The classification of periodontal diseases and conditions in the past and present presented to you by Dr. Salam Jawad and Dr. Rusul Mohammed

1. Classification of periodontal diseases and
conditions past and present
By:
Abd AL Salam Jawad Kadhim
Rusul Mohammed Mando
Fifth grade
Supervised by:
Dr. Ali Abbas Abdul Kareem
B.D.S,MSc.

3. INTRODUCTION
Over the years, discernment of the nature of periodontal diseases was achieved
successfully due to extensive research in this field. experts have worked
towards periodically developing a new classification system for periodontal
diseases or to improve an existing one. The concept of classification systems is
considered as uninteresting by many, but it provides us with a framework to
come to a diagnosis. The intricacy of periodontal diseases can be understood
by classifying various diseases. Its goals are:
To provide a foundation to study the etiology, susceptibility traits,
pathogenesis, and treatment of diseases in an organized manner.
To give clinicians a way to organize the health care needs of their patients.
Assemble similar disease phenotypes in more homogeneous syndromes.

4. Three paradigms that reflected the understanding of the nature of periodontal
diseases were noticed during the evolution of periodontal diseases :
(~1870–1920): Clinical characteristics paradigm. For the period from
approximately 1870 to 1920, the researchers had insufficient information
about the etiopathogenesis of periodontal diseases.
(~1920–1970): Classical pathology paradigm. During this time a new
concept developed that periodontal diseases can be of 2 types-inflammatory
and non-inflammatory (‘degenerative’ or ‘dystrophic’).
(~1970–present): Infection/ host response paradigm. After the publication
of Robert Koch’s postulates (1876), researchers stressed upon the
infectious nature of periodontal diseases.
paradigm Classification systems in the modern era represent a blend of all
three paradigms since there is a certain amount of gravity to some of the
earliest thoughts about the nature of periodontal diseases. History reveals that
people in the past opposed the modification of these entities. They were
adamant to accept a particular classification in spite of it having many flaws.
But in the true sense, they should be periodically modified based on modern
thinking and concepts.

5. CHRONOLOGICAL CLASSIFICATION OF
PRIODONTAL DISEASES
1.Kantorowicz (1924)
2.McCall and Box (1925)
3.Simonton (1927)
4.Haupi and Lang (1927)
5.Gottlieb (1928)
6.Becks (1929/1931)
7.Jaccard (1930/1933)
8.Roy (1935)
9.Robinson (1935)
10.Weski (1937)
11.Isadore Weinmann (1934-1957)
12.Thoma and Goldman (1937)
13.Fish (1944/1952)

6. 14.Hine and Hine (1944)
15.Orban (1942/1949)
16.Hulin (1949)
17.Held (1949)
18.Pucci (1950)
19.Lyons (1951)
20.Miller (1950)
21.Kerr (1951)
22.Goldman (1956)
23.McCall (1956)
24.American Academy of Periodontology (1957)
25.Robinson (1959)
26.Carranza (1959)
27.Ray (1962)
28.Glickman (1964)

7. 29.Drum (1975)
30.American Academy of Periodontology (1987)
31.World Workshop in Clinical Periodontics Classification (1989)
32.European Workshop in Periodontology Classification (1993)

8. 33.American Academy of Periodontology (1999)
I. Gingival Diseases
i. Dental plaque-induced gingival diseases
A. Gingivitis associated with dental plaque only
1. without other local contributing factors
2. with local contributing factors (see VIII A)

9. B. Gingival diseases modified by systemic factors
1. associated with the endocrine system
a) puberty-associated gingivitis
b) menstrual cycle-associated gingivitis

10. c) pregnancy-associated
1) gingivitis
2) Pyogenic Granuloma

11. d) diabetes mellitus-associated gingivitis
2. associated with blood dyscrasias
a) leukemia-associated gingivitis
b) other

12. C. Gingival diseases modified by medications
1.drug-influenced gingival diseases
a)drug-influenced gingival enlargements
b)drug-influenced gingivitis
1)oral contraceptive-associated gingivitis
2)other

13. ii. Non-plaque-induced gingival lesions
A. Gingival diseases of specific bacterial origin
1. Nesseria gonorrhea-associated lesions
2. Treponema pallidum-associated lesions
3. Streptococcal species-associated lesions
4. Other

