By Dr. Pradnya Kadam

1. DR. PRADNYA D. KADAM
DEPT.OF PERIODONTICS.

2. Contents
•What is classification?
•Why classification ?
•Historical perspective
•Desirable characteristics of a classification system
•Need for classification
•Dominant paradigms in the historical development of classification
systems.
•Classification of American acadamy of periodontology 1999
•Changes in the classification system till present
•A lacuna in AAP classification 1999
•How was 2017 classification framed?
•Key changes in 2017
•2017 classification system
•Staging and grading system
•Implementation of the new classification of Periodontal diseases:
decision-making

3. PERIODONTAL DISEASES
“It is defined as the inflammation of the
supporting tissue of the teeth caused by specific
micro organism or groups of micro organism,
resulting in progressive destruction of the
periodontal ligament and alveolar bone with
increased probing depth,recession or both”.

4. What is classification?
•Systematic collection of data or knowledge
& its arrangement in sequential manner in
order to facilitate its understanding or
knowledge.

5. •To provide maximum assistance in diagnosis & treatment
planning diseases have been classified mainly on the basis of
three criteria:-
CLINICAL
FEATURES
PATHOLOGICAL
CHANGES
ETIOLOGY

6. Helps in the development of frameworks to
study the -
I. aetiology,
II. Pathogenesis &
III. treatment of diseases;
•Common systems of classification allow
effective communication between health care
professionals using a common language.
Why Classification ?

7. HISTORICAL PERSPECTIVE
Girolamo Cardano is the
first person to differentiate
periodontal diseases.
 Fauchard (1723)-Scurvy of the gums

8.  Early 19th century- Riggs disease
 Introduced by John W Riggs (1810-1885)
 Known as “Father of Periodontology”
RIGGS disease-loss of alveoli
without loss of gums
•Death of periodontal membrane
•Deprives the alveoli of nutrition
•Death of alveolar bone

9. DESIRABLE CHARACTERISTICS OF A CLASSIFICATION
SYSTEM
1. Should have suitable organising
principle matching the nature of
the items being classified.
2. Every item should fall into at least
one of the classes.
3. No item should fall into more than
one of the classes.
4. Should serve its users.
5. Simpler the classification easier it
will be to remember and use.

10. NEED FOR CLASSIFICATION

11. •Dominant Paradigms in the historical
development of classification systems.
year Paradigms
1870–1920 The clinical features of the
diseases
1920–1970
•The concepts of classical
pathology
1970– present
Infectious etiology of the diseases

12. The clinical features of the diseases

13. •A paper was published by C.G. Davis in 1879 who believed that there
were three distinct forms of destructive periodontal disease:
C.G. Davis 1879

14. 1. No emphasis was given on age of onset of diseases
and rate of progression.
2. Inadequate or unclear classification criteria.
3. Little or no scientific evidence was used to support
the opinions of the clinicians of that time.
4. Periodontitis which can be due to systemic diseases
is not considered.
Limitations

15. G.V. Black (1886)
1. Constitutional gingivitis- scurvy, mercurial gingivitis,potassium iodide
gingivitis.
2. Painful form of gingivitis- a clinical condition that resembled what is
now termed acute necrotizing ulcerative gingivitis
(NUG).
3. Simple gingivitis - Associated with the accumulation of
debris / plaque.
4. Calcic inflammation of the peridental membrane-
5. Phagedenic pericementitis
(phagedenic = spreading ulcer or necrosis)
In a later publication Black replaced the term "Phagedenic
Pericementitis” with “chronic suppurative pericementitis”.

16. Drawbacks
Little or no scientific evidence was used.
No accepted terminology adopted.
Inappropriate emphasis on age of onset of diseases and
rates of progression of this diseases.
Inadequate or unclear classification criteria.
Periodontitis which can be due to systemic diseases is not considered.

17. Classical pathology
paradigm
(1920-1970)

18. During this period, the dominant term used for
destructive periodontal disease was pyorrhea
alveolaris. (Toirez , 1779)

19. •As the field 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
• The concept was introduced by Gottlieb and Orban based on
the over-interpretation of histopathological studies.
• Two forms of destructive periodontal diseases.
-Inflammatory
-Degenrative

20. •Gottlieb, in particular, 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”.
•Later called as “PERIODONTOSIS”
• He believed that he had discovered histological evidence of an
impairment in the continuous deposition of cementum.
(i.e. ‘cementopathia’).

