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classification of periodontal diseases
- 1. Classification of periodontaldiseases DR. BENITAMARIAREGI 1ST MDS
- 2. CONTENTS • INTRODUCTION • NEEDFOR CLASSIFICATION • HISTORICAL BACKGROUND • DOMINANT PARADIGMS • VARIOUS CLASSIFICATION SYSTEMS • CONCLUSION • REFERENCES
- 3. INTRODUCTION • PERIODONTITIS…… • Theclassification of periodontal diseases has come a long way over the past hundred years. • Classifying periodontal diseases is essential to provide a framework to scientifically study the aetiology, pathogenesis and treatment of disease in an orderly fashion.
- 4. • Disease classificationis useful for the purpose of diagnosis, prognosis and treatment planning. To provide maximum assistance in diagnosis & treatment planning, diseases have been classified mainly on the basis of three criteria:-
- 5. NEED FOR CLASSIFICATION •Diagnosis, prognosis & treatment planning. • To understand the etiology & pathology of the disease affecting the periodontium. • For logical, systematic separation & organization of knowledge about disease. • Facts can be filed for future references. • Helps to communicate among clinicians, researchers, students , epidemiologists & public health workers.
- 6. HISTORY Giralamo Cardono -1st to differentiate periodontal diseases Fauchard (1723) – ‘Scurvy’ of the gums Early 19th century – Riggs Disease (John W Riggs 1811-1885)
- 7. Dominant paradigms inthe historical development of classification system 1870-1920 • Clinical features of the diseases 1920-1970 • The concepts of classical pathology 1970- present • Infectious etiology of diseases
- 8. Clinical features ofthe disease
- 9. John M. Riggs(1875) margins of the gums showed inflammatory action & bleeding at slightest touch of the brush inflammation extends over the thinner alveolar border causing absorption of bone & gum tissue, forming small pockets filled with pus. thicker portions of the process are involved absorbing it most rapidly. the disease has swept away all of the alveoli & much of the gum
- 10. C.G. Davis (1879) •Gingival recession with little or no inflammation • Periodontal destruction secondary to lime deposits • “ RIGG’S DISEASE” the hallmark of which was loss of alveolus without loss of gums
- 11. shortcomings • No emphasiswas given on age of onset of diseases and rate of progression. • Inadequate or unclear classification criteria. • Little or no scientific evidence was used to support the opinions of the clinicians of that time. • Periodontitis which can be due to systemic diseases was not considered.
- 12. G. V. BLACKCLASSIFICATION (1886) Constitutional Gingivitis Phagedenic Pericementitis (PHAGEDENIC) Calcic Inflammation Of The Periodontal Membrane Painful Form Of Gingivitis Simple Gingivitis
- 13. SHORTCOMINGS • Little orno scientific evidence was used to support the opinions of the clinicians of that time • No accepted terminology or classification system was adopted. During this period, the dominant term used for destructive periodontal disease was ‘PYORRHEA ALVEOLARIS’.(Toirez in 1779)
- 14. In the latterpart of 19th century, periodontitis underwent numerous modifications in names: PYORRHOEA ALVEOLARIS (MOST COMMON) CHRONIC SUPPURATIVE PERICEMENTITIS CALCIC INFLAMMATION OF PERIDENTAL MEMBRANE PHAGEDENIC PERICEMENTITIS. RIGGS DISEASE
- 15. • This conceptwas introduced by GOTTLIEB AND ORBAN. Two forms of destructive periodontal disease. CLASSICAL PATHOLOGY PARADIGM (1920- 1970) Inflammatory Non inflammatory (degenerative, dystrophic)
- 16. • As thefield of periodontology began to mature scientifically in the first half of the 20th century, many clinical scholars in both Europe and North America began to develop, and argue about, nomenclature and classification systems for periodontal diseases. • What emerged from this debate was the concept that there were at least two forms of destructive periodontal disease, Inflammatory and Non-inflammatory (‘degenerative’ or ‘dystrophic’). • This conclusion was primarily based on the over-interpretation of histopathological studies from a group of investigators led by Gottlieb and Orban.
- 17. • Gottlieb, inparticular, had a significant influence on the field when he postulated that certain forms of destructive periodontal disease were due to degenerative changes in the periodontium. • He believed that he had discovered histological evidence of an impairment in the continuous deposition of cementum (i.e. ‘cementopathia’). This cemental defect was presumably initiated by the degeneration of the principal fibers of the periodontal ligament that eventually resulted in detachment of connective tissue from the tooth followed by resorption of adjacent bone.
