Is the classification of periodontal

diseases now agreed or should

classification systems always be
considered a work in progress?

Name: Grace Girgis

Supervisor: Dr. Timothy McSwiney
Provider: Dr.Denise MacCarthy
What is periodontal disease?
• Inflammation of the periodontal
tissues which causes attachment loss
around teeth and destruction of
alveolar bone due to pathogenic
microorganisms, which can lead to
loss of dentition (1)
• It negatively affects chewing function
and aesthetics, and it may be a
source of social inequality, and
impair QOL (1)
• It is a ‘silent disease’, and affected
individuals will likely remain unaware
until the later stages of the disorder,
when they experience symptoms
such as drifting teeth or mobility (2)
 Framework for etiology,
Differentiate between disease
pathogenesis, and treatment of
processes (3)
disease (1,3,4)

Why is Classification
Important?

Provides the healthcare community

For diagnosis, prognosis, and
with a way of communicating in a
treatment planning (3)
common language (3)
 Why is classification difficult?

• Classification is difficult due to the lack of

understanding of the true nature of the
differences between the different clinical
presentations of disease (5)
• For example, it is not understood if
whether phonetically different case
presentations represent different diseases
or just variations of a single disease
process
• And there are differing personal
preferences of committee members for
different nomenclature (6)
Historical Development of Classification
System Clinical
characteristics
Paradigm (1870 to
1920)

Classical Pathology
Paradigm (1920 to 1970)

Infection/Host Paradigm (1970 to

present)
Clinical Characteristics Paradigm
(1870-1920)
• From 1870 to 1920 and PD was classified according to its clinical presentation(3,7)
• Knowledge of the etiology and pathogenesis of PD was limited (3,7)
• Publications during this time presented opinion of a single person

Periodontal Disease underwent numerous modifications in names:

• Pyorrhea Alveolaris
• Riggs Disease
 Classical Pathology Paradigm (1920-1970)
• Throughout this period, PD was assumed to be a degenerative non-
inflammatory condition wherein patients would progressively lose all
their teeth unless therapy was administered (8)
• This false knowledge led to dentists routinely extracting hopeless teeth
(9)
• Now it is understood that such hopeless teeth can be preserved (9)
 • W.D. Miller was an early proponent of the
infectious nature of PD (7)
Infection/Host • Loe et al., (1965) observed that specific
changes occurred in the dental plaque flora
Paradigm (1970- during the development of gingivitis
present) • This is why sometimes periodontal therapy
includes antimicrobial prescriptions due to
the microbial etiology of inflammatory PD
• Antimicrobials can lessen bacterial load by
targeting explicit microbes of which
mechanical therapy at times cannot, which
resolves periodontal pocket inflammation
Classification Systems of Periodontal
Disease

1) 1989 2) 1999 3) 2017

Overview of 1989 World Workshop
Classification
Merits
✔Inclusion of ”Periodontitis Associated with Systemic Disease”
Disadvantages
The criticisms largely related to the emphasis on age of onset and rates
of progression in the classification which was felt to be inappropriate
Gingival disease category was absent
The dividing line between “early onset periodontitis” and “adult
periodontitis” was 35 years old which is not evidence-based
 1999 Classification of
Periodontal Diseases and
Conditions
1999 Classification system: Addition of a section on “gingival diseases”
 Overview of 1999 classification
• Merits
✔Criteria of age and rate of progression removed
✔Heterogenous disease categories of pubertal, refractory, and rapidly
progressive periodontitis eliminated
✔A gingivitis category was added
• Disadvantages
Complex classification as numerous disease categories are listed
Did not clearly communicate differences between chronic and aggressive
periodontitis overlap between the diagnostic categories
Diabetes associated gingivitis included but not diabetes associated
periodontitis
Developments since 1999 classification