21. Almost all classification systems from 1920–1970 included disease
categories labeled as
•‘dystrophic’-
(disorder due to defective or faulty nutrition)
•‘atrophic’-
(A wasting or decrease in size of a body organ, tissue)
•‘degenerative’-
(characterized by progressive deterioration and loss of
function in the organs or tissues)

22. 1.Schmutz-Pyorrhoe Inflammatory, deposits with shallow
pockets and resorption of the alveolar crest
2. Alveolar atrophy or Diffuse
atrophy
Non inflammatory disease ,
loosening of teeth,
No any deposits.
Pockets are formed only in later stages
3. Paradental-Pyorrhoe Irregularly distributed pockets - shallow
to extremely deep. May start as Schmutz-
Pyorrhoe or as diffuse atrophy
4.Occlusal trauma Physical overload which results in
resorption of the alveolar bone and
loosening of teeth.
Gottlieb (1928)

23. Limitations
• No microbial analysis.
• Inflammatory process is over interpretated as degenerative
process.
• Gingival diseases not included

24. Beck’s classification -1931

25. •Orban based this classification on a combination of his
perceptions of the etiologic,clinical, and pathologic features of
the diseases.
• He grouped them according to the ‘‘pathologic’’ categories of
Inflammation, Degeneration, Atrophy, Hypertrophy, and
Traumatism.
Orban’s classification(1942)

26. Orban’s classification(1942)
1. Inflammation
A. Gingivitis
a)Local
Calculus, food impaction, irritating restorations, etc.
b)Systemic
Pregnancy
Diabetes and other endocrine dysfunctions
Tuberculosis & Syphilis
Nutritional disturbances & Drug action
Allergy
B. Periodontitis
Simplex (secondary to gingivitis).
Complex ( secondary to periodontosis)

27. 2. Degeneration: Periodontosis
A. Systemic disturbances
Diabetes and other Endocrine dysfunctions
Blood dyscrasias
Nutritional disturbances
Nervous disorders
Infectious diseases
B. Hereditary
C. Idiopathic

28. 3. Periodontal Atrophy (Recession, no inflammation, no pockets;
osteoporosis.)
1. Local trauma (from toothbrush)
2. Presenile
3. Senile
5. Following inflammation
6. Idiopathic
4. Gingival Hypertrophy
1. Chronic irritation
2. Drug action (e.g.. Dilantin sodium)
3. Idiopathic
5. Periodontal Traumatism
A. Occlusal trauma

29. Demerits
1. Degeneration is not an appropriate word to be used, rather it
should be called Inflammatory diseases.
2. Microbiological bases were not given much importance.

30. Infection/ host response
Paradigm
(1970- present)

31. Soon after the 1876 publication of Robert Koch in which he
provided experimental proof of the germ theory of disease,
some dentists began to suggest that periodontal diseases
might be caused by bacteria.
(Harlan et al.)
W.D. Miller , in particular, was an early proponent of the
infectious nature of periodontal diseases.

32. Miller also recognized that certain systemic conditions (e.g.
diabetes, pregnancy) could modify the course of disease.
He was, however, an early advocate of the ‘Infection/Host
Response Paradigm’ that would come to dominate the field nearly
a hundred years later.

33. ‘Three factors are to be taken into
consideration in every case of pyorrhea
alveolaris: (1) predisposing circumstances, (2)
local irritation, (3) bacteria. ‘... pyorrhea
alveolaris is not caused by any specific
bacterium, which occurs in every case ..., but
various bacteria may participate in it ...’
Ref -(Miller WD, The Micro-organisms of
the Human Mouth . Philadelphia: The
S.S White Dental Mfg.Co,1890:328-334)

34. •The next major discovery in periodontal microbiology was
the preliminary demonstration in 1976–1977 of microbial
specificity at sites with periodontosis.
• This finding, coupled with the demonstration in 1977–
1979 that neutrophils from patients with juvenile
periodontitis (periodontosis) had defective chemotactic and
phagocytic activities .
• This marked the beginning of the dominance of
the Infection/Host Response paradigm.

35. •The classical ‘experimental gingivitis’ studies published by Harald
Loe et al,1965-1968 made infection / host response paradigm to be the
dominant paradigm.
•Their research work showed that host response is an important factor
in determining the disease progression and its outcome.