- 18. • MCCALL &BOX(1925)- introduced the term ‘PERIODONTITIS’ to denote those inflammatory diseases in which gingiva, bone and PDL are involved. • Based on systemic etiological factors- 2) Complex periodontitis. 1) Simple periodontitis
- 19. GOTTLEIB’S CLASSIFICATION-(1928) • Schmutz-pyorrhea ( poor oral hygiene)INFLAMMATORY • Diffuse alveolar atrophy (systemic or metabolic causes) (non – inflammatory) • Paradental- pyorrhea (irregularly distributed pockets) DEGENERATIVE OR ATROPHIC- OCCLUSAL TRAUMA
- 20. Demerits No microbialanalysis. Inflammatory process is over interpretated as degenerative process. Gingival diseases not included.
- 21. BECKS CLASSIFICATION- (1931) •1) Paradentitis (originates from the gum disease in the form of gingivitis) 2) Genuine paradentosis (originates in the bony alveolus)
- 22. ORBAN CLASSIFICATION (1942) •PERIODONTOSIS-to designate the ‘non-inflammatory disease’ & was a separate distinct disease entity. INFLAMMATORY GINGIVITIS PERIODONTITIS 1)LOCAL 2)SYSTEMIC 1) SIMPLE 2) COMPLEX
- 23. DEGENERATIVE • Systemic disturbances •Hereditary • Idiopathic PERIODONTOSIS ATROPHIC CONDITIONS- Periodontal atrophy- a) following inflammation b) local Trauma c) idiopathic
- 24. HYPERTROPHY- TRAUMATISM- Gingival hypertrophy a)chronic irritation b)drug reaction c)idiopathic Periodontal traumatism a)occlusal trauma
- 25. • Conclusion thatsome forms of periodontal diseases were caused by non-inflammatory or degenerative process was primarily based on over-interpretation of histopathological studies. • No scientific basis for retaining the concept that there were non-inflammatory or degenerative forms of destructive periodontal diseases. Demerits
- 26. WHO expert committeeon the dental health in 1961 suggested: • Etiology plays secondary & accessory part in classification • Clinical assessment lack sufficient precision to serve as a foundation for classification • The most valid basis for classification is therefore one based on general pathology
- 27. WHO CLASSIFICATION -1961 GINGIVITIS Acute ulcerative gingivitis Acute non-specific gingivitis ACUTE Chronic gingivitis Chronic hyperplastic gingivitis CHRONIC
- 28. PERIODONTITIS periodontal abscess ulcerative periodontitis ACUTE Periodontitis simplex (marginal horizontalbone loss) Periodontitis complex (irregular bone loss) CHRONIC
- 29. • MERITS Acute& chronic conditions are easily identified. • DEMERITS Degenerative & neoplastic process are left out. Considered only inflammatory periodontal diseases. Not considered periodontal traumatism. Systemic diseases not included.
- 30. • During 1950& 1960s the importance of dental plaque as the major etiologic factor for periodontal diseases became more and more evident. • The ultimate proof of association between plaque and gingival inflammation was shown by Loe and coworkers in their experimental gingivitis studies(1965,1966). • In 1966 the workshop in periodontics concluded the report: ‘Evidence to support the conventional concept of periodontosis is unsubstantiated’.
- 31. • It wasthe consensus of the section that the term periodontosis is ambiguous and it should be eliminated from nomenclature. • Nevertheless, the committee is aware that some evidence exists to indicate that a clinical entity different from adult periodontitis may occur in adolescents and young adults’. • Soon after the workshop a study was published by Butler(1969) introducing the JUVENILE PERIODONTITIS instead of periodontosis.
