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https://www.mayoclinic.org/es-es/diseases-conditions/periodontitis/symptoms-causes/syc-20354473

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Encías inflamadas o hinchadas.

Encías de color rojo brillante, rojo oscuro o morado.

Encías sensibles al tacto.

Encías que sangran fácilmente.

Cepillo de dientes teñido de rosa después del cepillado.

Escupir sangre al cepillarse los dientes o al usar el hilo dental.

Mal aliento.

Pus entre los dientes y las encías.

Dientes flojos o pérdida de dientes.

Dolor al masticar.

Se crean nuevos espacios entre los dientes.

Encías que se retraen de los dientes (se reabsorben), lo que hace que los dientes se vean más largos de lo normal.

Cambio en la manera en que se unen los dientes al morder.

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Periodontitis - Síntomas y causas - Mayo Clinic

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Esta grave infección de las encías daña el tejido blando y puede destruir el hueso que sostiene los dientes. Puede causar el aflojamiento o la pérdida de dientes.

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https://onlinelibrary.wiley.com/doi/10.1111/j.1834-7819.2009.01140.x

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Adjunct Associate Professor John HighfieldDiscipline of PeriodonticsFaculty of DentistryThe University of Sydney2 Chalmers StreetSydney NSW 2010Email: johnh@dentistry.usyd.edu.au

Abstract

Periodontal diseases have been recognized and treated for at least 5000 years. Clinicians have recognized for many years that there are apparent differences in the presentation of periodontal diseases and have attempted to classify these diseases. Systems of classifications of disease have arisen allowing clinicians to develop structures which can be used to identify diseases in relation to aetiology, pathogenesis and treatment. It allows us to organize effective treatment of our patients' diseases. Once a disease has been diagnosed and classified, the aetiology of the condition and appropriate evidence-based treatment is suggested to the clinician. Common systems of classification also allow effective communication between health care professionals using a common language. Early attempts at classification were made on the basis of the clinical characteristics of the diseases or on theories of their aetiology. These attempts were unsupported by any evidence base. As scientific knowledge expanded, conventional pathology formed the basis of classification. More recently, this has been followed by systems of classification based upon our knowledge of the various periodontal infections and the host response to them. Classification of periodontal diseases has, however, proved problematic. Over much of the last century clinicians and researchers have grappled with the problem and have assembled periodically to review or develop the classification of the various forms of periodontal disease as research has expanded our knowledge of these diseases. This has resulted in frequent revisions and changes. A classification, however, should not be regarded as a permanent structure. It must be adaptable to change and evolve with the development of new knowledge. It is expected that systems of classification will change over time. This review examines the past and present classifications of the periodontal diseases.

Abbreviations and acronyms

AST

aspartate aminotransferase

CAL

clinical loss of attachment

GCF

gingival crevicular fluid

LJP

localized juvenile periodontitis

NUG

necrotizing ulcerative gingivitis

NUP

necrotizing ulcerative peridontitis

Introduction

Periodontal disease is a disease, or more likely a number of diseases of the periodontal tissues that results in attachment loss and destruction of alveolar bone. The natural history of periodontal disease, in some but not all patients, results in tooth loss.1 Periodontal disease, however, encompasses a wider spectrum of diseases than just periodontitis and the recognition of these diseases requires a diagnosis be made.

Diagnosis is the recognition of the presence of a disease.2 Clinical diagnosis of periodontal disease is made by the recognition of various signs and symptoms in the periodontal tissues which herald a departure from health. The diagnosis of periodontal disease demands a firm knowledge of what constitutes periodontal health. The healthy periodontium,3 of which only the gingival tissues may be directly observed, is described as being stippled, pale pink or coral pink, in the Caucasian ( Fig 1), with various degrees of pigmentation in other races. It is tightly adapted to the underlying tissues, with a knife edge margin where it abuts the tooth, The gingival margin is located, in the absence of pathology, at the cemento-enamel junction. It displays a scalloped edge configuration highest interdentally, where it constitutes the interdental papilla and lowest buccally and lingually. There is a gingival crevice where it abuts the tooth which in health is 1-3 mm deep. There is an absence of bleeding from the crevice on gentle probing. The crevice in health will show a small amount of interstitial fluid, gingival crevicular fluid.4 The lateral wall of the crevice constitutes the free gingival margin. From the most apical extent of the free gingival to the mucogingival junction is the attached gingival which varies in width from 1 to 9 mm and has a stippled surface. It is an immobile tissue tightly bound down to the bone as a mucoperiostium and is a keratinized mucosa well suited to resist injury. Apical from the mucogingival junction and continuous with the lining mucosa of the mouth is the alveolar mucosa, which is freely mobile and surmounted by a non-keratinized epithelium. It is generally thought that alveolar mucosa functions poorly as a marginal tissue and areas where there is lack of attached gingival may constitute mucogingival problems. Departures from this concept of the healthy periodontium may suggest the presence of disease. The relevant changes which are diagnostic of the presence of disease will be discussed later in this paper.

Systems of classifications of disease have arisen to allow clinicians to develop a structure which can be used to identify diseases in relation to aetiology, pathogenesis and treatment. It allows us to organize effective treatment of our patient's disease. Once a disease has been diagnosed and classified, the aetiology of the condition and appropriate evidence-based treatment is suggested to the clinician. Classification systems also allow the clinicians and researchers everywhere to communicate with a common language.

The most commonly accepted systems of classification of periodontal disease have been those of the American Academy of Periodontology (AAP). Over much of the last century, the Academy has struggled to identify and classify the various forms of periodontal disease as research has expanded knowledge. This has led to frequent revisions and changes but has created some confusion. A classification, however, should not be regarded as a permanent structure. It must be adaptable to change and evolve with the development of new knowledge. It must be expected that systems of classification will change over time, however much this may be confusing and perhaps annoying to practitioners.

This article is a review of the historical and contemporary attempts to classify periodontal diseases.

Historical perspective

Recognition and treatment of periodontal disease can be traced back to antiquity. Descriptions of treatment are found in ancient Egyptian and Chinese writings and would suggest that periodontal diseases were recognized possibly 5000 years ago.5 The first modern writings were by Abu I Quasim, also known as Abuccusis of Cordova Spain in the 10th century.6 More recently, descriptions of treatment of periodontal disease were made by Pierre Fauchard7 who published the first dental textbook, "The Surgeon Dentist" in 1728 and John Hunter8 who published "The Natural History of the Human Teeth" in 1771 and "A Practical Treatise on the Diseases of the Teeth" in 1778. Although there was already a considerable body of writings on dentistry, possibly in excess of 450 treatises in existence before this one,9 Hunter provided the scientific foundations of modern dentistry. The presence of bacteria around the teeth was recognized by Von Leeuwenhoek5, 10 in the 17th century. He described what he saw as "animicules" and related them by inference to disease. He was also probably the first person to recognize the protective effect on bacteria of the properties of biofilms when he described the effect of vinegar upon the animicules in vivo and in vitro. His observations were not remarked upon and the bacterial aetiology of periodontitis was not accepted until the latter part of the 19th century following the seminal work on the germ theory of disease of Pasteur, Koch and Lister.11 Adolph Witzel12 (1847-1906) appears to be the first individual to identify bacteria as the cause of periodontal disease but the first true oral microbiologist was WD Miller13 (1853-1907). Until then it was widely accepted that periodontal disease was largely related to systemic factors. The importance of local factors was, however, recognized by many practitioners. John W Riggs14 (1811-1885), a leading authority on the treatment of periodontal disease, and who incidentally was Mark Twain's periodontist, clearly recognized the importance of local irritants in the aetiology of periodontal disease. Although he published little he lectured extensively, if controversially, on the treatment of periodontal disease with the emphasis on the removal of local factors rather than on systemic factors. For many years, particularly in America, periodontitis was known as "Riggs' disease".

In the 19th century, little was understood about the aetiology and pathogenesis of periodontal diseases. Classification was made on the basis of their clinical characteristics or theories on their aetiology and was unsupported by any evidence base. The term "pyorrhea alveolaris" was introduced early in the 19th century to describe periodontitis and literally meant "pus oozing out of the alveolus". This suggested that the bone in periodontitis was infected. This, unfortunately, was incorrect but influenced treatment of periodontitis for many years toward the removal of infected marginal bone via flap surgery.

It had long been recognized clinically that there appeared to be different types of periodontal disease and various attempts were made to define them. Gottlieb in 1921 attempted to split up the broad field of pyorrhea alveolaris into schmutz pyorrhea or filth pyorrhea, paradontal pyorrhea where there is deep seated disease within the gingival crevice that hygiene measures do not alleviate, diffuse atrophy of the alveolar bone and accelerated eruption.16 Fish17 described pyorrhea simplex where there is gradual equal deepening of the sulcus and pyorrhea profunda where isolated deep pockets existed with little general deepening of the sulcus around most teeth. Stillman and McCall18 argued for the terms, gingivitis, ulatrophia, alveoloclasia, and pericementoclasia for disease processes attacking primarily the gingival tissues, the pericementum or the alveolar bone. Box19 divided chronic periodontitis into complex and simplex, and forcefully ascribed a prominent role for occlusal trauma in the aetiology of complex and, interestingly, cites in support of his theory an article published in the Dental Science Journal of Australia in 1926 by R Morse Withycombe, the first periodontist to practise in Sydney, Australia.