36. AAP -1977
•Juvenile Periodontitis
•Chronic Marginal
Periodontitis
RAMJFORD & ASH -1979

37. MERITS
1. simple & convenient way of categorizing periodontal
diseases.
2. Gingival atrophy or recession as a separate category.
DEMERITS
1. Periodontal abscess & perio-endo lesions not included.

38. PAGE AND SHROEDER (1982)
Based on age, pocket flora, leukocyte function tests, serum
antibodies, clinical & radiographic pictures, progression & history .

39. MERITS
• Simplified, convenient and uncomplicated.
• 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.
• Periodontal Abscess not included.
• Periodontic-endodontic lesions not included.
• Occlusal trauma not included.

40. Modification of Page & Schroeder,1982 hypothesis for the
pathogenesis of the disease:
1. Direct tissue destruction by bacteria &
metabolic products
2. Immune hyper-responsiveness
3. Immune deficiencies involving neutrophil
function (chemotaxis and phagocytosis)
Suzuki, 1988

41. SUZUKI, 1988
1.Adult periodontitis >35yrs
2.Rapidly progressive periodontitis
3.Juvenile periodontitis 12-26yrs
4.Post juvenile periodontitis 26-35yrs
5.Pre pubertal periodontitis <14yrs

42. American Acadamy of Periodontology (1986)
I. Juvenile Periodontitis
• A. Prepubertal
• B. Localized juvenile
periodontitis
• C. Generalized juvenile
periodontitis
II. Adult
Periodontitis
III. Necrotizing
Ulcerative Gingivo-
Periodontitis
IV. Refractory
Periodontitis

43. Demerits
1. Absence of a gingival diseases component .
2. Periodontitis which can be due to systemic diseases has not been
considered .
3. Periodontal abscess and periodontic-endodontic lesions were not
included.
4. Extensive overlap among the categories.
5. Age dependent classification of periodontitis appears invalid.

44. WORLD WORKSHOP OF CLINICAL
PERIODONTOLOGY, 1989
-depended heavily on the age of the patient and rates of
progression.

45. Merits:
• Inclusion of ‘Periodontitis Associated with Systemic
Disease’
• Inclusion of ‘Refractory periodontitis’

46. Drawbacks with the 1989 classification
•Did not include a gingivitis or gingival disease category.
•There was extensive crossover in rates of progression of the different
categories of periodontitis.
•'Refractory periodontitis‘,'Rapidly progressive periodontitis‘ &
'Prepubertal periodontitis' were heterogeneous category.

47. • As a consequence of these problems, the 1989 classification was criticized
shortly after it was published and a different system was proposed by Ranney in
1993.
• He suggested elimination of the ‘Refractory Periodontitis’ category since it
was a heterogeneous group and it was impossible to standardize the
treatment that necessarily would have to be given prior to making the
diagnosis.
• He recommended elimination of the ‘Periodontitis Associated with Systemic
Disease’ category since the, expression of all forms of periodontitis can be
modified by some systemic diseases or abnormalities,

48. Ranney 1993
I. Gingivitis
Gingivitis, (Plaque Bacteria )
-Non - Aggravated
-Systemically Aggravated
-Related To Sex Hormones
-Related To Drugs
-Related To Systemic Diseases
Necrotising Ulcerative Gingivitis
-Systemic Determinants Unknown
-Related To HIV
Gingivitis, Non-Plaque
-Associated With Skin Disease
-Allergic
-Infectious

49. II. Periodontitis
Adult Periodontitis
-Non-Aggravated
-Systemically Aggravated
(Neutropenia, Leukemias, Lazy Leukocyte Syndrome,
AIDS, Diabetes Mellitus)
Early Onset Periodontitis
1)Localised Early Onset Periodontitis
Neutrophil Abnormality
2)Generalised Early Onset Periodontitis
Neutrophil Abnormality,
Immunodeficient
3)Early Onset Periodontitis Related To Systemic Disease
AIDS,
Papillon-Lefevre Syndrome,
Chediak Higashi Syndrome,
Diabetes Mellitus Type I,
Trisomy 21,
4)Early onset periodontitis, systemic determinants unknown

50. Modifications:
• Elimination of the ‘Refractory Periodontitis’ category.
• Elimination of the ‘Periodontitis Associated with Systemic Disease’ category
Shortcomings:
• Lenghty.
• Trauma from occlusion factor was not considered.
• Periodontic-endodontic lesions were not included.
• Term adult periodontitis created a diagnostic dilemma for clinicians, needed to be
replaced with term chronic.