- 32. Other Classifications (ClassicalPathology Paradigm) • Fish – 1944 • Hine & Hine – 1944 • Lyons - 1946 • Coolidge & Hine – 1951 • Goldman et al – 1956 • Wade - 1960 • Goldman & Cohen – 1968 • Grant et al - 1968
- 33. • W.D Miller- suggested that 3 factors are to be considered in every case of pyorrhea alveolaris – predisposing circumstances, local irritants, bacteria. Specific bacteria do not cause pyorrhea alveolaris but various bacteria may participate in it. Miller also recognized that systemic conditions (diabetes, pregnancy) could modify the course of the disease. INFECTION/HOST RESPONSE PARADIGM (1970-present)
- 34. • Harald &Loe in 1965-1968 studied on experimental gingivitis and concluded there is a significant relationship between plaque flora and development of gingivitis. • The next major discovery in periodontal microbiology was the preliminary demonstration in 1976-1977 of microbial specificity at sites with periodontitis. • This finding is coupled with demonstration in 1977-1979 that neutrophils from patients with juvenile periodontitis had defective chemotactic and phagocytic activities, marked the beginning of the dominance of infection/host response paradigm.
- 35. Classifications under Infection/Host response paradigm: • Goldman & cohen 1972 • Prichard – 1972 • Ramford & Ash – 1979 • Page & Schroeder - 1982 • American Dental Association – 1982 • Weatherford Classification -1987 • Suzuki’s Classification- 1988 • Grant, Stern, Listgarten, 1988
- 36. • World Workshopin Clinical Periodontology – 1989 • Short comings of 1989 classification • Genco 1990 • Ranney’s Classification – 1993 • European Workshop on Periodontics – 1993 • World workshop– 1999
- 37. CLASSIFICATION BY RAMFJORD& ASH( 1979)- GINGIVITIS simplex complex traumatic GINGIVAL ATROPHY OR RECESSION Systemic local TRAUMA FROM OCCLUSION PERIODONTITIS Simple complex
- 38. MERITS • Simple &convenient way of categorizing periodontal diseases. • Gingival atrophy or recession as a separate category. DEMERITS • Periodontal abscess & perio-endo lesions not included.
- 39. CLASSIFICATION BY PAGE& SCHRODER,1982 Based on age, pocket flora, leukocyte function tests, serum antibodies, clinical & radiographic pictures, progression & history. 1)PREPUBERTAL PERIODONTITIS- 2) JUVENILE PERIODONTITIS 3) RAPIDLY PROGRESSIVE PERIODONTITIS 4) ADULT TYPE PERIODONTITIS
- 40. MERITS • Simplified, convenientand uncomplicated. • systemic & local factors. • Age of onset is taken into consideration which is adopted in subsequent classifications • Designed to accommodate additional forms of diseases as new insights are gained & additional forms are identified. DEMERITS • Gingival diseases not included. • Non-validated age-dependent criteria. • Periodontal Abscess not included. • Periodontic-endodontic lesions not included. • Occlusal trauma not included.
- 41. American Academy OfPeriodontology (1986) 1. Juvenile Periodontitis • Prepubertal periodontitis • Localized juvenile periodontitis • Generalized juvenile periodontitis 2. Adult periodontitis 3. Necrotizing Ulcerative gingivo-Periodontitis 4. Refractory Periodontitis
- 42. CLASSIFICATION OF THEWORLD WORKSHOP, 1989 • Major landmark in the classification emerged from 1989 World Workshop in Clinical periodontitis based on this paradigm a. Adult periodontitis. b. Early-onset periodontitis: i. Prepubertal periodontitis: 1. Local 2. Generalized ii. Juvenile periodontitis 1. Localized 2. Generalized iii. RPP c. Periodontitis associated with systemic diseases d. Necrotising ulcerative periodontitis e. Refractory periodontitis
- 43. 1989 classificationhad many shortcomings including : 1 Considerable overlap in clinical characteristics of the different disease categories 2 Inappropriate emphasis on age of onset of disease and rates of progression 3 Absence of a gingival disease component. 4 Rapidly progressive & prepubertal periodontitis and refractory periodontitis were heterogenous category. 5. The 1989 classification did not include a section on the connection between periodontitis and endodontic lesions. DRAWBACKS
- 44. • Ranney: • Eliminatedthe “Refractory Periodontitis” category since it was heterogeneous group & it was impossible to standardized the treatment that necessarily would have to be given prior to making diagnosis. • Eliminated the “Periodontitis associated with systemic disease” category since the expression of all forms of periodontitis can be modified by some systemic disease or abnormality Compared to WWS class – 1989
- 45. RANNEY, 1993 • GINGIVITIS •Gingivitis plaque induced * Systemically aggravated by sex hormones, drugs, systemic diseases. • NUG * Systemic determinants unknown * Related to HIV • Gingivitis, non-plaque induced * Associated with skin diseases: allergic, infections
- 46. • PERIODONTITIS • Adultperiodontitis * Non-aggravated * Systemically aggravated • Early-onset periodontitis * Localised / generalized * Related to systemic diseases * Systemic determinants unknown • NUP * Systemic determinants unknown * Related to HIV * Related to nutrition • Periodontal abscess
- 47. Merits • This systemincludes not only forms of gingivitis & Periodontitis other than those caused by plaque but also modifying factors, for ex. Systemic aggravating factors, general diseases status, viral infections & so on.