The terms simplex and complex gained fairly wide acceptance. Definitions, however, varied. MacPhee and Cowley21 defined simplex as being characterized by pocket formation of regular depth throughout the mouth and a pattern of horizontal bone loss. Complex was characterized by advanced tissue destruction relative to the age of the patient, pocket formation of irregular depth around the mouth and irregular vertical bone loss. Complex also inferred that the disease was not a simple response to local irritants but suggested a co-factor in the aetiology, such as systemic factors or local co-factors such as occlusal trauma. Many texts, however, continued to classify inflammatory periodontal disease simply as gingivitis and periodontitis.22, 23

I.
Adult periodontitis

II.
Early-onset periodontitis

III.
Periodontitis associated with systemic disease

IV.
Necrotizing ulcerative periodontitis

V.
Refractory periodontitis

This classification was based upon:

1
Presence/absence of clinically detectable inflammation.

2
Extent and pattern of attachment loss.

3
Patient's age at onset.

4
Rate of progression.

5
Presence/absence of miscellaneous signs and symptoms, including pain, ulceration and amount of observable plaque and calculus.

There were, however, voices of dissent at the workshop regarding this process. Hubert Newman, for example, argued that all periodontal diseases could be classified along the lines of conventional pathology as had been done previously.

Classification - the current situation

The 1999 AAP Classification28 ( Fig 2) is encyclopaedic. It is very complete, detailed and complex and perhaps does not lend itself for use in its entirety on a daily basis by practitioners. A more convenient and simplified summary is:

I.
Gingival diseases

A.
Plaque induced

B.
Non-plaque induced

II.
Chronic periodontitis

A.
Localized

B.
Generalized

III.
Aggressive periodontitis

A.
Localized

B.
Generalized

IV.
Periodontitis as a manifestation of systemic disease

V.
Necrotizing periodontal diseases

VI.
Abscesses of the periodontium

VII.
Periodontitis associated with endodontic lesions

VIII.
Developmental or acquired deformities and conditions.

Gingival conditions

This is an important inclusion in the classification. Gingival lesions are classified into two broad categories. Plaque induced and non-plaque induced. Dental plaque induced lesions (gingivitis) may be purely plaque related with or without local contributing factors ( Fig 3) or may be modified by systemic factors, medications ( Fig 4) or by malnutrition. It should be noted that, although by definition gingivitis has been traditionally described as being associated with a periodontium where there has been no loss of attachment, it is possible for gingivitis to occur on a periodontium with a reduced attachment level which is stable and not experiencing progressive loss of attachment. Non-plaque induced gingival lesions encompass those caused by specific bacterial, fungal or viral infections, genetic origin, systemic conditions (dermatological conditions, allergic reactions), foreign body reactions, trauma lesions and a catch all, not otherwise specified, for forms of gingivitis that do not fit neatly into any of the other areas. Figure 5 illustrates a dermatological disease, lichen planus which is common, may occur in the mouth without skin lesions and is frequently confused and misdiagnosed as plaque induced gingivitis. Note the severe erythema of the attached gingiva and the presence of cheek lesions and an ulcer opposite the second molar.

Chronic periodontitis

"Chronic periodontitis", in the 1999 classification, has replaced the term "adult periodontitis". It was felt that adult periodontitis was an inappropriate term as, although it was the most common form of periodontitis in adults, it could also be seen in adolescents and occasionally children. The term "chronic" was chosen as it was felt to be non-specific and not age dependant and thus less restrictive. It may be either localized or generalized, depending upon the number of sites affected. Localized periodontitis is described as 30 per cent or less of sites affected and generalized periodontitis being more than 30 per cent of sites affected.

*
most prevalent in adults, but can occur in children and adolescents;

*
amount of destruction is consistent with the presence of local factors;

*
subgingival calculus is a frequent finding;

*
associated with a variable microbial pattern;

*
slow to moderate rate of progression, but may have periods of rapid progression;

*
can be further classified on the basis of extent and severity;

*
can be associated with local predisposing factors (e.g., tooth-related or iatrogenic factors);

*
may be modified by and/or associated with systemic diseases (e.g., diabetes mellitus, HIV infection);

*
can be modified by factors other than systemic disease such as cigarette smoking and emotional stress.

The workshop also produced the following working definition and features of chronic periodontitis: "An infectious disease resulting in inflammation within the supporting structures of teeth, progressive attachment and bone loss. It is characterized by pocket formation and/or gingival recession. It is recognized as the most frequently occurring form of periodontitis. Its onset may be at any age but is most commonly detected in adults. The prevalence and severity of the disease increases with age. It may affect a variable number of teeth and has variable rates of progression."

As a guide, severity of the disease has traditionally been characterized as being slight or early where bone loss is in the coronal third of the root, moderate where bone loss is in the middle third of the root and advanced when in the apical third of the root length. The workshop categorized a general guide for severity on the basis of clinical loss of attachment (CAL) as follows: slight = 1-2 mm CAL; moderate = 3 to 4 mm CAL; and severe = 5 mm CAL.

Signs of inflammation are often variable depending upon the patient's plaque control. As the disease progresses mobility and migration of teeth, which may be individual or segmental, may occur. Figure 6 shows a generalized advanced chronic periodontitis in a 55-year-old female. Note the lack of marked inflammation, presence of gingival recession, calculus and anterior migration with the opening of a diastema. The radiograph shows advanced bone loss which is both horizontal and vertical.

Aggressive periodontitis

Aggressive periodontitis replaces the category "early onset periodontitis" which in the 1989 AAP and 1993 European classifications embraced a number of diseases affecting young patients. It was felt that the use of this new term addressed the clinical characteristics of the disease while avoiding the controversial age barrier. While generally patients in this category would be under the age of 30, it is recognized that older patients may also experience periods of more rapid attachment loss. It also avoids the dilemma frequently confronted using the 1989 classification as to where to place certain patients. For example, deciding whether a young adult with generalized periodontal destruction has rapidly progressive periodontitis or generalized juvenile periodontitis under the 1989 classification highlights the problem with age dependency and rates of progression. A diagnosis of generalized juvenile periodontitis, which has persisted into adulthood, requires knowledge of the time of onset. Alternatively, the condition may be a rapidly progressive periodontitis. However, making this diagnosis requires knowledge of rates of progression and time of onset which can only be gained from previous records, which in many cases may or may not be available ( Fig 7). Further, is it appropriate to classify it as a juvenile periodontitis when the patient is now an adult? Should the classification be changed to something else and, if so, what? It may not fit into any of our categories. One purpose of a classification system is to provide a framework in which to undertake orderly treatment of a disease. In this instance the classification system is contributing to confusion and is not suggesting appropriate treatment. Should we be carrying out treatment appropriate for a rapidly progressive disease or treatment for a generalized juvenile periodontitis which may no longer be rapidly progressive? Localized juvenile periodontitis has a circumpubertal onset and progresses very rapidly for a number of years then frequently goes into remission,32 becoming more generalized and, as Suzuki33 suggests, clinically similar to adult (chronic) periodontitis. Thus, we may be treating what under the 1999 classification is a chronic periodontitis. The new classification system attempts to avoid these problems by simplifying the diagnosis. The treatment dilemma, however, may still exist with the new classification when we have imperfect knowledge of the disease history.

The workshop decided to discard all classifications that were age dependant or where knowledge of rates of progression was required. Patients previously classified as having rapidly progressive periodontitis were classified as having either generalized aggressive periodontitis or chronic periodontitis, depending upon their clinical characteristics. The term localized juvenile periodontitis was replaced by localized aggressive periodontitis, and prepubertal periodontitis was removed as a separate disease category. In most patients given the classification of generalized prepubertal periodontitis, the periodontitis was found to be a manifestation of a systemic disease. Those prepubescent children with periodontitis without any modifying systemic conditions would fit under the chronic or aggressive disease categories.

Secondary features that are generally, but not universally, present are:

*
amounts of microbial deposits are inconsistent with the severity of periodontal tissue destruction;

*
elevated proportions of Actinobacillus actinomycetemcomitans ( Aggregatibacter actinomycetemcomitans) and, in some populations, Porphyromonas gingivalis may be elevated;

*
phagocyte abnormalities;

*
hyper-responsive macrophage phenotype, including elevated levels of PGE ₂ and IL-1β;

*
progression of attachment loss and bone loss may be self arresting.

Further specific features were identified:

Localized aggressive ( Fig 8)

*
circumpubertal onset;

*
localized first molar/incisor presentation 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 to infecting agents.

Generalized aggressive ( Fig 9)

*
usually affecting persons under 30 years of age, but patients may be older;

*
poor serum antibody response to infecting agents;

*
pronounced episodic nature of the destruction of attachment and alveolar bone;

*
generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors.