51. SO AGAIN A CLASSIFICATION SYSTEM WAS PROPOSED IN 1993 BY
EUROPEAN WORKSHOP IN PERIODONTOLOGY.
(ATTSTROM & VANDER VELDEN)
• Adult Periodontitis - Begins at the 4th decade of life, slow rate of progression of
disease.
• Early onset Periodontitis - Begins before the 4th decade of life, rapid rate of
progression of disease, altered host response is seen.
• Necrotizing Periodontitis -Tissue necrosis with clinical attachment and bone loss is
seen.

52. Elaboration of the broad spectrum of periodontal diseases encountered in clinical
practice was absent in the 1993 European classification.
during the 1996 World Workshop in Periodontics, the need for a revised
classification system for periodontal diseases was stressed.
In 1997, the 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.
The International Workshop for a Classification of Periodontal Diseases and
Conditions was held and a new classification was agreed upon in 1999.
(Oct 30-Nov 2)

53. So why we acknowledged previous classification systems?
Because to understand present status of our understanding in field
of periodontology we first have to know our journey to present so
that we can understand upcoming classification systems.

54. •Classification of American acadamy of periodontology 1999
•Changes in the classification system
•New classification 2017
•Implementation of the New Classification of Periodontal
diseases
Part 2

55. 1999 classification of periodontal diseases

56. American acadamy of periodontology 1999
GINGIVAL DISEASES
Dental plaque induced
Non plaque induced
CHRONIC PERIODONTITIS
Localised
Generalised
AGGRESSIVE PERIODONTITIS
Localised
Generalised
PERIODONTITIS AS MANIFESTATION SYSTEMIC DISEASES
Associated with hematological disorders
Associated with genetic disorders
Not otherwise specified

57. NECROTIZING PERIODONTAL DISEASES
Necrotizing Ulcerative gingivitis
Necrotizing Ulcerative periodontitis
ABSCESSES OF THE PERIODONTIUM
Gingival abscess
Periodontal abscess
Periocoronal abscess
PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS
Endodontic –periodontal lesion
Periodontal – endodontic lesion
Combined lesion
DEVELOPMENTAL OR ACQUIRED DEFORMITIES OR CONDITIONS
Localized tooth related
Mucogingival deformities around teeth
Mucogingival deformities in edentulous area
Occlusal trauma

61. CHANGES IN THE CLASSIFICATION SYSTEM FOR
PERIODONTAL DISEASE

63. Addition of a ‘Gingival Disease’ Category
• Important inclusion in the classification.
• Split into ‘plaque-induced’ and ‘nonplaque- induced’ gingival
diseases.
Highlights of classification

64. Dental Plaque–Induced Gingival Diseases
•Most common.
•occur on a periodontium with no attachment loss or on a periodontium
with attachment loss that is stable and not progressing (i.e., reduced
periodontium).
•Treated cases, where gingival inflammation recurs around teeth with
existing attachment loss due to a history of treated periodontitis, the
appropriate diagnosis would be gingivitis on a reduced periodontium.

65. Sub classification of ‘Periodontal Disease as a
Manifestation of Systemic Disease’
‘ ‘
Periodontitis associated
with systemic disease’
(1989)
periodontal disease as a
manifestation of
systemic disease’(1999)
•Diabetes mellitus has not been included in this subclass as it can modify all forms
of periodontal disease, and there is insufficient information to conclude that there
is a specific diabetes mellitus-associated form of periodontitis.
•smoking, which is therefore also not included because it is considered a
significant modifier of all periodontal diseases

66. Replacement of ‘ANUG’ and ‘ANUP’ with ‘Necrotizing
Periodontal Diseases’
•The workshop agreed that ANUG and ANUP were clinically distinguishable
disease entities, although they were unsure whether they were two separate
diseases or part of the same disease process.
• Insufficient evidence to warrant two separate categories and the term
‘necrotizing periodontal diseases’ was introduced.
• 1999 classification omitted ‘acute necrotizing stomatitis’ which would have
been a useful inclusion.