- 48. EUROPEAN WORKSHOP ONPERIODONTICS - 1993 • In 1993, the first European Workshop on periodontology was organized by Attstrom R, Vander Velden U. • It was divided into 3 types based on host-parasitic interaction. • ADULT PERIODONTITIS. * Onset 4th decade, slow rate of progression, * no host response defect. EARLY ONSET PERIODONTITIS. * Onset prior to 4th decade, rapid rate of progression, defect in host response. NECROTIZING PERIODONTITIS * Tissue necrosis with attachment & bone loss.
- 49. • In caseof early-onset periodontitis , no knowledge when the disease started. • No mention on gingival diseases • There is uncertainty about the upper age-limit for patients with early-onset periodontitis. So the need for a revised classification system was emphasized during 1996 world workshop in periodontics. DRAWBACKS
- 50. • 1996 WorldWorkshop in Periodontics - The need for a revised classification system for periodontal diseases was emphasized • 1997 - American Academy of Periodontology responded to this need and formed a committee to plan and organize an International Workshop to revise the classification system for periodontal diseases. • October 30-November 2, 1999 - The International Workshop for a Classification of Periodontal Diseases and Conditions was held and a new classification was agreed upon.
- 51. • October 30-November 2, 1999 a new classification system was agreed upon. • CHANGES IN THE CLASSIFICATION SYSTEM FOR PERIODONTAL DISEASE- • ADDITION OF A SECTION ON “ GINGIVAL DISEASES” • REPLACEMENT OF “ADULT PERIODONTITIS” WITH “CHRONIC PERIODONTITIS” • REPLACEMENT OF “EARLY ONSET PERIODONTITIS” (EOP) WITH “AGGRESSIVE PERIODONTITIS” (AP) • ELIMINATION OF A SEPARATE DISEASE CATEGORY FOR “REFRACTORY PERIODONTITIS” (RP) INTERNATIONAL WORKSHOP FOR CLASSIFICATION OF PERIODONTAL DISEASE & CONDITIONS- 1999(ARMITAGE GC)
- 52. • CLARIFICATION OFTHE DESIGNATION “PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC DISEASES” • REPLACEMENT OF “NECROTIZING ULCERATIVE PERIODONTITIS(NUP) WITH “NECROTIZING PERIODONTAL DISEASES” (NPD) • ADDITION OF A CATEGORY ON “PERIODONTAL ABSCESS” • ADDITION OF A CATEGORY ON “PERIODONTIC ENDODONTIC LESIONS” • ADDITION OF A CATEGORY ON “DEVELOPMENT OR ACQUIRED DEFORMITIES AND CONDITIONS”
- 53. • I. GingivalDiseases • A. Dental plaque-induced gingival diseases • B. Non-plaque-induced gingival lesions • II. Chronic Periodontitis (slight: 1-2 mm CAL; moderate: 3-4 mm CAL; severe: > 5 mm CAL) • A. Localized • B. Generalized (> 30% of sites are involved) • III. Aggressive Periodontitis (slight: 1-2 mm CAL; moderate: 3-4 mm CAL; severe: > 5 mm CAL) • A. Localized • B. Generalized (> 30% of sites are involved)
- 54. • IV. Periodontitisas a Manifestation of Systemic Diseases • A. Associated with hematological disorders • B. Associated with genetic disorders • C. Not otherwise specified • V. Necrotizing Periodontal Diseases • A. Necrotizing ulcerative gingivitis • B. Necrotizing ulcerative periodontitis • VI. Abscesses of the Periodontium • A. Gingival abscess • B. Periodontal abscess • C. Pericoronal abscess
- 55. • VII. PeriodontitisAssociated With Endodontic Lesions • A. Combined periodontic-endodontic lesions • VIII. Developmental or Acquired Deformities and Conditions A. Localized tooth-related factors that modify or predispose to plaque-induced gingival diseases and deformities. B. Mucogingival deformities and conditions around teeth C. Mucogingival deformities and conditions on edentulous ridges D. Occlusal trauma
- 56. Gingival diseases 1) Dentalplaque induced gingival diseases • Gingivitis that is associated with dental plaque formation is the most common form of the gingival disease. • It has been proved that plaque induced gingivitis may occurs on periodontium with no attachment loss or on periodontium with previous attachment loss that is stable and not progressing.