The workshop noted that factors which modify risk, such as cigarette smoking, stress, drugs or sex hormones, which affect the course of all types of periodontal disease, may be added to these primary descriptors to further describe the type of disease being managed or studied.

Periodontitis as a manifestation of systemic disease

This category has been redefined to include only those diseases where the periodontal disease is a manifestation of the disease process and excludes those which act as modifiers of all types of periodontal disease. This includes various haematological disorders such as acquired neutropenia and leukaemia; various genetic disorders such as familial and cyclic neutropenia ( Fig 10), Down syndrome ( Fig 11), leukocyte adhesion deficiency syndrome, Papillon-Lefèvre syndrome, Chediak-Higashi syndrome, histiocytosis syndromes, hypophosphatasia and others.35 Other diseases such as HIV and diabetes ( Fig 12) were considered to be modifiers of both chronic and aggressive periodontitis. It was concluded that there was insufficient evidence that there is a specific periodontitis associated with these diseases.28

Necrotizing periodontal disease

The workshop recognized that necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative peridontitis (NUP) were clinically distinguishable disease entities but were unsure as to whether they were part of the same disease process or were two distinct diseases. They concluded that there was insufficient data to resolve this problem, thus they decided to place both conditions in the one category of "necrotizing periodontal disease".36 Certainly clinical observation would suggest that they are part of a continuum with initial infections perhaps showing little or no clinically recognizable attachment loss despite soft tissue destruction of the papillary tissue. However, with recurrent infections, to which these patients are prone, the attachment loss becomes more apparent. Figure 13 shows necrotizing ulcerative gingivitis in a 21-year-old law student taken during his final year examinations. This patient was under stress, was smoking tobacco heavily and had a history of "bleeding gums" (pre-existing gingivitis). These are common predisposing factors for necrotizing periodontal disease. He complained of painful gingival tissues, of sudden onset. Note the marked gingival erythema and oedema, loss of papillary tissue with punched out crater ulcers and spread of the ulceration to the marginal tissue with obvious bleeding. Necrotizing ulcerative gingivitis tends to be recurrent if predisposing factors remain and progresses to necrotizing ulcerative periodontitis, in some cases causing severe destruction of the periodontal tissues ( Fig 14). This condition is commonly associated also with HIV infection ( Fig 12) and because of this there has been some discussion as to whether it should be included under manifestation of systemic diseases. However, it is likely that HIV acts as a predisposing factor by lowering host resistance.

Periodontal abscess

Periodontal abscess was added as a separate category. It was felt that, although periodontal abscess formation is a clinical feature of both chronic and aggressive periodontitis, it presents as a distinct clinical entity that requires specific diagnosis and treatment and thus deserves a separate classification. In most cases periodontal abscess formation reflects the acute exacerbation of a pre-existing periodontal pocket ( Fig 15). It may be more correctly called an acute periodontitis. Abscesses may occur because of other causes such as foreign body impaction, trauma, including occlusal trauma causing vertical and horizontal root fractures or cemental tears. They can present a diagnostic dilemma, so perhaps a separate classification is justified.

Periodontal-endodontic lesions

The workshop included a single category, the "combined lesion" where an endodontic lesion is draining through a pre-existing periodontal pocket.

Developmental or acquired deformities and conditions

This category appears to have been added for completeness. It includes localized tooth related factors and mucogingival conditions which may modify or predispose to disease. Many of these conditions do not constitute disease entities in their own rights but they modify and alter susceptibility to disease. Therefore, it is debatable whether they should be included in a disease classification. Occlusal trauma, primary and secondary is included. Primary occlusal trauma, where an injury to the attachment or tooth is the result of excessive occlusal forces, is recognized as a condition. However, secondary occlusal trauma, where normal forces cause a traumatic lesion in a periodontium with reduced support is a debatable and perhaps doubtful phenomena. Conditions such as recession, excessive gingival display and ridge deformities which may require treatment for reasons other than treatment of disease, are also included and this is easier to justify.

Diagnosis

Once a diagnosis of disease has been made, the disease may be classified according to the criteria of the classification system. This process of diagnosis, while it may be valid for diagnosis of periodontal disease for clinical management in dental practice presents problems when trying to determine what constitutes periodontal disease in order to undertake clinical studies.39 The problem is that our diagnosis is made upon an assessment of the destruction caused by the disease and not by an assessment of the presence of a destructive disease process within the periodontal tissues using the means usually used in assessing other diseases in medicine, such as the identification through biochemical markers, identification of responsible microbes or identification by histopathology. As Caton40 says "periodontitis by definition is inflammation of the supporting structures of the teeth - usually a progressive destructive change leading to loss of bone and periodontal ligament. Periodontal disease activity refers to the stage of the disease characterized by loss of supporting bone and tissue attachment. This implies the natural history of periodontal disease is marked by periods of active destruction and relative quiescence, even though the periodontal tissues remain relatively inflamed". This may not appear on the surface to be of great consequence in clinical practice when confronted with a patient with obvious periodontal inflammation, attachment loss and probing depth. However, it does pose problems in recognizing the presence or absence of a destructive disease process in the tissues particularly when monitoring treatments and in designing research studies. Does a patient who has been treated with non-surgical periodontal treatment and now has a number of sites with residual probing depths that bleed on probing still have a periodontitis that requires further active therapy or surgical treatment, or is the condition stable and the disease in remission? Similarly, do patients recruited into a research study on the basis of certain criteria such as more than 30 per cent of teeth affected with pockets of ≥ 4 mm all have active periodontitis, and are the results of these studies valid and comparable? This may partly explain the confusing and often contradictory results of published research on the same topic in the literature. Problems in using different criteria for defining periodontal disease were illustrated in a recent article by Manau et al.,41 where the authors reanalysed their original data on the relationship between periodontitis and pregnancy using 14 different periodontitis definitions obtained from other publications. They found that the periodontal disease definition used influenced the association found between the presence of periodontitis and the association with adverse outcomes. Six of the 14 definitions of periodontitis resulted in a statistically significant association of periodontitis with adverse pregnancy outcomes while the other eight found no significant association.

Our diagnostic tools, as Preshaw25 says, are "crude". He further states "we do not (yet) have the luxury of accurate, precise and reproducible indicators of periodontal disease". Much research has been done to determine accurate markers or indicators of disease.29, 40 In addition to traditional diagnostic procedures, assessments of inflammation and damage to the periodontal tissues, these indicators include biochemical mediators as markers, microbiological diagnostic procedures, immunological methods and genetic methods. Despite extensive research into biochemical and microbiological markers, several of which have been developed into commercial products, little of value to the clinician has evolved. One product which was marketed for a brief time used the ability of three putative periodontal pathogens, B. gingivalis, B. forsythus and Trepenoma denticola, to hydrolyze the synthetic trypsin substrate, N-benzoyl-DL-arginine-2-naphthylamide (BANA) forming a colour reaction to detect the presence of these putative periodontal pathogens in the subgingival plaque.42 Another detected the presence of aspartate aminotransferase (AST) in the gingival fluid.43 AST is an enzyme present in all cells and released in abundance on cell death. In medicine it is used as a non-specific marker of cell death and routinely used as a diagnostic indicator of myocardial infarction. Gingival crevicular fluid (GCF) levels of AST have been shown to increase with inflammation and there is evidence that AST levels in GCF correlate with disease activity as assessed by probing attachment loss and with severe gingivitis.44 The problem with the test was in distinguishing between severe gingivitis and disease activity. These tests added little to our diagnostic ability and their place in clinical practice was unclear. There was uncertainty about their ability to reliably distinguish between sites that were progressing and sites that were inflamed but not progressing. Periodontal pathogens are found in sites with and without disease activity and also in population groups resistant to periodontitis.45 AST is found at sites with gingivitis, non-progressing and progressing lesions thus the ability of the test to discriminate is questionable.46 Some microbiologic investigations such as DNA probes and monoclonal antibody investigations may be of use particularly in the treatment of refractory forms of periodontitis.

Therefore, despite enormous research there has been no major breakthrough in diagnosis of periodontal diseases. Although there have been major advances in our understanding of periodontal diseases, we still must rely upon our traditional diagnostic procedures, assessment of inflammation and assessment of damage to the periodontal tissues. Signs of inflammation indicate that the tissues are no longer healthy but cannot distinguish between gingivitis and periodontitis. Signs of inflammation must be evaluated in combination with evidence of attachment loss and probing depth. Inflamed periodontal tissues may exhibit some or all of the cardinal signs of inflammation, rubor (redness), tumor (swelling), calor (heat), dolor (pain) and functio laesa (loss of function), although the two last signs usually occur late in the disease process. In periodontal disease we may also diagnose bleeding on probing, suppuration, and increased gingival fluid flow. Bleeding on probing and suppuration are generally used by clinicians as presumptive indicators of disease activity. Bleeding on probing, while a reliable indicator of gingival inflammation,47 correlates poorly with disease activity and is a poor predictor of the progression of periodontitis.48, 49 A good diagnostic test should have high sensitivity, the ability to detect true negatives (unlikely to be negative if someone has the disease), and high specificity, the ability to detect true positives (unlikely to be positive if someone truly does not have the disease). Sensitivity, however, often comes at the expense of specificity and vice versa. Bleeding on probing has low specificity for predicting disease activity, however sensitivity is apparently high.40 The use of bleeding on probing as a primary diagnostic tool means that we may be treating sites which are inactive. Conversely, the absence of bleeding on probing is used by clinicians as an indicator of periodontal stability.50 Suppuration has a high specificity for further disease progression in populations with a high prevalence of periodontitis.29, 51 One would suspect that most practitioners would find the presence of suppuration disturbing.

Conclusions

Despite intensive research efforts to develop new technologies to improve diagnostic ability, traditional diagnostic procedures based upon clinical signs of inflammation, probing depths and clinical attachment loss still form the basis upon which periodontal diagnosis is made. Absence of gingival inflammation and shallow probing depths have a strong negative predictive values for periodontal stability.48, 53 The clinician should strive to achieve this endpoint in the treatment of our patients.

Diagnosis of the disease also involves classification. Systems of classification are continually evolving. Classification of periodontal diseases is difficult and all classification systems produced to date have their imperfections and their critics. Van der Velden54 argued that the 1999 reclassification was not helpful and suggested a classification based on age, which appears to be a simplified version of the 1989 AAP classification, and further classified on the basis of extent, severity and clinical characteristics. This classification allows the possibility of making an accurate clinical diagnosis for any patient with periodontitis. Milward and Chapple,56 while recognizing the 1999 World Workshop attempted to produce a classification from an evidence-based perspective, criticized the 1999 classification as being unnecessarily complex and not suited for routine general dental practice. Lopez and Baelum57 argue from an epidemiological point of view that there is little justification for the use of complicated classification systems and favour an approach based upon simple clinical attachment loss measurements such as ≥ 3 mm etc., a minimalist approach that does not try to differentiate between different types of periodontitis.

Why is classification of periodontal disease so difficult and so controversial? The answer lies in the heterogenicity of the clinical presentation and our lack of understanding of the true nature of the differences between the different clinical presentations of the disease. We attempt to classify using evidence based upon the different infections represented and on the host response. However, in most cases our knowledge is incomplete or confused. Much of the certitude that was felt in the 1980s that we had reached a point where we could truly distinguish between the different disease presentations in a scientific manner, has largely evaporated. It is of interest that localized juvenile periodontitis (LJP), one disease which has long been recognized as being a distinct or separate disease entity on the basis of clinical characteristics, microbiological factors and host response, the features of which are well documented, has been discarded as a distinct disease entity and has been reclassified as localized aggressive periodontitis. This apparently was done to conform to the predetermined criteria of the classification and in particular the removal of the emphasis on age. However, I have yet to see an LJP in anyone other than a juvenile and the circumpubertal age of onset is an integral part of the disease description and its deletion does not appear to have been a progressive step. We should also consider that perhaps there is just one periodontitis with different clinical expressions in different hosts.

Armitage,15 in a thoughtful article on classification, stated that "the classification system proposed by the '1999 International Workshop for a Classification of Periodontal Diseases and Conditions' has corrected some of the problems associated with the previous system that had been in use since 1989. Nevertheless, the new system is far from perfect and will need to be modified once there are sufficient new data to justify revisions". He is of the opinion that current disease designations such as "chronic periodontitis" are constellations of polymicrobial and polygenic infections whose clinical expression is altered by important environmental and host modifying conditions.

It would seem that we are trying to classify diseases of which we do not have sufficient knowledge. The present classification of periodontitis looks surprisingly like a return to simplex and complex. Until we have greater understanding of the aetiology, the bacteria associated with different periodontal infections and the pathogenesis and genetics of periodontal diseases, it is very likely that we will see further reclassifications at regular intervals.

Abstract

Periodontal diseases have been recognized and treated for at least 5000 years. Clinicians have recognized for many years that there are apparent differences in the presentation of periodontal diseases and have attempted to classify these diseases. Systems of classifications of disease have arisen allowing clinicians to develop structures which can be used to identify diseases in relation to aetiology, pathogenesis and treatment. It allows us to organize effective treatment of our patients' diseases. Once a disease has been diagnosed and classified, the aetiology of the condition and appropriate evidence-based treatment is suggested to the clinician. Common systems of classification also allow effective communication between health care professionals using a common language. Early attempts at classification were made on the basis of the clinical characteristics of the diseases or on theories of their aetiology. These attempts were unsupported by any evidence base. As scientific knowledge expanded, conventional pathology formed the basis of classification. More recently, this has been followed by systems of classification based upon our knowledge of the various periodontal infections and the host response to them. Classification of periodontal diseases has, however, proved problematic. Over much of the last century clinicians and researchers have grappled with the problem and have assembled periodically to review or develop the classification of the various forms of periodontal disease as research has expanded our knowledge of these diseases. This has resulted in frequent revisions and changes. A classification, however, should not be regarded as a permanent structure. It must be adaptable to change and evolve with the development of new knowledge. It is expected that systems of classification will change over time. This review examines the past and present classifications of the periodontal diseases.

Abbreviations and acronyms

AST

aspartate aminotransferase

CAL

clinical loss of attachment

GCF

gingival crevicular fluid

LJP

localized juvenile periodontitis

NUG

necrotizing ulcerative gingivitis

NUP

necrotizing ulcerative peridontitis

Introduction

Periodontal disease is a disease, or more likely a number of diseases of the periodontal tissues that results in attachment loss and destruction of alveolar bone. The natural history of periodontal disease, in some but not all patients, results in tooth loss.1 Periodontal disease, however, encompasses a wider spectrum of diseases than just periodontitis and the recognition of these diseases requires a diagnosis be made.

Diagnosis is the recognition of the presence of a disease.2 Clinical diagnosis of periodontal disease is made by the recognition of various signs and symptoms in the periodontal tissues which herald a departure from health. The diagnosis of periodontal disease demands a firm knowledge of what constitutes periodontal health. The healthy periodontium,3 of which only the gingival tissues may be directly observed, is described as being stippled, pale pink or coral pink, in the Caucasian ( Fig 1), with various degrees of pigmentation in other races. It is tightly adapted to the underlying tissues, with a knife edge margin where it abuts the tooth, The gingival margin is located, in the absence of pathology, at the cemento-enamel junction. It displays a scalloped edge configuration highest interdentally, where it constitutes the interdental papilla and lowest buccally and lingually. There is a gingival crevice where it abuts the tooth which in health is 1-3 mm deep. There is an absence of bleeding from the crevice on gentle probing. The crevice in health will show a small amount of interstitial fluid, gingival crevicular fluid.4 The lateral wall of the crevice constitutes the free gingival margin. From the most apical extent of the free gingival to the mucogingival junction is the attached gingival which varies in width from 1 to 9 mm and has a stippled surface. It is an immobile tissue tightly bound down to the bone as a mucoperiostium and is a keratinized mucosa well suited to resist injury. Apical from the mucogingival junction and continuous with the lining mucosa of the mouth is the alveolar mucosa, which is freely mobile and surmounted by a non-keratinized epithelium. It is generally thought that alveolar mucosa functions poorly as a marginal tissue and areas where there is lack of attached gingival may constitute mucogingival problems. Departures from this concept of the healthy periodontium may suggest the presence of disease. The relevant changes which are diagnostic of the presence of disease will be discussed later in this paper.

Systems of classifications of disease have arisen to allow clinicians to develop a structure which can be used to identify diseases in relation to aetiology, pathogenesis and treatment. It allows us to organize effective treatment of our patient's disease. Once a disease has been diagnosed and classified, the aetiology of the condition and appropriate evidence-based treatment is suggested to the clinician. Classification systems also allow the clinicians and researchers everywhere to communicate with a common language.

The most commonly accepted systems of classification of periodontal disease have been those of the American Academy of Periodontology (AAP). Over much of the last century, the Academy has struggled to identify and classify the various forms of periodontal disease as research has expanded knowledge. This has led to frequent revisions and changes but has created some confusion. A classification, however, should not be regarded as a permanent structure. It must be adaptable to change and evolve with the development of new knowledge. It must be expected that systems of classification will change over time, however much this may be confusing and perhaps annoying to practitioners.

This article is a review of the historical and contemporary attempts to classify periodontal diseases.

Historical perspective

Recognition and treatment of periodontal disease can be traced back to antiquity. Descriptions of treatment are found in ancient Egyptian and Chinese writings and would suggest that periodontal diseases were recognized possibly 5000 years ago.5 The first modern writings were by Abu I Quasim, also known as Abuccusis of Cordova Spain in the 10th century.6 More recently, descriptions of treatment of periodontal disease were made by Pierre Fauchard7 who published the first dental textbook, "The Surgeon Dentist" in 1728 and John Hunter8 who published "The Natural History of the Human Teeth" in 1771 and "A Practical Treatise on the Diseases of the Teeth" in 1778. Although there was already a considerable body of writings on dentistry, possibly in excess of 450 treatises in existence before this one,9 Hunter provided the scientific foundations of modern dentistry. The presence of bacteria around the teeth was recognized by Von Leeuwenhoek5, 10 in the 17th century. He described what he saw as "animicules" and related them by inference to disease. He was also probably the first person to recognize the protective effect on bacteria of the properties of biofilms when he described the effect of vinegar upon the animicules in vivo and in vitro. His observations were not remarked upon and the bacterial aetiology of periodontitis was not accepted until the latter part of the 19th century following the seminal work on the germ theory of disease of Pasteur, Koch and Lister.11 Adolph Witzel12 (1847-1906) appears to be the first individual to identify bacteria as the cause of periodontal disease but the first true oral microbiologist was WD Miller13 (1853-1907). Until then it was widely accepted that periodontal disease was largely related to systemic factors. The importance of local factors was, however, recognized by many practitioners. John W Riggs14 (1811-1885), a leading authority on the treatment of periodontal disease, and who incidentally was Mark Twain's periodontist, clearly recognized the importance of local irritants in the aetiology of periodontal disease. Although he published little he lectured extensively, if controversially, on the treatment of periodontal disease with the emphasis on the removal of local factors rather than on systemic factors. For many years, particularly in America, periodontitis was known as "Riggs' disease".

In the 19th century, little was understood about the aetiology and pathogenesis of periodontal diseases. Classification was made on the basis of their clinical characteristics or theories on their aetiology and was unsupported by any evidence base. The term "pyorrhea alveolaris" was introduced early in the 19th century to describe periodontitis and literally meant "pus oozing out of the alveolus". This suggested that the bone in periodontitis was infected. This, unfortunately, was incorrect but influenced treatment of periodontitis for many years toward the removal of infected marginal bone via flap surgery.

It had long been recognized clinically that there appeared to be different types of periodontal disease and various attempts were made to define them. Gottlieb in 1921 attempted to split up the broad field of pyorrhea alveolaris into schmutz pyorrhea or filth pyorrhea, paradontal pyorrhea where there is deep seated disease within the gingival crevice that hygiene measures do not alleviate, diffuse atrophy of the alveolar bone and accelerated eruption.16 Fish17 described pyorrhea simplex where there is gradual equal deepening of the sulcus and pyorrhea profunda where isolated deep pockets existed with little general deepening of the sulcus around most teeth. Stillman and McCall18 argued for the terms, gingivitis, ulatrophia, alveoloclasia, and pericementoclasia for disease processes attacking primarily the gingival tissues, the pericementum or the alveolar bone. Box19 divided chronic periodontitis into complex and simplex, and forcefully ascribed a prominent role for occlusal trauma in the aetiology of complex and, interestingly, cites in support of his theory an article published in the Dental Science Journal of Australia in 1926 by R Morse Withycombe, the first periodontist to practise in Sydney, Australia.

The terms simplex and complex gained fairly wide acceptance. Definitions, however, varied. MacPhee and Cowley21 defined simplex as being characterized by pocket formation of regular depth throughout the mouth and a pattern of horizontal bone loss. Complex was characterized by advanced tissue destruction relative to the age of the patient, pocket formation of irregular depth around the mouth and irregular vertical bone loss. Complex also inferred that the disease was not a simple response to local irritants but suggested a co-factor in the aetiology, such as systemic factors or local co-factors such as occlusal trauma. Many texts, however, continued to classify inflammatory periodontal disease simply as gingivitis and periodontitis.22, 23

I.
Adult periodontitis

II.
Early-onset periodontitis

III.
Periodontitis associated with systemic disease

IV.
Necrotizing ulcerative periodontitis

V.
Refractory periodontitis

This classification was based upon:

1
Presence/absence of clinically detectable inflammation.

2
Extent and pattern of attachment loss.

3
Patient's age at onset.

4
Rate of progression.

5
Presence/absence of miscellaneous signs and symptoms, including pain, ulceration and amount of observable plaque and calculus.

There were, however, voices of dissent at the workshop regarding this process. Hubert Newman, for example, argued that all periodontal diseases could be classified along the lines of conventional pathology as had been done previously.

Classification - the current situation

The 1999 AAP Classification28 ( Fig 2) is encyclopaedic. It is very complete, detailed and complex and perhaps does not lend itself for use in its entirety on a daily basis by practitioners. A more convenient and simplified summary is:

I.
Gingival diseases

A.
Plaque induced

B.
Non-plaque induced

II.
Chronic periodontitis

A.
Localized

B.
Generalized

III.
Aggressive periodontitis

A.
Localized

B.
Generalized

IV.
Periodontitis as a manifestation of systemic disease

V.
Necrotizing periodontal diseases

VI.
Abscesses of the periodontium

VII.
Periodontitis associated with endodontic lesions

VIII.
Developmental or acquired deformities and conditions.

Gingival conditions

This is an important inclusion in the classification. Gingival lesions are classified into two broad categories. Plaque induced and non-plaque induced. Dental plaque induced lesions (gingivitis) may be purely plaque related with or without local contributing factors ( Fig 3) or may be modified by systemic factors, medications ( Fig 4) or by malnutrition. It should be noted that, although by definition gingivitis has been traditionally described as being associated with a periodontium where there has been no loss of attachment, it is possible for gingivitis to occur on a periodontium with a reduced attachment level which is stable and not experiencing progressive loss of attachment. Non-plaque induced gingival lesions encompass those caused by specific bacterial, fungal or viral infections, genetic origin, systemic conditions (dermatological conditions, allergic reactions), foreign body reactions, trauma lesions and a catch all, not otherwise specified, for forms of gingivitis that do not fit neatly into any of the other areas. Figure 5 illustrates a dermatological disease, lichen planus which is common, may occur in the mouth without skin lesions and is frequently confused and misdiagnosed as plaque induced gingivitis. Note the severe erythema of the attached gingiva and the presence of cheek lesions and an ulcer opposite the second molar.

Chronic periodontitis

"Chronic periodontitis", in the 1999 classification, has replaced the term "adult periodontitis". It was felt that adult periodontitis was an inappropriate term as, although it was the most common form of periodontitis in adults, it could also be seen in adolescents and occasionally children. The term "chronic" was chosen as it was felt to be non-specific and not age dependant and thus less restrictive. It may be either localized or generalized, depending upon the number of sites affected. Localized periodontitis is described as 30 per cent or less of sites affected and generalized periodontitis being more than 30 per cent of sites affected.

*
most prevalent in adults, but can occur in children and adolescents;

*
amount of destruction is consistent with the presence of local factors;

*
subgingival calculus is a frequent finding;

*
associated with a variable microbial pattern;

*
slow to moderate rate of progression, but may have periods of rapid progression;

*
can be further classified on the basis of extent and severity;

*
can be associated with local predisposing factors (e.g., tooth-related or iatrogenic factors);

*
may be modified by and/or associated with systemic diseases (e.g., diabetes mellitus, HIV infection);

*
can be modified by factors other than systemic disease such as cigarette smoking and emotional stress.

The workshop also produced the following working definition and features of chronic periodontitis: "An infectious disease resulting in inflammation within the supporting structures of teeth, progressive attachment and bone loss. It is characterized by pocket formation and/or gingival recession. It is recognized as the most frequently occurring form of periodontitis. Its onset may be at any age but is most commonly detected in adults. The prevalence and severity of the disease increases with age. It may affect a variable number of teeth and has variable rates of progression."

As a guide, severity of the disease has traditionally been characterized as being slight or early where bone loss is in the coronal third of the root, moderate where bone loss is in the middle third of the root and advanced when in the apical third of the root length. The workshop categorized a general guide for severity on the basis of clinical loss of attachment (CAL) as follows: slight = 1-2 mm CAL; moderate = 3 to 4 mm CAL; and severe = 5 mm CAL.

Signs of inflammation are often variable depending upon the patient's plaque control. As the disease progresses mobility and migration of teeth, which may be individual or segmental, may occur. Figure 6 shows a generalized advanced chronic periodontitis in a 55-year-old female. Note the lack of marked inflammation, presence of gingival recession, calculus and anterior migration with the opening of a diastema. The radiograph shows advanced bone loss which is both horizontal and vertical.