67. Removal of ‘Refractory Disease’ as a Term
Refractory disease can be defined by the 1989 classification as continued loss of
attachment despite the provision of adequate treatment and the patient
maintaining a good level of oral hygiene.
1999 Workshop considered that ‘refractory disease’ was not a separate disease
entity, suggesting that any periodontal disease could be termed ‘recurrent
disease’ (‘recurrent aggressive periodontitis’, ‘recurrent chronic periodontitis’,
etc.).

68. ‘Chronic Periodontitis’ Instead of ‘Chronic Adult
Periodontitis’
• In the 1999 classification, ‘chronic periodontitis’ was subdivided into localized and
generalized on the basis of the number of sites affected, localized being up to 30% of
sites, and generalized being more than 30% of sites.
• 1999 Workshop suggested that the severity of disease could be categorized on the
basis of clinical attachment loss (CAL):
• Mild : CAL 1–2 mm.
• Moderate : CAL 3–4 mm.
• Severe : CAL 5 mm or more.

69. •Traditionally, the term ‘adult periodontitis’, used by previous
classification systems, relates to patients over the age of 35 years, and
approximately 16% of the population over this age will have disease.
• However, it is important to note that adolescents also suffer from
slowly progressive attachment loss; hence chronic disease.

70. ‘Aggressive Disease’ in place of ‘Early-
onset Periodontitis’
•In the 1999 classification, ‘aggressive disease’ was defined as
disease in patients who were systemically healthy, had rapid
loss of attachment and alveolar bone, and a high incidence of a
familial link.
• Is useful as it addresses the clinical behavior of the disease but
avoids the controversial age barrier.

71. • Clearly, older subjects can experience episodes of more
rapid attachment loss; whilst this is rare ,it is embraced by
the new system.
• However, it is accepted that most patients falling into this
category will be less than 30 years old.

72. Addition of ‘Periodontal– Endodontic Lesions’
The 1989 classification did not include this group,
and this was amended in 1999 to include only one
category: the ‘combined lesion’.
This had been recommended in an earlier
publication
(Chapple ILC, Lumley PJ. The
periodontal endodontic interface.
Dent Update 1999)
Was welcomed because it implied a single
treatment regimen based on the pathology
present and not on the aetiology of the lesion

73. • The removal of this diagnostic category from the classification systems
is unfortunate because localized juvenile periodontitis is the most well
defined of all periodontal diseases.
• Features include-
• a strong association with Actinomyce’s actinomycetemcomitans.
• reduced chemotactic and phagocytic activity of the host’s
polymorphonuclear cells;
• strong family history, suggesting a genetic association.
Removal of ‘Localized Juvenile Periodontitis’

74. • It is an 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)
DRAWBACKS

75. • 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.

76. Update of AAP 1999 to be revised in 2017
• The Academy announced that an update to the 1999
Classification would commence in 2017.
• Three specific areas of concern:-
• ATTACHMENT LEVEL
• CHRONIC versus AGGRESSIVE PERIODONTITIS
• LOCALIZED versus GENERALIZED PERIODONTITIS

77. They added other parameters to the 1999
Classification of Periodontal Diseases and Conditions such as
radiographic bone loss in association with clinical
attachment loss.
2015 Task Force Report by the American
Academy of Periodontology
Mild periodontitis-
Reduction of 1–2 mm CAL and up to 15% of root length
or ≥2 mm & ≤3 mm bone loss .
Moderate Periodontitis
3–4 mm CAL and 16–30% or >3 mm & ≤5 mm bone
loss.
Severe Periodontitis
CAL ≥ 5 mm and bone loss >30%

78. •The New Classification is the product of the World Workshop on the
Classification of Periodontal and Peri-implant Diseases and
Conditions, held in Chicago in November 2017.
•The New Classification updates the previous classification made in
1999.
•The new classification was presented formally by the two
organisations at the EuroPerio congress in Amsterdam in June 2018.

79. HOW WAS 2017 CLASSIFICATION FRAMED?
• Two organisation involved –AAP & EFP.
• Aimed to create a consensus knowledge base to enable the two
organisation to promote a new classification globally.
• Involved 130 experts & review authors who reviewed the scientific
evidence to update the classification scheme.
• 4 working groups of the world workshop are:
1. Periodontal health, gingival health and conditions
2.Periodontitis
3. Periodontal manifestation of systemic disease
4. Peri implant health and condition

80. • The organising committee commissioned 19 review
paper and 4 consensus reports .
• One of the key task of working group was to define
what is meant by periodontal health , because unless
you define health you cannot define disease.