- 57. Gingivitis associated withdental plaque • The plaque host interaction can be altered by the effects of local factors, systemic factors or both, medications and malnutrition that can influence the severity and duration of the response.
- 58. A)Gingival Diseases Modifiedby Systemic Factors • Associated with the endocrine system- such as the endocrine changes associated with puberty, menstrual cycle, pregnancy and diabetes may be exacerbated because of the alterations in the gingival inflammatory response to plaque Puberty gingivitis Pregnancy gingivitis
- 59. Associated with blooddyscrasias • Blood dyscrasias such as leukemia may alter immune function by disturbing the normal balance of immunologically competent white cells supplying periodontium. • Gingival enlargement and bleeding are common findings and may be associated with, swollen, spongy gingival tissues caused by excessive infiltration of blood cells.
- 60. B)Gingival Diseases Modifiedby medications • Gingival diseases modified by medications are increasingly prevalent because of the increased use of anticonvulsant drugs, known to induce gingival enlargement. • Such as phenytoin, immunosuppressive drugs such as cyclosporine A, and calcium channel blockers such as nifedipine, verapamil, amlodipine and felodipine.
- 61. C)Gingival disease modifiedby Malnutrition • Clinical descriptions of bright red, swollen and bleeding gingiva associated with severe ascorbic acid deficiency or scurvy. • Nutritional deficiencies are known to affect immune function & may have an impact on the hosts ability to protect itself against some of the detrimental effects of cellular products such as oxygen radicals.
- 62. Gingival Disease ofSpecific Bacterial Origin • These disease are increasing in prevalance especially as a result of sexually transmitted disease such as gonorrhea and to a lesser degree syphillis. • Oral lesions may be secondary to systemic infections or may occur through direct infection. • Streptococcal gingivitis or gingivo stomatitis is a rare condition that may present as an acute condition with fever, malaise and pain associated with acutely inflammed diffuse red, and swollen gingiva with increased bleeding and occasional gingival abscess formation. B. Non – Plaque Induced Gingival Lesions
- 63. Gingival disease ofViral Origin • It may be caused by a variety of deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) viruses, the most common being the herpes viruses. • Lesions are frequently related to reactivation of latent viruses especially as a result of reduced immune function.
- 64. Gingival Disease ofFungal Origin • It occurs most frequently on individuals who are immunocompromised or in whom the normal oral flora has been disturbed by long term use of antibiotics. • The most common oral fungal infection is candidiasis caused by infection with candida albicans • A generalized candidal infection may manifest as white patches on the gingiva, tongue or oral mucous membrane that can be removed with a gauze leaving a red, bleeding surface. • In HIV infected individuals, candidal infection may present as erythema of attached gingiva and has been referred to as linear gingival erythema or HIV associated gingivitis.
- 65. Gingival Disease ofGenetic Origin • One of the most clinically evident conditions is hereditary gingival fibromatosis that exhibits autosomal dominant or (rarely) autosomal recessive modes of inheritance. • The gingival enlargement may completely cover the teeth, delay eruption and present as an isolated finding or be associated with several more generalized syndromes.
- 66. Gingival Manifestations ofSystemic Conditions- • It may appear as desqumative lesions, ulceration of gingiva or both. • Allergic reactions that manifest with gingival changes are uncommon but have been observed in association with several restorative materials, tooth pastes, mouth washes, chewing gum and foods.
- 67. Traumatic Lesions • Traumaticlesions may be factitial (produced by artifical means; unintentionally produced) as in the case of tooth brush trauma resulting in gingival ulceration, recession or both; iatrogenic (trauma to the gingiva induced by the dentist or health professional) as in the case of preventive or restorative care that may lead to traumatic injury of the gingiva; or accidental as in the case of damage to the gingiva through minor burns from hot food and drinks.