14. B. Gingival diseases of viral origin
1. herpesvirus infections
a) primary herpetic gingivostomatitis
b) recurrent oral herpes
c) varicella-zoster infections
2. other

15. C. Gingival diseases of fungal origin
1. Candida-species infection
a) generalized gingival candidiasis
2. linear gingival erythema
3. histoplasmosis
4. other

16. D. Gingival lesions of genetic origin
1. hereditary gingival fibromatosis
2. other
E. Gingival manifestations of systemic conditions
1. mucocutaneous disorders
a) lichen planus

17. b) pemphigoid
c) Pemphigus vulgaris
d) Erythema multiforme

18. e) lupus erythematosus
f) drug-induced
g) other

19. 2. allergic reactions
a) dental restorative materials
1) mercury
2) nickel
3) acrylic
4) other

20. b) reactions attributable to
1) toothpastes/dentifrices
2) mouth rinses/mouth washes
3) chewing gum additives
4) foods and additives
c) other

21. F . Traumatic lesions (factitious, iatrogenic, accidental)
1. chemical injury
2. physical injury
3. thermal injury

22. G. Foreign body reactions
H. Not otherwise specified (NOS)

23. II. Chronic Periodontitis
i. Localized
ii. Generalized
III. Aggressive Periodontitis
i. Localized
ii. Generalized

24. IV. Periodontitis as a manifestation of Systemic Diseases
i. Associated with hematological disorders
A. Acquired Neutropenia
B. Leukemias
C. Other

25. ii. Associated with genetic disorders
A. Familial and Cyclic Neutropenia
B. Down syndrome

26. C. Leukocyte adhesion deficiency syndromes
D. Papillon-Lefėvre syndrome
E. Chediak-Higashi syndrome

27. F. Histocytosis syndromes
G. Glycogen storage disease
H. Infantile genetic Agranulocytosis

28. I. Cohen syndrome
J. Ehlers-Danlos syndrome (Types IV and V)
K. Hypophosphatasia
L. Other

29. iii. Not otherwise specified (NOS)
V. Necrotizing Periodontal Diseases
i. Necrotizing ulcerative gingivitis (NUG)
ii. Necrotizing ulcerative Periodontitis (NUP)

30. VI. Abscesses of the Periodontium
i. Gingival abscess
ii. Periodontal abscess
iii. Pericoronal abscess

31. VII. Periodontitis associated with Endodontic Lesions
i. combined periodontic-endodontic lesions
VIII. Developmental or Acquired Deformities and conditions
i. Localized tooth-related factors that modify or predispose to plaque-induced
gingival diseases/ Periodontitis
A. Tooth anatomic factors

32. B. Dental restorations/appliances
C. Root fractures
D. Cervical root resorption and cemental tears

33. ii. Mucogingival deformities and conditions around teeth
A. Gingival/soft tissue recession
1. facial or lingual surfaces
2. interproximal (papillary)
B. Lack of keratinized tissue

34. C. Decreased vestibular depth
D. Aberrant frenum/muscle position

35. E. Gingival excess
1. Pseudopocket
2. inconsistent gingival margin
3. excessive gingival display

36. 4. gingival enlargement
F. Abnormal color

37. iii. Mucogingival deformities and conditions on edentulous ridges
A. Vertical and horizontal ridge deficiency
B. Lack of gingival/keratinized tissue
C. Gingival/soft tissue enlargement
D. Aberrant frenum/muscle position
E. Decreased vestibular depth
F. Abnormal color

38. iv. Occlusal trauma
A. Primary occlusal trauma
B. Secondary occlusal trauma

39. Changes in the classification of periodontal diseases :
Addition of a section on “Gingival Diseases”.
Replacement of “Adult Periodontitis” with “Chronic Periodontitis”.
Replacement of “Early-Onset Periodontitis” with “Aggressive Periodontitis”.
Elimination of a separate disease category for “Refractory Periodontitis”.
Clarification of the designation “Periodontitis as a Manifestation of Systemic
Diseases”.
Replacement of “Necrotizing Ulcerative Periodontitis” With “Necrotizing
Periodontal Diseases”.
Addition of a category on “Periodontal Abscess”.
Addition of a category on “Periodontic-Endodontic Lesions”.
Addition of a category on “Developmental or Acquired Deformities and
Conditions”.

40. It appears that throughout history we went from short to lengthy to moderate to longer
classifications as we realized the multiple complications of pure periodontitis to the
role of medical factors in the periodontal disease process and the role of periodontal
disease in contributing to medical problems. Now we are considering the enormity of
periodontal disease as it relates to the patients’ overall health. While most of the
classifications listed are for pure historical comparison the only classifications that are
of significant importance are those of Dr. I. Weinmann (1934-1957), Dr. I. Glickman
(1964), and The American Academy of Periodontology (1987 and 1999). These all
show the value of a good and thorough classification .
But in the 1999 classification the following are points of disagreement :
The word “other” too freely used.
Under “drug-influenced gingival diseases” it does not mention the effects of
alcohol, cocaine, and heart medications as causing increased plaque formation and
stimulating gingival overgrowth.
There is no discussion of TMJ and stress as an aggravating factor in periodontal
disease.
There is no mention of the biochemical mediators of the gingival crevicular fluid
and their affects upon the periodontal tissues .

41. The section on occlusal trauma does not in our opinion adequately cover the
magnitude of the pathology associated with occlusion, malocclusion, and the habit
neuroses.
We still believe in the breakdown of “adult Periodontitis” over “chronic
Periodontitis” .
With Juvenile (early onset) Periodontitis which is age-related instead of
“Aggressive Periodontitis” which means Rapidly Progressing Periodontitis (RPP)
independent of age despite totally adequate periodontal therapy.
in aggressive Periodontitis we have two categories that involve. Localized Juvenile
Periodontitis (LAP) and Generalized Juvenile Periodontitis (GAP). Both forms
share the following features - rapid loss of attachment and bone; patients are
clinically healthy except for the presence of Periodontitis; and familial aggregation.
LAP patients have a big serum antibody response; whereas, GAP patients have a
poor antibody response to the infecting agents.
NUP involves a great deal of alveolar bone and attachment loss; whereas, in NUG
loss of clinical attachment is generally absent. as well as attempting to make the
classification of periodontal disease a more realistic, current concept as we become
aware of more medical problems that are influenced by periodontal diseases and the
more periodontal problems that are affected by medical diseases.

42. A new classification scheme for periodontal and peri‐implant
diseases and conditions 2017
PERIODONTAL HEALTH, GINGIVAL DISEASES/CONDITIONS
I. Periodontal health and gingival health
i. Clinical gingival health on an intact periodontium

43. ii. Clinical gingival health on a reduced periodontium
A. Stable periodontitis patient
B. Non-periodontitis patient

44. II. Gingivitis – dental biofilm-induced
i. Associated with dental biofilm alone
ii. Mediated by systemic or local risk factors
iii. Drug-influenced gingival enlargement

45. III. Gingival diseases – non-dental biofilm induced
i. Genetic/developmental disorders
ii. Specific infections
iii. Inflammatory and immune conditions

46. iv. Reactive processes
v. Neoplasms
vi. Endocrine, nutritional & metabolic diseases

47. vii. Traumatic lesions
viii. Gingival pigmentation

48. FORMS OF PERIODONTITIS
I. Necrotizing periodontal diseases
i. Necrotizing gingivitis
ii. Necrotizing periodontitis
iii. Necrotizing stomatitis

49. II. Periodontitis as manifestation of systemic diseases
Classification of these conditions should be based on the primary systemic disease
according to the international statistical classification of diseases and related health
problems (ICD) codes.

50. III. Periodontitis
i. Stages : based on severity and complexity of management
A. Stage I: initial periodontitis
B. Stage II: moderate periodontitis

51. C. Stage III: severe periodontitis with potential for additional tooth loss
D. Stage IV: severe periodontitis with potential for loss of the dentition

52. ii. Extent and distribution : localized; generalized; molar-incisor distribution
iii. Grades : evidence or risk of rapid progression , anticipated treatment response
A. Grade A: slow rate of progression
B. Grade B: moderate rate of progression
C. Grade C: rapid rate of progression.