81. Classification of periodontal health , gingival health ,diseases and conditions
was introduced.
 Peri implant diseases and conditions were added.
 Defination periodontal health given.
 Term plaque induced replaced by dental biofilm induced.
 Systemic risk factors newly added are smoking, hyperglycemia, nutrtional
factors, pharmacological agents, sex steroid harmones, haematological
condition.
 Mycobacterium tuberculosis added to specific infection of bacterial origin.
 Specific infection of viral origin is discussed in detail – coxsackie virus,
molluscum contagiosum.
key changes in 2017

82.  Candidosis is added to specific infection of fungal origin.
 Linear gingival erthyma is removed.
 Erythema multiforme and drug induced category is removed.
 Granulomatous inflammatory lesion and reactive process category
is added.
 Neoplasmas and gingival pigmentation category is newly added.
 Chronic and aggressive periodontitis is removed .
 Multi dimensional staging and grading added for periodontitis.

83. Four major advances from previous classification:
There is a widespread welcome for an updated classification :
1) Definition of periodontal health
2) Replacement of chronic and aggressive periodontitis with a model
based on stages and grades.
3) The support given to personalised medicine.
4) The inclusion of peri implant disease and condition

84. 2017 CLASSIFICATION OF PERIODONTAL DISEASES

85. •PERIODONTAL HEALTH ,GINGIVAL DISEASES AND
CONDITIONS
•FORMS OF PERIODONTITIS
• PERIODONTAL MANIFESTATION OF SYSYTEMIC DISEASES
AND DEVELOPMENTAL AND ACQUIRED CONDITIONS
•PERI-IMPLANT DISEASES AND CONDITION

86. 1. PERIODONTAL HEALTH AND GINGIVAL HEALTH.
• Clinical gingival health on an intact periodontium.
• Clinical gingival health on a reduced periodontium.
Stable periodontitis patient.
Non periodontitis patient.
2. GINGIVITIS DENTAL BIOFILM INDUCED
• Associated by dental biofilm alone.
• Mediated by systemic or local risk factors.
• Drug influenced gingival enlargement.
3. GINGIVAL DISEASES – NON DENTAL BIOFILM INDUCED
• Genetic/developmental disorders.
• Specific infections.
• Inflammatory and immune conditions.
• Reactive processes.
• Neoplasm.
• Endocrine, nutritional and metabolic diseases.
• Traumatic lesions.
• Gingival pigmentation.
Periodontal health ,gingival diseases and conditions

87. FORMS OF PERIODONTITIS
1. NECROTIZING PERIODONTAL DISEASES
•Necrotizing gingivitis
•Necrotizing periodontitis
•Necrotizing stomatitis
2. PERIODONTITIS AS MANIFESTATION OF SYSTEMIC DISEASES
Classification of theses conditions should be based on the primary systemic disease
according to the international statistical classification of diseases and related health
problems(ICD) codes

88. 3. PERIODONTITIS
• STAGES: Based on severity and complexity of management
Stage I: initial periodontitis
Stage II: Moderate periodontitis
Stage III: Severe periodontitis with potential for additional tooth loss
Stage IV: Severe periodontits with potential for loss of the dentition
• EXTENT AND DISTRIBUTION: Localized; Generalized; Molar-Incisor distribution
• GRADES: Evidence or risk of rapid progression, anticipated treatment resonse
Grade A: Slow rate of progression.
Grade B: Moderate rate of progression.
Grade C: Rapid rate of progression.

89. 3. PERIODONTITIS
• Staging –
– CAL, bone loss, PD, angular defect,
furcation, mobility,
tooth loss.
• Grading –
feature, history, rate, risk of
further progression.

90. 1
2
3
4

91. • Initial stage determined using CAL.
• Tooth loss – modify stage.
• Complexity factor shifts stage – high mobility.
• POST TREATMENT PATIENTS:
CAL, RBL, complexity factor eliminated – not retrogress –
consider always in maintanence.