• Since the 1999 workshop, substantial new

information has emerged from population
studies, basic science investigations, and the
evidence from prospective studies evaluating
environmental and systemic risk factors (11)
• This new research prompted the 2017
workshop to develop a new classification
framework for periodontitis in which more
than 100 experts worldwide were consulted
(11)
• The workshop agreed on a classification
framework for periodontitis further
characterized based on a multidimensional
staging and grading system that could be
adapted over time as new evidence emerges
(11)
2017 World
Workshop
• The new classification was agreed at the
joint meeting of the American Association
of Periodontology and European Federation
of Periodontology (11)
• It is split into 4 workshops
• Workshop 1: Periodontal Health and
Gingival Diseases and Conditions
• Workshop 2: Periodontitis
• Workshop 3: Periodontitis as a
manifestation of systemic diseases and
developmental and acquired conditions
Workshop 4: Peri-Implant Disease and
Conditions
• Workshop 4: Peri Implant Disease and
Conditions
 Workshop 1: Periodontal health and
gingival diseases and conditions on an
intact and reduced periodontium
 Workshop 1:Gingivitis
• Since the 1999 classification system, there have been advances in knowledge
of the microbiome and the gingival transcriptome (12) and there are new
definitions of periodontal health histologically and clinically
• Although the 1999 classification system was the first to recognize a need to
classify gingival diseases, but there was no attempt to define health--a critical
factor when establishing case definitions for disease and it was unnecessarily
complex, embedding both predisposing (plaque) and modifying factors
(medications) in the diagnosis (12)
• The reliability and reproducibility of these case definitions relies upon
standardization of probing protocols, which is only possible with the
implementation of an ISO probe (12)

Gingivitis on a reduced Gingival inflammation on

periodontium in a non- a reduced periodontium
Gingivitis on an intact in a successfully treated
periodontitis patient
periodontium periodontitis patient
(crown lengthening,
recession)
Workshop 1: Periodontal Health

• A case of clinical gingival health was therefore established on an intact and a reduced
periodontium in a non-periodontitis patient as <10% sites of bleeding on probing and probing
depths of ≤3 mm (12)
• A successfully treated periodontitis patient in whom sites of gingival bleeding appear remains
at high risk of disease recurrence at those sites and of progressive attachment loss (12)
• *Therefore gingivitis is defined as bleeding at a shallow site of ≤3 mm rather than ≤ 4 mm as in
the case of gingival health (12)
Workshop 2: Periodontitis
 Workshop 2: Defining Periodontitis
• In summary a periodontitis diagnosis for an individual patient should encompass three
dimensions:
• 1) Interdental CAL is detectable at  2 non-adjacent teeth OR buccal or oral CAL  3 mm with
pocketing  3 mm is detectable at 2 teeth (13)
• cannot be ascribed to non-periodontal causes such as 1) gingival recession of traumatic
origin
• 2) Identification of the form of periodontitis (13)
• Necrotizing Characterized by a hx of pain, presence of ulceration of the gingival margin,
and/or fibrin deposits at sites with decapitated gingival papillae, exposure of the marginal
alveolar bone
• Periodontitis as a manifestation of systemic disease
• Periodontitis
• 3) Description of the presentation and aggressiveness of the disease by stage and grade (13)
 Workshop 2: Defining Periodontitis continued

• Forms of the disease previously recognized as “chronic” or “aggressive” are now

grouped under a single category “periodontitis” (11)
• Chronic periodontitis is characterized by subgingival calculus and slow to moderate rates
of progression. It usually occurs in adults (11)
• Aggressive periodontitis is a rare form of periodontitis characterized by rapid attachment
loss, bone destruction, and a non-contributory medical history (11)
• The thought process followed in distinguishing between chronic and aggressive forms of
periodontitis in the 1999 classification system is dependent on:
• 1) the amount and pattern of periodontal destruction and
• 2) the patient’s age and medical status
 Chronic vs Aggressive Periodontitis
• Current evidence does not support the distinction between Chronic and Aggressive periodontitis as
defined by the 1999 classification workshop as 2 separate diseases despite substantial research (11)
• No apparent histopathological explanations for the different rates of destruction (11)
• Among the major overlapping histopathologic events in both diseases are:
•1) acute inflammatory changes in response to microbial colonization of the teeth
•2) influx of neutrophils toward microbial components of subgingival biofilms
•3) detachment of the junctional epithelium and its conversion to pocket epithelium
•4) inflammatory destruction of connective tissue adjacent to pocket epithelium
•5) apical migration of the epithelium onto the tooth root
•6) osteoclastic resorption of alveolar bone
Workshop 2: Staging
• Staging is largely dependent upon the severity of disease at
presentation, complexity of disease management, and a description
of the extent and distribution of disease in the dentition (15)