54. PERIODONTAL MANIFESTATIONS OF SYSTEMIC DISEASES AND
DEVELOPMENTAL AND ACQUIRED CONDITIONS
I. Systemic diseases or conditions affecting the periodontal
supporting tissues
II. Other periodontal conditions
i. Periodontal abscesses
ii. Endodontic-periodontal lesions

55. III. Mucogingival deformities and conditions around teeth
i. Gingival phenotype
ii. Gingival/soft tissue recession

56. ii. Lack of gingiva
iv. Decreased vestibular depth
v. Aberrant frenum/muscle position

57. vi. Gingival excess
vii. Abnormal color
viii. Condition of the exposed root surface

58. IV. Traumatic occlusal forces
i. Primary occlusal trauma
ii. Secondary occlusal trauma
iii. Orthodontic forces

59. V. Prostheses and tooth-related factors that modify or predispose
to plaque-induced gingival diseases/periodontitis
i. Localized tooth-related factors
ii. Localized dental prostheses-related factors

60. PERI-IMPLANT DISEASES AND CONDITIONS
I. Peri-implant health
II. Peri-implant mucositis
III. Peri-implantitis

61. IV. Peri-implant soft and hard tissue deficiencies

62. Peri‐implant health: Clinically, peri‐implant health is characterized by an absence of
visual signs of inflammation and bleeding on probing. Peri‐implant health can exist
around implants with normal or reduced bone support. It is not possible to define a
range of probing depths compatible with peri‐implant health.
Peri‐implant mucositis: Characterized by bleeding on probing and visual signs of
inflammation. While there is strong evidence that peri‐implant mucositis is caused by
plaque, there is very limited evidence for non‐plaque induced peri‐implant mucositis.
Peri‐implant mucositis can be reversed with measures aimed at eliminating the plaque.
Peri‐implantitis: Defined as a plaque‐associated pathologic condition occurring in the
tissue around dental implants, characterized by inflammation in the peri‐implant
mucosa and subsequent progressive loss of supporting bone. Peri‐implant mucositis is
assumed to precede peri‐implantitis. Peri‐implantitis is associated with poor plaque
control and with patients with a history of severe periodontitis. The onset of
peri‐implantitis may occur early following implant placement as indicated by
radiographic data. Peri‐implantitis, in the absence of treatment, seems to progress in a
non‐linear and accelerating pattern.

63. Hard and soft tissue implant site deficiencies: Normal healing following tooth
loss leads to diminished dimensions of the alveolar process/ridge that result in
both hard and soft tissue deficiencies. Larger ridge deficiencies can occur at
sites associated with severe loss of periodontal support, extraction trauma,
endodontic infections, root fractures, thin buccal bone plates, poor tooth
position, injury and pneumatisation of the maxillary sinuses. Other factors
affecting the ridge can be associated with medications and systemic diseases
reducing the amount of naturally formed bone, tooth agenesis, and pressure
from prostheses.
Changes in this classification :
Mucogingival conditions.
Occlusal trauma and traumatic occlusal forces.
Prosthesis‐ and tooth‐related factors.

68. The 2017 World Workshop Classification system for periodontal and peri-implant
diseases and conditions was developed in order to accommodate advances in
knowledge derived from both biological and clinical research, that have emerged since
the 1999 International Classification of Periodontal Diseases.
Importantly, it defines clinical health for the first time, and distinguishes an intact and
a reduced periodontium throughout. The term 'aggressive periodontitis' was removed,
creating a staging and grading system for periodontitis that is based primarily upon
attachment and bone loss and classifies the disease into four stages based on severity (I,
II, III or IV) and three grades based on disease susceptibility (A, B or C).
The workshop addressed unresolved issues with the previous classification by
identifying the difference between presence of gingival inflammation at one or more
sites and the definition of a gingivitis case.
It agreed that bleeding on probing should be the primary parameter to set thresholds for
gingivitis. The workshop also characterized periodontal health and gingival
inflammation in a reduced periodontium after completion of successful treatment of a
patient with periodontitis.

69. Specific definitions were agreed to with regard to cases of gingival health or
inflammation after completion of periodontitis treatment based on bleeding on probing
and depth of the residual sulcus/pocket.
This distinction was made to emphasize the need for a more comprehensive
maintenance and surveillance of the successfully treated patient with periodontitis. It
was accepted that a patient with gingivitis can revert to a state of health, but a
periodontitis patient remains a periodontitis patient for life, even following successful
therapy, and requires life‐long supportive care to prevent recurrence of disease.
The workshop also reorganized the broad spectrum of non‐plaque induced gingival
diseases and conditions based on primary etiology