92. GRADING

94. PERIODONTAL MANIFESTATION OF SYSYTEMIC DISEASES AND
DEVELOPMENTAL AND ACQUIRED CONDITIONS
1. SYSTEMIC DISEASES OR CONDITIONS AFFECTING THE PERIODONTAL SUPPORTING TISSUES
2. OTHER PERIODONTAL CONDITIONS
Periodontal abscesses
Endodontic periodontal lesions
3. MUCOGINGIVAL DEFORMITIES AND CONDITIONS AROUND TEETH
Gingival phenotypes
Gingival/soft tissue recession
Lack of gingiva
Decreased vestibular depth
Aberrant frenum/muscle position
Gingival excess
Abnormal color
Conditions of the exposed root surface

95. 4. TRAUMATIC OCCLUSAL FORCES
• Primary occlusal forces
• Secondary occlusal forces
• Orthodontic forces
5. PROSTHESES AND TOOTH RELATED FACTORS THAT MODIFY OR
PREDISPOSE TO PLAQUE INDUCED GINGIVAL DISEASES/PERIODONTITIS
• Localized tooth related factors
• Localized dental prosthesis related factors.

96. PERI-IMPLANT DISEASES AND CONDITION
1. PERI-IMPLANT HEALTH
2. PERI-IMPLANT MUCOSITIS
3. PERI-IMPLANTITIS
4. PERI-IMLANT SOFT AND HARD TISSUE DEFICIENCY

97. Peri-implant health presents with a core of connective tissue
covered by keratinized or nonkeratinized epithelium and the
intrabony part of the implant is in contact with mineralized
bone.
Peri-implant health

98. Peri-implant mucositis is indicated by the presence of bleeding on
probing and clinical signs of inflammation. It is primarily thought to
be caused by plaque as it often resolves with better home care and
a proper in-office treatment to reduce biofilm
Peri-implant mucositis

99. •Peri-implantitis is characterized by the presence of bleeding on
probing, clinical signs of inflammation, and radiographic bone loss.
•It is often seen in patients with a history of periodontitis and
progresses quickly in a nonlinear pattern.
Peri-implantitis

100. •Soft- and hard-tissue implant site deficiencies occur after tooth loss and
lead to diminished alveolar ridge/process.
•Prior to tooth removal, if a root fracture, abscess, thin buccal bone
plates, or endodontic infection is present, it can result in greater loss of
the alveolar ridge/process.
•Medications and systemic diseases also reduce the amount of natural
formed bone. In these cases, further treatment would be indicated prior
to implant placement.
Soft- and hard-tissue implant site deficiencies

101. Implementation of the New Classification of
Periodontal Diseases: Decision-making
Zerodonto/Marianosanz,tonetti/2april2019

102. STEP 1 – New patient

103. STEP 2 – Patient suspected of periodontitis

104. Patient is a periodontitis case whose stage
needs to be established

105. Stages III and IV versus I and II

106. STEP 3c –
Stages I, II, III, and IV

107. STEP 4a –
Grading when there
are no existing records
bone
loss/age
(BL/A)
ratio
<0.25 = Grade A
0.25 -1.0 = Grade B
>1.0 = Grade C
Bone loss in chronic periodontitis was
assessed from panoramic radiographs
by direct measurement from the
cemento-enamel junction (CEJ) and by
measuring the proportion of the tooth
length supported by bone

108. STEP 4b – Grading when there are existing
records
The rate of periodontitis
progression over the
previous five years should
be calculated.

109. •Classification systems for periodontal diseases have evolved based
on the understanding of the nature of the diseases.
•Although classification systems for periodontal diseases currently in
use are based on, the Infection/Host Response paradigm, some
features of the older paradigms are still valid and have been
retained.
•This new system is not perfect and will need to be modified.
•One of the interesting historical features of classification systems is
the often intense resistance to their modification. However,
classification systems should be viewed as dynamic works-in-
progress that needs to be periodically modified based on current
thinking and new knowledge
Conclusion

110. •Gary C. Armitage, Periodontal diagnosis and classification of periodontal diseases.
Periodontology 2000, Vol 34, 2004, 9-21
•Gary C. Armitage, Development of a classification system for periodontal diseases
and conditions. Ann Periodontol 1999;4:1-6.
•Classification of Periodontal Diseases: Where were we? Where are we now? Where
are we going? M.R. Milward and i.L.C. Chapple
•Classifying periodontal diseases – a long-standing Dilemma Development of a
Classification System Periodontal Diseases and Conditions Gary C. Armitage
•A new classification scheme for periodontal and peri-implant diseases and
conditions – Introduction and key changes from the 1999 classificationJ Periodontol.
2018;89(Suppl 1):S1–S8.
•clinical textbook of periodontology carranza.
References