pallidum, streptococci, and other organisms. The most important viral infections of gingiva are herpes simplex virus type 1 and 2 and varicella-zoster virus. Fungal infections may be caused by several fungi, the most important of these being Candida species including C. albicans, C. glabrata, C. krusei, C. tropicalis, C. parapsilosis, and C. guillermondii. Gingival histoplasmosis is a granulomatous disease caused by the fungus Histoplasma capsulatum and, as for the other specific infections of gingiva, a con- firmed diagnosis may require histopathologic examination and/or culture. Atypical gingivitis may also occur as gingiv...
81 citations
TL;DR: This review focuses on the relationship of lesions of endodontic origin with lesions of periodontal origin and their classification.
Abstract: Lesions of the periodontal ligament and adjacent alveolar bone may originate from infections of the periodontium or tissues of the dental pulp. This review focuses on the relationship of lesions of endodontic origin with lesions of periodontal origin and their classification. Ann Periodontol 1999;4:84-89.
71 citations
TL;DR: This focused review is limited to a number of investigations in an attempt to specifically address the histological and clinical effects of excessive occlusal forces on the teeth and periodontium and to provide a basis of classification for this interaction.
Abstract: This focused review is limited to a number of investigations in an attempt to specifically address the histological and clinical effects of excessive occlusal forces on the teeth and periodontium and to provide a basis of classification for this interaction. This review does not include the effects of occlusal forces on dental implants or dental prostheses/appliances.
69 citations
TL;DR: NUG and NUP should be classified together under the grouping of necrotizing periodontal diseases based on their clinical characteristics, and further studies are needed to define the complex interactions between the microbial, or viral, etiology of nec rotic lesions and the immunocompromised host.
Abstract: In patients with no known systemic disease or immune dysfunction, necrotizing periodontitis (NUP) appears to share many of the clinical and etiologic characteristics of necrotizing ulcerative gingivitis (NUG) except that patients with NUP demonstrate loss of clinical attachment and alveolar bone at affected sites. In these patients, NUP may be a sequela of a single or multiple episodes of NUG or may be the result of the occurrence of necrotizing disease at a previously periodontitis-affected site. The existence of immune dysfunction may predispose patients to NUG and NUP, especially when associated with an infection of microorganisms frequently associated with periodontal disease such as Treponema and Selenomonas species, Fuscobacterium nucleatum, Prevotella intermedia, and Porphyromonas gingivalis. The role of immune dysfunction is exemplified by the occasionally aggressive nature of necrotic forms of periodontal disease seen in patients with HIV infection or malnutrition, both of which may impact host defenses. Clinical studies of HIV-infected patients have shown that patients with NUP are 20.8 times more likely to have CD4+ cell counts below 200 cells/mm3. However, these same studies have demonstrated that most patients with CD4+ cell counts below 200 cells/mm do not have NUP, suggesting that other factors, in addition to immunocompromisation, are involved. Further studies are needed to define the complex interactions between the microbial, or viral, etiology of necrotic lesions and the immunocompromised host. It is, therefore, recommended that NUG and NUP be classified together under the grouping of necrotizing periodontal diseases based on their clinical characteristics.
[...]
TL;DR: Several factors related to tooth/root anatomy, restorative, and endodontic considerations have been associated with gingival inflammation, attachment loss, and bone loss and will be reviewed as they relate to their potential to promote damage to the periodontium.
Abstract: Several conditions exist around teeth that may predispose the periodontium to disease. These situations may occur as a result of the condition or position of teeth or as a result of tooth treatment. In certain cases these tooth-related factors may contribute to the initiation of periodontal disease. While the etiology of periodontal disease is bacterial, factors that enhance bacterial accumulation or allow the ingress of bacteria into the periodontium should be considered in the classification and diagnosis of periodontal diseases. This is because many times these tooth-related issues can cause site-specific problems that require treatment in an otherwise intact periodontium. Several factors related to tooth/root anatomy, restorative, and endodontic considerations have been associated with gingival inflammation, attachment loss, and bone loss. These factors will be reviewed as they relate to their potential to promote damage to the periodontium.
TL;DR: This is an infection characterized by necrosis of gingival tissues, periodontal ligament, and alveolar bone that is most commonly observed in individuals with systemic conditions including, but not limited to HIV infection, severe malnutrition, and immunosuppression.
Abstract: 78 Necrotizing ulcerative gingivitis. This is an infection characterized by gingival necrosis presenting as “punched-out” papillae, with gingival bleeding, and pain. Fetid breath and pseudomembrane formation may be secondary diagnostic features. Fusiform bacteria, Prevotella intermedia, and spirochetes have been associated with the gingival lesions. Predisposing factors may include: emotional stress, poor diet, cigarette smoking, and HIV infection. Necrotizing ulcerative periodontitis. This is an infection characterized by necrosis of gingival tissues, periodontal ligament, and alveolar bone. These lesions are most commonly observed in individuals with systemic conditions including, but not limited to HIV infection, severe malnutrition, and immunosuppression.