- 68. Foreign Body Reactions •Foreign body reactions lead to localized inflammatory conditions of the gingiva and are caused by the introduction of foreign material into the gingival connective tissues through breaks in epithelium • Eg. Introduction of amalgam into gingiva during the placement of restoration leaving an amalgam tattoo or the introduction of abrasives during polishing procedures.
- 69. Chronic periodontitis It isa common plaque induced periodontal infection that is major cause of tooth loss throughout the world. Its important clinical features are:- • Most prevalent in adults but can occur in children. • Amount of destruction is consistent with the presence of local factors. • Associated with a variable microbial pattern • Slow to moderate rate of progression but may have periods of rapid progression. • Subgingival calculus frequently found. • May be modified by or associated with systemic disease • Can be modified by other factors such as cigarette smoking and emotional stress.
- 70. Aggressive periodontitis • Aggressiveperiodontitis is much less common than chronic periodontitis and affects a narrower range of younger patients. • It occurs in localized and generalized forms and the two forms differ in many respects with regard to their etiology and pathogenesis. • LAP and GAP were once called localized and generalized juvenile periodontitis respectively. • However these terms were replaced with LAP and GAP terminology because they do not depend on questionable age based classification criteria.
- 71. Both forms ofaggressive periodontitis share the following common features:- • patients are otherwise clinically healthy • Rapid attachment loss and bone destruction • Familial aggregation of diseased individual • Amount of microbial deposits inconsistent with the diseases severity.
- 72. Specific features oflocalized and generalized aggressive periodontitis. Localized Aggressive Periodontitis • 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
- 73. Generalized Aggressive Periodontitis •Usually affecting individuals less than 30 years 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.
- 74. Periodontitis as amanifestation of systemic diseases There are two general categories of systemic disease that have periodontitis as a frequent manifestation 1. Certain hematologic disorders (eg acquired neutropenia, leukemia) and 2. Some genetic disease (eg. Familial / cyclic neutropenia, down syndrome, papillon lefevre syndrome, chediak-higashi syndrome, Cohen syndrome).
- 75. Necrotizing periodontal disease •Necrotizing periodontal infections include necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP). • In both the condition there is a rapid onset of pain associated with development of necrotic and ulcerative lesions of marginal gingiva, particularly involving interproximal sites.
- 76. NECROTIZING ULCERATIVE GINGIVITIS Thetwo most significant criteria used for the diagnosis of NUG are :- • Presence of interproximal necrosis and ulceration • A history of rapid onset of gingival soreness and pain. • The interproximal necrosis and ulceration take the form of eroded crater like depressions of one or more interproximal gingival papillae sometimes referred to as having “ Punched Out” appearance. • Marked halitosis is present in most patients with NUG. • Some patients have a pseudo membrane covering the ulcerated areas of the gingiva.
- 77. Predisposing factors forNUG in adult patients:- • Emotional stress • Heavy cigarette smoking • Lack of sleep • Poor dietary habits • Immunosuppression.
- 78. Necrotizing Ulcerative Periodontitis •Compared to NUG, NUP always involves considerable loss of periodontal attachment and alveolar bone. • Local ulceration, necrosis of gingival tissues with exposure & rapid destruction of underlying bone, bleeding & severe pain. • Severe immunosuppression from other sources such as cancer chemotherapy and malnutrition also can lead to the development of NUP.
- 79. Abscesses of periodontium 3 types- i. gingival abscess ii. periodontal abscess iii. peri coronal abscess
- 80. Periodontitis Associated withEndodontic Lesions • Infections of periapical tissues caused by the pulpal death (i.e. endodontic lesions) can often locally join with separate infections emenating from periodontal pockets. • This coalescence of endodontic and periodontal infections has termed combined periodontal–endodontic lesions.
- 81. Developmental or AcquiredDeformities and Conditions • They are included in most classifications of periodontal disease because they may be important modifiers of susceptibility to periodontal infections or can dramatically influence treatment outcomes.
- 82. Localized tooth relatedfactors that modify or predispose to plaque induced periodontal diseases. • Cervical enamel projections, enamel pearls, furcation anatomy, tooth position, root proximity and anomalous grooves in roots. • Defect in dental restorations such as poor contours and marginal discrepancies can increase the risk of periodontal infections.