Aggressive periodontitis

Aggressive periodontitis replaces the category "early onset periodontitis" which in the 1989 AAP and 1993 European classifications embraced a number of diseases affecting young patients. It was felt that the use of this new term addressed the clinical characteristics of the disease while avoiding the controversial age barrier. While generally patients in this category would be under the age of 30, it is recognized that older patients may also experience periods of more rapid attachment loss. It also avoids the dilemma frequently confronted using the 1989 classification as to where to place certain patients. For example, deciding whether a young adult with generalized periodontal destruction has rapidly progressive periodontitis or generalized juvenile periodontitis under the 1989 classification highlights the problem with age dependency and rates of progression. A diagnosis of generalized juvenile periodontitis, which has persisted into adulthood, requires knowledge of the time of onset. Alternatively, the condition may be a rapidly progressive periodontitis. However, making this diagnosis requires knowledge of rates of progression and time of onset which can only be gained from previous records, which in many cases may or may not be available ( Fig 7). Further, is it appropriate to classify it as a juvenile periodontitis when the patient is now an adult? Should the classification be changed to something else and, if so, what? It may not fit into any of our categories. One purpose of a classification system is to provide a framework in which to undertake orderly treatment of a disease. In this instance the classification system is contributing to confusion and is not suggesting appropriate treatment. Should we be carrying out treatment appropriate for a rapidly progressive disease or treatment for a generalized juvenile periodontitis which may no longer be rapidly progressive? Localized juvenile periodontitis has a circumpubertal onset and progresses very rapidly for a number of years then frequently goes into remission,32 becoming more generalized and, as Suzuki33 suggests, clinically similar to adult (chronic) periodontitis. Thus, we may be treating what under the 1999 classification is a chronic periodontitis. The new classification system attempts to avoid these problems by simplifying the diagnosis. The treatment dilemma, however, may still exist with the new classification when we have imperfect knowledge of the disease history.

The workshop decided to discard all classifications that were age dependant or where knowledge of rates of progression was required. Patients previously classified as having rapidly progressive periodontitis were classified as having either generalized aggressive periodontitis or chronic periodontitis, depending upon their clinical characteristics. The term localized juvenile periodontitis was replaced by localized aggressive periodontitis, and prepubertal periodontitis was removed as a separate disease category. In most patients given the classification of generalized prepubertal periodontitis, the periodontitis was found to be a manifestation of a systemic disease. Those prepubescent children with periodontitis without any modifying systemic conditions would fit under the chronic or aggressive disease categories.

Secondary features that are generally, but not universally, present are:

*
amounts of microbial deposits are inconsistent with the severity of periodontal tissue destruction;

*
elevated proportions of Actinobacillus actinomycetemcomitans ( Aggregatibacter actinomycetemcomitans) and, in some populations, Porphyromonas gingivalis may be elevated;

*
phagocyte abnormalities;

*
hyper-responsive macrophage phenotype, including elevated levels of PGE ₂ and IL-1β;

*
progression of attachment loss and bone loss may be self arresting.

Further specific features were identified:

Localized aggressive ( Fig 8)

*
circumpubertal onset;

*
localized first molar/incisor presentation 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 to infecting agents.

Generalized aggressive ( Fig 9)

*
usually affecting persons under 30 years of age, but patients may be older;

*
poor serum antibody response to infecting agents;

*
pronounced episodic nature of the destruction of attachment and alveolar bone;

*
generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors.

The workshop noted that factors which modify risk, such as cigarette smoking, stress, drugs or sex hormones, which affect the course of all types of periodontal disease, may be added to these primary descriptors to further describe the type of disease being managed or studied.

Periodontitis as a manifestation of systemic disease

This category has been redefined to include only those diseases where the periodontal disease is a manifestation of the disease process and excludes those which act as modifiers of all types of periodontal disease. This includes various haematological disorders such as acquired neutropenia and leukaemia; various genetic disorders such as familial and cyclic neutropenia ( Fig 10), Down syndrome ( Fig 11), leukocyte adhesion deficiency syndrome, Papillon-Lefèvre syndrome, Chediak-Higashi syndrome, histiocytosis syndromes, hypophosphatasia and others.35 Other diseases such as HIV and diabetes ( Fig 12) were considered to be modifiers of both chronic and aggressive periodontitis. It was concluded that there was insufficient evidence that there is a specific periodontitis associated with these diseases.28

Necrotizing periodontal disease

The workshop recognized that necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative peridontitis (NUP) were clinically distinguishable disease entities but were unsure as to whether they were part of the same disease process or were two distinct diseases. They concluded that there was insufficient data to resolve this problem, thus they decided to place both conditions in the one category of "necrotizing periodontal disease".36 Certainly clinical observation would suggest that they are part of a continuum with initial infections perhaps showing little or no clinically recognizable attachment loss despite soft tissue destruction of the papillary tissue. However, with recurrent infections, to which these patients are prone, the attachment loss becomes more apparent. Figure 13 shows necrotizing ulcerative gingivitis in a 21-year-old law student taken during his final year examinations. This patient was under stress, was smoking tobacco heavily and had a history of "bleeding gums" (pre-existing gingivitis). These are common predisposing factors for necrotizing periodontal disease. He complained of painful gingival tissues, of sudden onset. Note the marked gingival erythema and oedema, loss of papillary tissue with punched out crater ulcers and spread of the ulceration to the marginal tissue with obvious bleeding. Necrotizing ulcerative gingivitis tends to be recurrent if predisposing factors remain and progresses to necrotizing ulcerative periodontitis, in some cases causing severe destruction of the periodontal tissues ( Fig 14). This condition is commonly associated also with HIV infection ( Fig 12) and because of this there has been some discussion as to whether it should be included under manifestation of systemic diseases. However, it is likely that HIV acts as a predisposing factor by lowering host resistance.

Periodontal abscess

Periodontal abscess was added as a separate category. It was felt that, although periodontal abscess formation is a clinical feature of both chronic and aggressive periodontitis, it presents as a distinct clinical entity that requires specific diagnosis and treatment and thus deserves a separate classification. In most cases periodontal abscess formation reflects the acute exacerbation of a pre-existing periodontal pocket ( Fig 15). It may be more correctly called an acute periodontitis. Abscesses may occur because of other causes such as foreign body impaction, trauma, including occlusal trauma causing vertical and horizontal root fractures or cemental tears. They can present a diagnostic dilemma, so perhaps a separate classification is justified.

Periodontal-endodontic lesions

The workshop included a single category, the "combined lesion" where an endodontic lesion is draining through a pre-existing periodontal pocket.

Developmental or acquired deformities and conditions

This category appears to have been added for completeness. It includes localized tooth related factors and mucogingival conditions which may modify or predispose to disease. Many of these conditions do not constitute disease entities in their own rights but they modify and alter susceptibility to disease. Therefore, it is debatable whether they should be included in a disease classification. Occlusal trauma, primary and secondary is included. Primary occlusal trauma, where an injury to the attachment or tooth is the result of excessive occlusal forces, is recognized as a condition. However, secondary occlusal trauma, where normal forces cause a traumatic lesion in a periodontium with reduced support is a debatable and perhaps doubtful phenomena. Conditions such as recession, excessive gingival display and ridge deformities which may require treatment for reasons other than treatment of disease, are also included and this is easier to justify.

Diagnosis

Once a diagnosis of disease has been made, the disease may be classified according to the criteria of the classification system. This process of diagnosis, while it may be valid for diagnosis of periodontal disease for clinical management in dental practice presents problems when trying to determine what constitutes periodontal disease in order to undertake clinical studies.39 The problem is that our diagnosis is made upon an assessment of the destruction caused by the disease and not by an assessment of the presence of a destructive disease process within the periodontal tissues using the means usually used in assessing other diseases in medicine, such as the identification through biochemical markers, identification of responsible microbes or identification by histopathology. As Caton40 says "periodontitis by definition is inflammation of the supporting structures of the teeth - usually a progressive destructive change leading to loss of bone and periodontal ligament. Periodontal disease activity refers to the stage of the disease characterized by loss of supporting bone and tissue attachment. This implies the natural history of periodontal disease is marked by periods of active destruction and relative quiescence, even though the periodontal tissues remain relatively inflamed". This may not appear on the surface to be of great consequence in clinical practice when confronted with a patient with obvious periodontal inflammation, attachment loss and probing depth. However, it does pose problems in recognizing the presence or absence of a destructive disease process in the tissues particularly when monitoring treatments and in designing research studies. Does a patient who has been treated with non-surgical periodontal treatment and now has a number of sites with residual probing depths that bleed on probing still have a periodontitis that requires further active therapy or surgical treatment, or is the condition stable and the disease in remission? Similarly, do patients recruited into a research study on the basis of certain criteria such as more than 30 per cent of teeth affected with pockets of ≥ 4 mm all have active periodontitis, and are the results of these studies valid and comparable? This may partly explain the confusing and often contradictory results of published research on the same topic in the literature. Problems in using different criteria for defining periodontal disease were illustrated in a recent article by Manau et al.,41 where the authors reanalysed their original data on the relationship between periodontitis and pregnancy using 14 different periodontitis definitions obtained from other publications. They found that the periodontal disease definition used influenced the association found between the presence of periodontitis and the association with adverse outcomes. Six of the 14 definitions of periodontitis resulted in a statistically significant association of periodontitis with adverse pregnancy outcomes while the other eight found no significant association.

Our diagnostic tools, as Preshaw25 says, are "crude". He further states "we do not (yet) have the luxury of accurate, precise and reproducible indicators of periodontal disease". Much research has been done to determine accurate markers or indicators of disease.29, 40 In addition to traditional diagnostic procedures, assessments of inflammation and damage to the periodontal tissues, these indicators include biochemical mediators as markers, microbiological diagnostic procedures, immunological methods and genetic methods. Despite extensive research into biochemical and microbiological markers, several of which have been developed into commercial products, little of value to the clinician has evolved. One product which was marketed for a brief time used the ability of three putative periodontal pathogens, B. gingivalis, B. forsythus and Trepenoma denticola, to hydrolyze the synthetic trypsin substrate, N-benzoyl-DL-arginine-2-naphthylamide (BANA) forming a colour reaction to detect the presence of these putative periodontal pathogens in the subgingival plaque.42 Another detected the presence of aspartate aminotransferase (AST) in the gingival fluid.43 AST is an enzyme present in all cells and released in abundance on cell death. In medicine it is used as a non-specific marker of cell death and routinely used as a diagnostic indicator of myocardial infarction. Gingival crevicular fluid (GCF) levels of AST have been shown to increase with inflammation and there is evidence that AST levels in GCF correlate with disease activity as assessed by probing attachment loss and with severe gingivitis.44 The problem with the test was in distinguishing between severe gingivitis and disease activity. These tests added little to our diagnostic ability and their place in clinical practice was unclear. There was uncertainty about their ability to reliably distinguish between sites that were progressing and sites that were inflamed but not progressing. Periodontal pathogens are found in sites with and without disease activity and also in population groups resistant to periodontitis.45 AST is found at sites with gingivitis, non-progressing and progressing lesions thus the ability of the test to discriminate is questionable.46 Some microbiologic investigations such as DNA probes and monoclonal antibody investigations may be of use particularly in the treatment of refractory forms of periodontitis.

Therefore, despite enormous research there has been no major breakthrough in diagnosis of periodontal diseases. Although there have been major advances in our understanding of periodontal diseases, we still must rely upon our traditional diagnostic procedures, assessment of inflammation and assessment of damage to the periodontal tissues. Signs of inflammation indicate that the tissues are no longer healthy but cannot distinguish between gingivitis and periodontitis. Signs of inflammation must be evaluated in combination with evidence of attachment loss and probing depth. Inflamed periodontal tissues may exhibit some or all of the cardinal signs of inflammation, rubor (redness), tumor (swelling), calor (heat), dolor (pain) and functio laesa (loss of function), although the two last signs usually occur late in the disease process. In periodontal disease we may also diagnose bleeding on probing, suppuration, and increased gingival fluid flow. Bleeding on probing and suppuration are generally used by clinicians as presumptive indicators of disease activity. Bleeding on probing, while a reliable indicator of gingival inflammation,47 correlates poorly with disease activity and is a poor predictor of the progression of periodontitis.48, 49 A good diagnostic test should have high sensitivity, the ability to detect true negatives (unlikely to be negative if someone has the disease), and high specificity, the ability to detect true positives (unlikely to be positive if someone truly does not have the disease). Sensitivity, however, often comes at the expense of specificity and vice versa. Bleeding on probing has low specificity for predicting disease activity, however sensitivity is apparently high.40 The use of bleeding on probing as a primary diagnostic tool means that we may be treating sites which are inactive. Conversely, the absence of bleeding on probing is used by clinicians as an indicator of periodontal stability.50 Suppuration has a high specificity for further disease progression in populations with a high prevalence of periodontitis.29, 51 One would suspect that most practitioners would find the presence of suppuration disturbing.

Conclusions

Despite intensive research efforts to develop new technologies to improve diagnostic ability, traditional diagnostic procedures based upon clinical signs of inflammation, probing depths and clinical attachment loss still form the basis upon which periodontal diagnosis is made. Absence of gingival inflammation and shallow probing depths have a strong negative predictive values for periodontal stability.48, 53 The clinician should strive to achieve this endpoint in the treatment of our patients.

Diagnosis of the disease also involves classification. Systems of classification are continually evolving. Classification of periodontal diseases is difficult and all classification systems produced to date have their imperfections and their critics. Van der Velden54 argued that the 1999 reclassification was not helpful and suggested a classification based on age, which appears to be a simplified version of the 1989 AAP classification, and further classified on the basis of extent, severity and clinical characteristics. This classification allows the possibility of making an accurate clinical diagnosis for any patient with periodontitis. Milward and Chapple,56 while recognizing the 1999 World Workshop attempted to produce a classification from an evidence-based perspective, criticized the 1999 classification as being unnecessarily complex and not suited for routine general dental practice. Lopez and Baelum57 argue from an epidemiological point of view that there is little justification for the use of complicated classification systems and favour an approach based upon simple clinical attachment loss measurements such as ≥ 3 mm etc., a minimalist approach that does not try to differentiate between different types of periodontitis.

Why is classification of periodontal disease so difficult and so controversial? The answer lies in the heterogenicity of the clinical presentation and our lack of understanding of the true nature of the differences between the different clinical presentations of the disease. We attempt to classify using evidence based upon the different infections represented and on the host response. However, in most cases our knowledge is incomplete or confused. Much of the certitude that was felt in the 1980s that we had reached a point where we could truly distinguish between the different disease presentations in a scientific manner, has largely evaporated. It is of interest that localized juvenile periodontitis (LJP), one disease which has long been recognized as being a distinct or separate disease entity on the basis of clinical characteristics, microbiological factors and host response, the features of which are well documented, has been discarded as a distinct disease entity and has been reclassified as localized aggressive periodontitis. This apparently was done to conform to the predetermined criteria of the classification and in particular the removal of the emphasis on age. However, I have yet to see an LJP in anyone other than a juvenile and the circumpubertal age of onset is an integral part of the disease description and its deletion does not appear to have been a progressive step. We should also consider that perhaps there is just one periodontitis with different clinical expressions in different hosts.

Armitage,15 in a thoughtful article on classification, stated that "the classification system proposed by the '1999 International Workshop for a Classification of Periodontal Diseases and Conditions' has corrected some of the problems associated with the previous system that had been in use since 1989. Nevertheless, the new system is far from perfect and will need to be modified once there are sufficient new data to justify revisions". He is of the opinion that current disease designations such as "chronic periodontitis" are constellations of polymicrobial and polygenic infections whose clinical expression is altered by important environmental and host modifying conditions.

It would seem that we are trying to classify diseases of which we do not have sufficient knowledge. The present classification of periodontitis looks surprisingly like a return to simplex and complex. Until we have greater understanding of the aetiology, the bacteria associated with different periodontal infections and the pathogenesis and genetics of periodontal diseases, it is very likely that we will see further reclassifications at regular intervals.

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Diagnosis and classification of periodontal disease

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Adjunct Associate Professor John HighfieldDiscipline of PeriodonticsFaculty of DentistryThe University of Sydney2 Chalmers StreetSydney NSW 2010Email: johnh@dentistry.usyd.edu.au Periodontal diseases have been recognized and treated for at least 5000 years. Clinicians have recognized for many years that there are apparent differences in the presentation of periodontal diseases and have attempted to classify these diseases.

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Es una grave infección de las encías que daña el tejido blando, pudiendo agravarse al punto de destruir el hueso que sostiene los dientes, aflojándolos hasta que se caen.

Se origina por la inflamación continua de las encías, seguida por la formación de bolsas entre las mismas y los dientes, los cuales se llenan con placa, sarro dental y bacterias. Con el tiempo, estas bolsas se hacen más profundas, y acumulan más bacterias. Si no se tratan, estas infecciones profundas causan pérdida de tejido y hueso, y finalmente, la pérdida de uno o más dientes. Además, la inflamación crónica continua puede sobrecargar el sistema inmunitario.

Se trata de una enfermedad frecuente, principalmente resultado de una mala higiene bucal. Conlleva un largo proceso en el que esa falta de correcta limpieza y de intervención profesional, desemboca en el desarrollo de distintos problemas (placa, sarro, gingivitis) que evolucionan hasta alcanzar la gravedad de la periodontitis.

PERIODONTITIS CRÓNICA

Es más común en adultos, ya que la mala higiene bucal y el consecuente desarrollo de la periodontitis necesita de un tiempo prolongado y, sobre todo, porque entran en juego otros factores más comunes de la edad adulta. No obstante, pueden padecerla individuos adolescentes e infantes. Se caracteriza por:

•Ser más prevalente en adultos.
•La cantidad de destrucción según factores localizados.
•Frecuente presencia de cálculos sublinguales.
•Asociarse a patrones existentes de cambios microbióticos.
•Su media de progresión es lenta, aunque presenta estadios de rápido desarrollo.
•Se clasifica según su extensión y gravedad.
•En algunas ocasiones se asocia con factores genéticos o problemas dentales previos, entre otros.
•Tener comorbilidad con inmunodeficiencias.
•Existen factores ajenos que pueden influir, como el tabaco y el estrés.

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HÁBITOS EN CASA PARA PREVENIR LOS DIENTES CON SARRO

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HÁBITOS EN CASA PARA PREVENIR LOS DIENTES CON SARRO

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Para tener una buena higiene y así evitar enfermedades como la periodontitis debes:

Cepíllate los dientes y encías todos los días.

Escoge el cepillo y pasta de dientes adecuado (manual, eléctrico, blanqueante, protectora...)

Utiliza seda dental y cepillos interdentales.

Termina con un enjuague bucal.

Visita al dentista periódicamente.

Evita el consumo de tabaco, alcohol, café, té o alimentos muy ácidos que pueden estropear tus dientes.

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https://www.mayoclinic.org/es-es/diseases-conditions/periodontitis/diagnosis-treatment/drc-20354479

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Periodontitis - Diagnóstico y tratamiento - Mayo Clinic

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Esta grave infección de las encías daña el tejido blando y puede destruir el hueso que sostiene los dientes. Puede causar el aflojamiento o la pérdida de dientes.

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El objetivo del tratamiento de la periodontitis es limpiar exhaustivamente las bolsas alrededor de los dientes y prevenir daños en el hueso que las rodea. Las mejores posibilidades de éxito en el tratamiento se obtienen cuando se adopta una rutina diaria de buen cuidado bucal, se controlan las afecciones de salud que pueden tener repercusión en la salud dental y se deja de fumar.

Tratamientos no quirúrgicos

Si la periodontitis no está avanzada, el tratamiento puede consistir en procedimientos menos invasivos, incluidos:

Raspado. El raspado elimina el sarro y las bacterias de la superficie de los dientes y debajo de las encías. Puede realizarse con instrumentos, un láser o un dispositivo ultrasónico.

Alisado radicular. El alisado radicular alisa las superficies de las raíces, desalentando una mayor acumulación de sarro y bacterias, y elimina los subproductos bacterianos que contribuyen a la inflamación y retrasan la cicatrización o la reimplantación de la encía en las superficies de los dientes.

Antibióticos. Los antibióticos tópicos u orales pueden ayudar a controlar la infección bacteriana. Los antibióticos tópicos pueden consistir en enjuagues bucales o geles con antibiótico, que se aplican en el espacio entre los dientes y la encía o dentro de las bolsas después de una limpieza profunda. Sin embargo, pueden ser necesarios antibióticos orales para eliminar por completo las bacterias que causan la infección.

Tratamientos quirúrgicos

Si tienes periodontitis avanzada, el tratamiento puede requerir una cirugía dental, por ejemplo:

Cirugía con colgajos (cirugía de reducción de las bolsas). El periodoncista hace pequeñas incisiones en la encía para poder levantar una sección del tejido de la encía, lo que expone las raíces para un raspado y alisado de la raíz más eficaces. Debido a que la periodontitis causa pérdida de la masa ósea, el hueso oculto se puede volver a moldear antes de que se suture el tejido de la encía nuevamente en su lugar. Una vez que te cures, será más fácil limpiar estas áreas y mantener el tejido de la encía saludable.

Injertos de tejido blando. Cuando pierdes el tejido de las encías, la línea gingival retrocede. Podría ser necesario que te refuercen parte del tejido blando dañado. Por lo general, esto se hace extrayendo una pequeña cantidad de tejido del techo de la boca (paladar) o utilizando tejido de otra fuente donante y adhiriéndolo al sitio afectado. Esto puede ayudar a reducir la recesión gingival, cubrir las raíces expuestas y dar a los dientes una apariencia más agradable.

Injerto óseo. Este procedimiento se realiza cuando la periodontitis ha destruido el hueso que rodea la raíz del diente. El injerto puede estar compuesto por pequeños fragmentos de tu propio hueso, o bien, el hueso puede ser sintético o donado. El injerto óseo ayuda a prevenir la pérdida del diente al sostenerlo en su lugar. También sirve como plataforma para el nuevo crecimiento del hueso natural.

Regeneración tisular guiada. Esto permite que el hueso destruido por las bacterias vuelva a crecer. Una de las técnicas consiste en que el dentista coloque una pieza especial de tela biocompatible entre el hueso existente y el diente. El material evita que ingrese tejido no deseado en el área de cicatrización, lo que permite que el hueso vuelva a crecer.

Proteínas estimulantes de tejidos. Otra técnica supone aplicar un gel especial a la raíz del diente afectado. Este gel contiene las mismas proteínas que se encuentran en el esmalte de los dientes en desarrollo y estimula el crecimiento de huesos y tejidos saludables.

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Factores que aumentan el riesgo de periodontitis:

Gingivitis.

Hábitos de salud oral deficientes.

Fumar o mascar tabaco.

Cambios hormonales (como embarazo o menopausia).

El uso de drogas recreativas (fumar marihuana o vapear).

Obesidad.

Nutrición inadecuada.

La deficiencia de vitamina C.

Genética.

Medicamentos que provocan sequedad de la boca o cambios en las encías

Afecciones que causan una disminución de la inmunidad (leucemia, VIH/SIDA, tratamiento del cáncer).

Enfermedades (diabetes, artritis reumatoide, la enfermedad de Crohn).

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El dentista es el profesional apto y encargado para determinar la presencia y gravedad de este problema bucal. Por ello y porque su intervención es esencial para el tratamiento de la Periodontitis, es fundamental acudir a su consulta. Estas son las acciones que lleva a cabo para realizar el diagnóstico:

Revisa tus antecedentes médicos para identificar cualquier factor que pueda contribuir con los síntomas, como fumar o tomar ciertos medicamentos que provoquen sequedad de boca.

Examina tu boca para buscar la acumulación de placa y sarro, y comprobar si hay tendencia al sangrado.

Usa una sonda metálica que mide la bolsa entre la encía y los dientes, repitiendo el proceso en varias partes de la boca. Las bolsas con una profundad mayor a 4 mm pueden ser un indicio de periodontitis. Las bolsas con una profundad mayor a 5 mm no se pueden limpiar bien.

Toma radiografías dentales para verificar si hay disminución de la masa ósea en áreas donde el dentista observa bolsas de mayor profundidad.

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FALTA DE HIGIENE BUCAL
Es la causa principal aunque hay otros factores (genética o morbilidades). La fauna bacteriana bucal se desarrolla en distintas fases, cuando no se da una limpieza dental adecuada y no se acude al dentista, agravándose al punto de desarrollar Periodontitis. Sus evoluciones de desarrollo son:

LA PLACA.

Es una película pegajosa, que resulta de la interacción de las bacterias que se encuentran normalmente en la boca con almidones y azúcares. Esa película tiende a endurecerse y expandirse.

EL SARRO.

Es producto de la placa endurecida bajo la línea de la encía. Es más difícil de eliminar y está lleno de bacterias. Cuanto más tiempo permanezcan la placa y el sarro dental en los dientes, más daño pueden hacer.

LA GINGIVITIS.

Es la irritación e inflamación de la parte del tejido de la encía que rodea la base de los dientes (tejido gingival).

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La importancia de la dieta en nuestra salud oral

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La importancia de la dieta en nuestra salud oral

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Para tener una buena salud oral es muy importante tener una dieta equilibrada, ayudando a prevenir la aparición de más caries que los alimentos ricos en azúcares favorecen en su actuación.

¿Cómo evitar la aparición de caries?
Evita comidas y bebidas que contengan mucho azúcar,  ya que contienen ácidos que tienen la capacidad de descalcificar el esmalte dental provocando desgaste, sensibilidad y caries. Ejemplos: golosinas, bollería industrial, refrescos, chocolates...

Junto a esto, las revisiones periódicas al dentista con los controles pertinentes harán que tu salud bucodental sea excelente.

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https://centroodontologicointegral.es/como-prevenir-la-periodontitis/

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Centro Odontológico Integral Mallorca | Un servicio de calidad con atención personalizada

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Cómo prevenir la periodontitis | Centro Odontológico Integral Mallorca

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La periodontitis, el estado más avanzado de las patologías periodontales, es irreversible, pero puede prevenirse siguiendo una serie de pautas en el día a día.

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Cómo prevenir la periodontitis

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Tratamiento periodontal y beneficios de este

Los procedimientos para combatir el avance de la periodontitis varían en función del estado y la gravedad de esta. En nuestra clínica dental en Palma de Mallorca contamos con tratamientos que van desde la profilaxis – o limpieza bucal profesional – hasta el curetaje o la cirugía periodontal. El objetivo último de todos ellos es evitar que la enfermedad avance y mantener una funcionalidad y una estética bucal apropiadas.

Un buen estado de las encías y de los tejidos orales no solo favorece una salud bucodental óptima, sino también una salud general adecuada. Gracias a los procedimientos de Periodoncia conseguimos:

La mejora de la funcionalidad y de la estética de la boca.

La eliminación de la placa bacteriana, el sarro y las bolsas periodontales.

La reducción del riesgo de perder piezas dentales.

La disminución de los problemas con el mal aliento o halitosis.

La atenuación del peligro de desarrollar diabetes o enfermedades cardiovasculares.

Si tus encías sangran durante el cepillado, las sientes inflamadas y enrojecidas, ponte en contacto con nosotros. Una detección a tiempo y un tratamiento precoz de los problemas periodontales es fundamental para evitar complicaciones más graves.