TL;DR: This map shows the main categories of genetic disorders associated with Down's syndrome, as well as some of the other conditions not specified (NOS).
Abstract: 64 B. Associated with genetic disorders 1. Familial and cyclic neutropenia 2. Down syndrome 3. Leukocyte adhesion deficiency syndromes 4. Papillon-Lefevre syndrome 5. Chediak-Higashi syndrome 6. Histiocytosis syndromes 7. Glycogen storage disease 8. Infantile genetic agranulocytosis 9. Cohen syndrome 10. Ehlers-Danlos syndrome (Types IV and VIII) 11. Hypophosphatasia 12. Other C. Not otherwise specified (NOS)
TL;DR: The following working definitions for these lesions were developed by the group: Gingival abscess, periodontal abscess and pericoronal abscess.
Abstract: 83 The following working definitions for these lesions were developed by the group: Gingival abscess. A localized purulent infection that involves the marginal gingiva or interdental papilla. Periodontal abscess. A localized purulent infection within the tissues adjacent to the periodontal pocket that may lead to the destruction of periodontal ligament and alveolar bone. Pericoronal abscess. A localized purulent infection within the tissue surrounding the crown of a partially erupted tooth.
TL;DR: The group endorsed the definition of mucogingival therapy as described in the 1996 World Workshop in Periodontics (i.e., “Non-surgical and surgical correction of defects in morphology, position, and/or amount of soft tissue and underlying bone”) and recommended that a classification system for mucogedival deformities around dental implants be similar to the one suggested above for teeth.
Abstract: of the oral mucosa that covers the alveolar process including the gingiva (keratinized tissue) and the adjacent alveolar mucosa. Mucogingival deformity. A departure from the normal dimension and morphology of and/or interrelationship between gingiva and alveolar mucosa. The abnormality may be associated with a deformity of the underlying alveolar bone. The group endorsed the definition of mucogingival therapy as described in the 1996 World Workshop in Periodontics (i.e., “Non-surgical and surgical correction of defects in morphology, position, and/or amount of soft tissue and underlying bone.”).1 In addition the current definition of gingival recession was also endorsed (i.e., “Location of the gingival margin apical to the cemento-enamel junction.”).2 Note: The group recommended that a classification system for mucogingival deformities around dental implants be similar to the one suggested above for teeth (i.e., “I. Mucogingival Deformities Around Teeth”). The group also recommended that the current classification of implant-related conditions (e.g., peri-implantitis) be retained until a new classification system for implant-related issues can be formulated.
TL;DR: The group agreed that in those cases where there is any coalescence of endodontic and periodontal lesions, these situations should be termed, “Combined Periodontal-Endodontal Lesions.”
Abstract: 90 sive forms of periodontitis can gain access to pulpal tissues through accessory canals or the tooth apex and lead to pulpal infection. In those cases where there is any coalescence of endodontic and periodontal lesions, the group agreed that these situations should be termed, “Combined Periodontal-Endodontic Lesions.” This classification is not based on the initial etiology of the lesion. Either the periodontal or endodontic lesion may be the cause or the result of the other or both may develop independently. Therefore, the group recommended the following classification:
TL;DR: The following working definitions for the types of occlusal trauma were developed by the group; injury resulting in tissue changes within the attachment apparatus as a result of Occlusal force, primary and secondary.
Abstract: The following working definitions for the types of occlusal trauma were developed by the group: Occlusal trauma. Injury resulting in tissue changes within the attachment apparatus as a result of occlusal force(s). Primary occlusal trauma. Injury resulting in tissue changes from excessive occlusal forces applied to a tooth or teeth with normal support. It occurs in the presence of: 1) normal bone levels, 2) normal attachment levels, and 3) excessive occlusal force(s). Secondary occlusal trauma.* Injury resulting in tissue changes from normal or excessive occlusal forces applied to a tooth or teeth with reduced support. It occurs in the presence of: 1) bone loss, 2) attachment loss, and 3) “normal”/excessive occlusal force(s).
TL;DR: The group agreed upon the following classification of these tooth-related issues: gingivitis, periodontitis, and gingival diseases.
Abstract: fashion by the research community. It should be emphasized that these tooth-related conditions are not separate disease entities, but may serve as localized predisposing and/or modifying factors in the onset or progression of plaque-induced gingival diseases and periodontitis. These conditions could be relevant to any of the gingivitis or periodontitis classifications. The group agreed upon the following classification of these tooth-related issues: