4. LIMITATIONS OF 1999 CLASSIFICATION
• Understanding of periodontal disease is not complete enough to base our classification
on etiology.
• The 1999 classification system depends upon assessing the rate of progression spread
over multiple appointments in order to diagnose aggressive periodontitis. It is not
possible for patient to repeat clinical visits just to place him/her under a specific disease
entity such as aggressive or chronic periodontitis.
Flemingson J. Lazarus et al Periodontal Disease Classification:Controversies, Limitations and the Road
Ahead- A Proposed New Classification Journal of the International Academy of Periodontology 2012 14/4:84-
90.
5. • In spite of rapid advancement in the field of implantology, there is no provision in the
present classification for the diseases around implants, leaving a significant void
(Armitage, 1999; Devi and Pradeep, 2009)
• All the risk factors are not considered, e.g., smoking and diabetes (Armitage, 1999)
Jack G. Caton et al A new classification scheme for periodontal and peri‐implant diseases and conditions
– Introduction and key changes from the 1999 classification J Clin Periodontol. 2018;45:45(Suppl 20);S1–
9. Dental plaque induced gingival conditions
REVISED CLASSIFICATION
1) description of the extent and severity
of the gingival inflammation,
2) description of the extent and severity
of gingival enlargements,
3) a reduction in gingival disease
taxonomy, and
4) discussion of whether mild localized
gingivitis should be considered a
disease or variant of health.
11. FEATURES OF 2017 CLASSIFICATION
• Staging levels indicate the severity of the disease and the complexity of disease
management and is determined after considering several variables including clinical
attachment loss, amount and percentage of bone loss, probing depth, presence and
extent of angular bony defects and furcation involvement, tooth mobility, and tooth
loss due to periodontitis.
• Grading structure considers supplemental biologic characteristics of the patient in
estimating the rate and likelihood of periodontitis progression.
12. • The four categories of periodontitis staging are determined by a number of
variables and range from the least severe Stage I to most severe Stage IV.
• The three levels of periodontitis grading—which consider a patient’s overall health
status and risk factors such as smoking and metabolic control of diabetes—
indicate low risk of progression (Grade A), moderate risk of progression (Grade
B), and high risk of progression (Grade C).
22. Mucogingival conditions and deformities
(Cortellini & Bissada)
• Periodontal” “Biotype”/ “Morphotype” / “Phenotype
The distinction among different biotypes is based upon anatomic characteristics of
components of the masticatory complex, including:
1) Gingival biotype, which includes in its definition gingival thickness (GT) and
keratinized tissue width (KTW);
2) Bone morphotype (BM); and 3) Tooth dimension.
23.
24. • A recent systematic review using the parameters reported previously, classified the
“biotypes” in three categories:
• Thin scalloped biotype in which there is a greater association with slender triangular crown,
subtle cervical convexity, interproximal contacts close to the incisal edge and a narrow zone of
KT, clear thin delicate gingiva, and a relatively thin alveolar bone.
• • Thick flat biotype showing more square‐shaped tooth crowns, pronounced cervical convexity,
large interproximal contact located more apically, a broad zone of KT, thick, fibrotic gingiva,
and a comparatively thick alveolar bone.
• • Thick scalloped biotype showing a thick fibrotic gingiva, slender teeth, narrow zone of KT,
and a pronounced gingival scalloping.
25. Gingival thickness, is assessed by:
– Transgingival probing
– Ultrasonic measurement.
– Probe visibility
• Gingiva was defined as thin (≤1.0 mm) or thick (>1 mm) upon the observation of the
periodontal probe visible through the gingiva.
• A color‐coded probe was proposed to identify four gingival biotypes (thin, medium,
thick and very thick).
26. • Keratinized tissue width(KTW)
– Thin biotype - 2.75 mm to 5.44mm
– Thick biotype - 5.09 mm to 6.65 mm
• Gingival thickness(GT)
– Thin biotype – 0.63mm
– Thick biotype - 1.79 mm.
• Bone morphotype
– Thin biotype – 0.343mm
– Thick biotype - 0.754 mm.
27. • Recession Type 1 (RT1):
Gingival recession with no loss of interproximal attachment. Interproximal CEJ is
clinically not detectable at both mesial and distal aspects of the tooth.
• Recession Type 2 (RT2):
Gingival recession associated with loss of interproximal attachment. The amount of
interproximal attachment loss (measured from the interproximal CEJ to the depth of
the interproximal sulcus/pocket) is less than or equal to the buccal attachment loss
(measured from the buccal CEJ to the apical end of the buccal sulcus/pocket).
28. • Recession Type 3 (RT3):
Gingival recession associated with loss of interproximal attachment. The amount of
interproximal attachment loss (measured from the interproximal CEJ to the apical end
of the sulcus/pocket) is greater than the buccal attachment loss (measured from the
buccal CEJ to the apical end of the buccal sulcus/pocket).
Cairo F, Nieri M, Cincinelli S, Mervelt J, Pagliaro U. The interproximal clinical attachment level to
classify gingival recessions and predict root coverage outcomes: an explorative and reliability study. J Clin
Periodontol. 2011;38:661–666.
29. Impact of Orthodontics in GR
• According to Kim DM et al, the direction of the tooth movement and the buccolingual
thickness of the gingiva may play important roles in soft tissue alteration during
orthodontic treatment.
– Higher probability of recession during tooth movement in areas with <2 mm of gingiva.
Gingival augmentation can be indicated before the initiation of orthodontic treatment in
areas with <2 mm.
– These conclusions are mainly based on historic clinical observations and recommendations
(low level of evidence).
30.
31.
32. Peri‐implant health:
• Was defined both clinically and histologically.
• Clinically, 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.
33. 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.
• It can be reversed with measures aimed at eliminating the plaque.
34. Peri‐implantitis:
• 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.
• Onset: 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.
35. 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 pneumatization of the maxillary sinuses.
• Other factors: medications and systemic diseases reducing the amount of naturally
formed bone, tooth agenesis, and pressure from prostheses.
36. References
1. Classification and diagnosis of aggressive periodontitis.Daniel H. Fine. J Clin
Periodontol. 2018;45(Suppl 20):S95–S111.
2. Mucogingival conditions in the natural dentition: Narrative review, case definitions, and
diagnostic considerations.Pierpaolo Cortellini. J Clin Periodontol. 2018;45(Suppl
20):S190–S198.
3. Periodontal health and gingival diseases and conditions on an intact and a reduced
periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the
Classification of Periodontal and Peri‐Implant Diseases and Conditions .Iain L.C.
Chapple. J Clin Periodontol. 2018;45(Suppl 20):S68–S77.
4. Papapanou PN, Sanz M, et al. Periodontitis: Consensus report of workgroup 2 of the
2017 World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and
Conditions. J Clin Periodontol. 2018;45(Suppl 20):S162–S170.
37. 5. Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis:
Framework and proposal of a new classification and case definition. J Clin Periodontol.
2018;45(Suppl 20):S149–S161.
6. Cortellini P, Bissada NF. Mucogingival conditions in the natural dentition: Narrative
review, case definitions, and diagnostic considerations. J Clin Periodontol.
2018;45(Suppl 20):S199–S206.
7. Berglundh T, Armitage G, et al. Peri‐implant diseases and conditions: Consensus report
of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and
Peri‐Implant Diseases and Conditions. J Clin Periodontol. 2018;45(Suppl 20):S286–
S291.
8. Araujo MG, Lindhe J. Peri‐implant health. J Clin Periodontol. 2018;45(Suppl 20):S36–
S36.
Editor's Notes
On June 21, 2018 in Chicago, AAP published official proceedings frm d 9- 11 nov.2017 World Workshop
The periodontal classification system had an unstable past with a relatively stable future. This classification system is based on the knowledge of infection and host response paradigm. this was a scientifically sound and well accepted system back den that is 19yrs back and it has several limitations.
Hence, recent classification scheme for periodontal and peri‐implant diseases and conditions is necessary for clinicians to properly diagnose and treat patients as well as for scientists to investigate etiology, pathogenesis, natural history, and treatment of the diseases and conditions.
This is a schematic table for the new classification of peridontal and peri implant disseases and condition.this article summarises the proceedings of the world workshop on the classification of periodontal and peri implant diseases and conditions .the workshop was held in chicago in nov.2017.
The workshop also characterized periodontal health and gingival inflammation in a reduced periodontium after completion of successful treatment of a patient with periodontitis.
This distinction was made to emphasize the need for a more comprehensive maintenance 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.
4 levels of periodontal health, depending upon whether the periodontium has normal attachment and bone level or reduced support, as well as the ability to control modifying factors and relative treatment outcomes.
These 4 categories include 1) pristine periodontal health, defined as a total absence of clinical inflammation and physiological immune surveillance on a periodontium with normal support (no attachment or bone loss). Pristine periodontal health is not likely to be observed clinically; 2) clinical periodontal health, characterized by an absence or minimal levels of clinical inflammation in a periodontium with normal support; 3) periodontal disease stability in a reduced periodontium; 4) periodontal disease remission/control in a reduced periodontium. Periodontal disease stability and periodontal disease remission/control are differentiated based on the ability to control modifying factors and therapeutic response. Stability is characterized by minimal inflammation and optimal therapeutic response, with control of modifiable risk factors; it is a major treatment goal for periodontitis. For patients in whom it is not possible to fully control modifying and predisposing factors, remission/control may be the more
realistically achievable therapeutic goal. Remission/control is characterized by a significant decrease in inflammation, some improvement in other clinical parameters, and a stabilization of disease progression. Ideally, restoration to periodontal stability should be a major treatment goal and can be attained by controlling inflammation and infection, reducing predisposing factors, and controlling any modifying factors. While
remission/control should be a clear target, based on available evidence, low disease activity may be an acceptable alternative therapeutic goal, particularly in long-standing disease.
Extent: less than or equal to 30% teeth affected- localized; more- generalized inflammation
Mild inflame: Minor change in color; mod- glazing, redness, edema, BOP and severe- overt redness and edema wid tendency towards bleeding when touched rather than probing. {Loe,1967}
Enlargement : Ellis J, Seymour et al: mild- papilla; mod: papilla+ ging margin; severe:papilla+margin+attached gingiva
This framework builds upon a notable change: Forms of periodontal disease are now defined as one of three distinct forms which include periodontitis (formerly aggressive and chronic), necrotizing periodontitis, and periodontitis as a manifestation of systemic conditions.
“The new staging and grading system provides a structure for treatment planning and for monitoring a patient’s response to therapy,”
With current knowledge on pathophysiology and With emerging scientific evidence the workshop agreed that, three forms of periodontitis can be identified: necrotizing periodontitis, periodontitis as a manifestation of systemic disease,and a single category, “periodontitis”. Which was earlier classified as chronic or aggressive.
Futher peridontitis is classified based on a staging and grading system. There are rare systemic disorders, such as Papillon Lefèvre Syndrome, that generally result in the early presentation of severe periodontitis. Such conditions are grouped as “Periodontitis as a Manifestation of Systemic Disease”, and classification should be based on the primary systemic disease.
Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management.
grading provides supplemental information about biological features of the disease, including a history based analysis of the rate of disease progression, assessment of the risk for further progression, anticipated poor outcomes of treatment, and assessment of the risk that the disease or its treatment may negatively affect the general health of the Patient.
Clinical procedures involved in the fabrication of indirect restorations was added because of new data indicating that these procedures may cause recession and loss of clinical attachment.
Pblms in 1999: (1) the differentiation between gingival and PA, which could be confusing, as it was simultaneously based on location and etiology;
(2) considering a PA as chronic or acute may not be adequate,because an abscess, by definition, is an acute lesion;
and (3) the inclusion of pericoronitis and periapical abscesses in the classification together with PA might not be appropriate.
Pericoronal abscesses were included in the 1999 classification, but no solid scientific basis for this was found in
the article associated with the topic.
grouping all EPL under a single section entitled “Periodontitis Associated with Endodontic Lesion” was not ideal, as these lesions may occur in subjects with or without periodontitis;
the single category presented, “Combined Periodontal-Endodontic Lesions”, was too generic and not sufficiently discriminative to help the clinician to determine the most effective treatment for a particular lesion.
Finally, EPL should be classified according to signs and symptoms feasible to be assessed at the time that the lesion is detected and that have direct impact on their treatment, such as presence or absence of fractures
and perforations, presence or absence of periodontitis, and the extent of the periodontal destruction around the affected teeth
The “biotype” has been labeled by different authors as “gingival” or “periodontal” “biotype”, “morphotype” or “phenotype”.
The assessment of periodontal biotype is considered relevant for outcome assessment of therapy.
Keratinized tissue width is easily measured with a periodontal probe positioned between the gingival margin and the mucogingival junction.
Although bone thickness assessment through CBCT
A modern recession classification based on the interdental CAL measurement has been proposed by Cairo et al.
The new classification includes additional information such as recession severity, dimension of the gingiva ,presence or absence of caries and non carious cervical lesions, esthetic concern of the patient and presence or absence of hypersensitivity.
This classification overcomes some limitations of the widely used Miller classification such as the difficult identification between Class I and II, and the use of “bone or soft tissue loss” as interdental reference to diagnose a periodontal destruction in the interdental area.
In addition, Miller classification is no longer matching the treatment outcomes of the most advanced surgical techniques.
when a facially positioned tooth is moved in a lingual direction within the alveolar process, the apico-coronal tissue dimension on its facial aspect will increase in width.
Fan J et al
Was 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.
Conclusion:
Classifications are used to assess clinical conditions in an individual and in groups of individuals.
Diagnosis is used to guide treatment on an individual level.
Case definitions are used to differentiate groups of individuals who share similar features with regard to causes, prognosis, and response to treatment.
Classification is difficult if a gold standard is lacking.