- 83. Mucogingival Deformities andconditions around Teeth Mucogingival deformities refer to a group of congenital, developmental, or acquired defects in the normal relation between keratinized gingival tissues and nonkeratinized alveolar mucous. These deformities are:- 1. Gingival/soft tissue recession - Facial or lingual surfaces - Inter proximal (papillary) 2. Lack of keratinized gingiva 3. Decreased vestibular depth 4. Aberrant frenum/muscle position 5. Gingival excess 6. Abnormal colour
- 84. Mucogingival Deformities andConditions on Edentulous Ridges. There are:- Vertical and/or horizontal ridge deficiency Lack of gingival /keratinized tissue Gingival / soft tissue enlargement Aberrant frenum /muscle position Decreased vestibular depth Abnormal colour.
- 85. Occlusal Trauma: • Damageto periodontal tissues can occur during a variety of conditions involving occlusal loads and forces that exceed the capacity of the periodontium to with stand them.
- 86. • It isan extremely complex classification with over 100 disease categories listed and, owing to its complexity, its clinical application is difficult. • Periodontal diagnosis around implants were not included • No research revealed specific bacterial characteristic in AP( Kinane & Attstrom, 2002) • It does not solve the problems as how severe a case must be in order to be classified as AP. • Knowledge about the rate of progression is still needed. • The use of AP implies that the person is systemically healthy but has periodontal diseases. But is not seen in all cases. DRAWBACKS
- 87. • According toSherp in 1964- one obvious problem is that one of the most important components of periodontitis is expressed in all patients in the same way, i.e. the amount of loss of attachment. • Essentialistic idea implies the real existence of a disease caused by a class of agents. • Since periodontitis is a syndrome, present & future classification have to be based on nominalistic concept. ESSENTIALISTIC OR NOMINALISTIC DISEASES CLASSIFICATION- (VANDER VELDON,2000)
- 88. Classification based onthis should be • Simple to apply. • Not susceptible to multiple interpretations. • Determined on the basis of documented differences regarding the consequences of the diagnosis. At present a classification which comes closest to these principles was published by Van der Velden in 2000. Based on a) Extent b) Severity c) Age d) Clinical characteristics.
- 93. As we enterthe postgenomic era with our increased understanding of the bacteria associated with periodontal infections & the genetic factors controlling host responses to these infections, it would seem that a more mechanistic or etiological classification could be devised. One of the problem associated with any attempt at subclassifying chronic periodontitis or other forms of periodontitis is that these infections are polymicrobial & polygenic. FUTURE CHALLENGES IN CLASSIFYING PERIODONTAL DISEASES
- 94. • The clinicalexpression of these diseases is altered by important environmental & host modifying conditions. • It may eventually be possible to subclassify the multiple forms of chronic periodontitis into discrete micro-organism / host genetic polymorphism groups. • It is also necessary to superimpose on these microorganism / host genetic polymorphisms groupings the effect of environmental or host-modification factors. i.e. “Smoking-induced Periodontitis” or “Diabetic Periodontitis”.
- 95.
- 96. REFERENCES 1. Clinical periodontology-Carranza9th edition. 2. Critical issues in periodontal diagnosis- Periodontology 2000;vol 39:2005. 3. Controversies in periodontology- Periodontology 2000; vol 30:2002. 4. Classification & Epidemiology of periodontal diseases-Periodontology 2000; vol 2:1993. 5. Annals of periodontology 1999.
Editor's Notes
- #4 periodontitis is an inflammatory disease of supporting tissues of the teeth caused by specific micro org resulting in progressive attachment loss and bone loss.
- #7 1875
- #8 Thoughts that guided the classification of periodontal disease can be placed into 3 dominant paradigms-
- #9 Clinicians case descriptions and their personal interpretations of what they saw clinically was the primary basis for classifying periodontal diseases.
- #10 John M Riggs lectured on the treatment of periodontal disease.After that periodontitis was called “Rigg’s disease”
- #11 published a paper ,he believed that there were three distinct forms of destructive periodontal disease: 2. the gum retires slowly and the alveolar border deprived of nutrition,at the point of pressure is consentaneously absorbed 3. the perceived problem was a necrosed alveolus or death of the periodontal membrane.
- #13 classification based on their clinical characteristics and his understanding of their cause into five groups:- e.g.- mercurial gingivitis, scurvy. 2. Now termed as NUG 3. associated with accumulation of debris that eventually led to calcic inflammation of the peridental membrane. 4. associated with salivary & serumal calculus (CP) .the destruction of alveolar bone slowly in even or generalized pattern. 5. the pattern of alveolar bone destruction is irregular.it may occur rapidly or slowly. - Spreading ulcer or necrosis Later (1915) publication replaced to ‘chronic suppurative pericementitis’
- #15 The point of these historical examples is to emphasize that little or no scientific evidence was used to support the opinions of the clinicians of the time. What caused the periodontal disease, how they should be classified, and the terminology used to describe them, seem to have approached the number of clinicians who treated the patients with these diseases. Hence it is not surprising then, that no generally accepted terminology or classification system for periodontal diseases was not adopted during this era.
- #19 1. due to local bacterial factors 2.due to systemic etiologic factors.
- #20 due to accumulation of deposits on the teeth and was characterised by inflammation, shallow pockets, and resorption of alveolar crest. Non inflammatory disease exhibiting loosening of teeth,elongation of and wandering of teeth in individuals who were free of caries & dental deposits,pockets are formed in later stages Irregularly distributed pockets varying from shallow to extremely deep.this may be started as Schmutz-pyorrhoe or diffuse atrophy A form of physical overload was believed to result in resorption of the alveolar bone and loosening of teeth.
- #23 Periodontosis was considered a separate disease entity,distinctly different from periodontitis,which was considered as the sequel of gingivitis of deeper periodontal structures and therefore of a inflammatory origin. It is not mentioned specifically that it was a disease entity particular to young patients. Orban classified periodontal diseases according to the “pathologic” categories of Inflammation Degeneration Atrophy Hypertrophy Traumatism. A.local- calculus,foodimpaction,irritating restorations,drug action etc. B.systemic- pregnancy,diabetes,tuberculosis,syphilis,nutritional disorders,drug action,allergy,hereditary,idiopathic etc. II.periodontitis A.simplex(secondary to gingivitis)-bone loss,pockets,abscess can form:cases have calculus. B.complex(secondary to periodontosis)-etiologic factors similar to periodontitis:cases have little,if any calculus.
- #24 DegenerationI.Periodontosis) A.Systemic disturbances 1.Diabetes 2.Endocrine dysfunctions 3.Bood dyscrasias 4.Nutritional disturbances 5.Nervous disorders 6.Infectious diseases(acute &chronic)B.HereditaryC.Idiopathic
- #32 2. Although this era included a degenerative disease category , question was raised in 1966 workshop about the existence of periodontosis as a distinct entity. In 1977 world workshop it was renamed as juvenile periodontitis (BUTLER) 5. According to him there was no proof of degeneration as suffix “osis” implies. It was further concluded that this was actually an infection, rather than a degenerative condition
- #38 Based on the concept that most PD is inflammatory in nature.
- #40 They suggested four different forms Onset- soon after the eruption of primary teeth. Generalized form- Localized form- of periodontitis.
- #43 Rapidly progressive periodontitis
- #47 In 1993 Ranney suggested to consider these in specific context rather than treating them as a unique category.
- #50 X. In 1993 first European Work Shop on periodontology given a statement on the basis of the reports produced by papapanou. ‘There is a insufficient knowledge to separate truly different diseases (disease heterogenicity)from differences in the presentation/severity of the same disease(phenotypic variation)
- #59 Without local contributing factors. With local contributing factors.
- #75 Robust serum antibody to infecting agents
- #81 2. The term necrotizing ulcerative periodontitis did not appear in classification systems for periodontal disease until the later 1980s at the peak of the AIDS epidemic. It was added to the classification systems primarily because of the increasing appearance of a rapidly destructive and intensely painful form of periodontitis in HIV infected patients.
- #82 An abscess is a circumscribed collection of pus. A periodontal abscess is a localized purulent infection of periodontal tissues that may result in severe destruction of the underlying periodontal tissues. Factors that predispose to abscess formation are Deep periodontal pockets. Incomplete removal of subgingival calculus during scaling and root planing Occlusion of the pocket orifice by foreign bodies
- #86 5. Includes – Pseudopockets - Inconsistent gingival margin - Excessive gingival display - Gingival enlargement
- #98 Classification of periodontal diseases has proved problematic. Over much of the last cent., 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.