Stage
Stage 4
Stage 3
Stage 2
I
Workshop 2: Stage 1 periodontitis
• Is borderline between gingivitis and periodontitis and represents the early
stages of attachment loss (11)
• If patients show CAL at a relatively early stage, these patients may have
heightened susceptibility to disease onset (11)
• Early diagnosis may be a challenge in general dental practice because
periodontal probing depths may be inaccurate (11)
Workshop 2: Stage 2 periodontitis
• Represents established periodontitis in which a carefully performed clinical
periodontal exam identifies the characteristic damages that periodontitis has caused
to tooth support (11)
• Careful evaluation of the stage 2 patient’s response to standard treatment principles
is essential, and the case grade plus treatment response may guide more intensive
management for specific patients (11)
Workshop 2: Stage 3 periodontitis
• At stage 3, periodontitis has produced significant damage to the attachment
apparatus, and in the absence of advanced treatment, tooth loss may occur (11)
• Masticatory function is preserved, and treatment of periodontitis doesn’t require
complex rehabilitation of function (11)
Workshop 2: Stage 4 periodontitis
• At the more advanced stage 4, periodontitis causes considerable damage to
the periodontal support and may cause significant tooth loss, and this
translates to loss of masticatory function (11)
• In the absence of proper control of the periodontitis and adequate rehab, the
dentition is at risk of being lost (11)
Workshop 2: Staging chart
 Workshop 2: 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 (11)
• Grading allows the clinician to incorporate individual patient factors into the
diagnosis which are vital to case management (e.g. smoking, diabetes) (11)
 Grade A-Low Grade B- Grade C-High
rate of Moderate rate rate of
progression of progression progression

• There are three levels which represent increasing periodontitis progression

• A risk factor should therefore shift the grade score to a higher value independently of the primary criterion represented
by the rate of progression (11)
• For example, if a patient is Grade B but has poorly controlled T2D ➔Grade C (11)
Workshop 2: Grading chart
Risk Factors
Diabetes
Smoking
Biomarkers
Workshop 2: Diabetes
• There are no characteristic phenotypic features that are unique to
periodontitis in patients with diabetes mellitus
• Thus there is insufficient data to conclude that there there is a
specific diabetes mellitus-associated form of periodontitis, but it is an
important modifier
• RCTs demonstrate that mechanical periodontal therapy associates
with ∼ 0.4% reduction in HBA1C at 3 months  a clinical impact
equivalent to adding a second pharmacological regime for diabetes
• The level of glycemic control in diabetes influences the grading of
periodontitis
Workshop 2: Cigarette smoking
• Similarly, the new classification doesn’t contain a separate disease
category for the effects of cigarette smoking on periodontitis (13,27)
• Smoking is a modifier of multiple forms of periodontitis
• Probing depths, clinical attachment loss, and alveolar bone loss have
been shown to be both more prevalent and more severe among smokers
as compared with non-smoking controls
• Smokers have increased prevalence and more severe extent of PD as
well as higher prevalence of tooth loss and edentulism
• Smoking causes  vascular alterations, altered fibroblast attachment
and function, difficulty in eliminating pathogens by mechanical therapy,
and negative local effects of cytokine and growth factor production
Workshop 2: Biomarkers
• A biomarker is a biological molecule by which a pathological or
physiological process can be identified (11, 24)
• Biomarkers may contribute to improved diagnostic accuracy in the early
detection of periodontitis and are likely to provide decisive contributions
• This is because some individuals are more susceptible to develop
periodontitis, more susceptible to develop progressive severe generalized
periodontitis, less responsive to standard bacterial control principles for
treating and preventing periodontitis, and more likely to have periodontitis
adversely impact systemic diseases
• Biomarkers may assist both in staging and grading of periodontitis
 Workshop 3:
Periodontitis as a
manifestation of
systemic diseases and
developmental and
acquired conditions
Workshop 3 Reviews
• 1) Periodontal manifestations of systemic diseases and conditions
• 2) Mucogingival conditions around natural teeth
• 3) Traumatic occlusal forces and occlusal trauma
• 4) Dental prostheses and tooth related factors
 Workshop 3: Periodontal manifestations
of systemic diseases and conditions
• 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
• Other systemic conditions such as neoplastic diseases may affect the periodontal apparatus
independent of dental plaque biofilm-induced periodontitis (16)
Workshop 3: Mucogingival Deformities and
Conditions around Teeth

• ‘Periodontal phenotype’ is determined by gingival

phenotype and bone morphotype and replaces the
original term “periodontal biotype” (16)
• Thin phenotype, as opposed to thick phenotype,
increases risk of gingival recession43,50 which is
associated with attachment loss, impaired esthetics,
dentin hypersensitivity, and caries/non-carious
cervical lesions (16)
 Workshop 3: Traumatic Occlusal Force
• Group replaced ”excessive occlusal force” (1999) with ”traumatic occlusal force” (2017)
• Definition: The presence can be indicated by one or more of the following fremitus,
tooth mobility, thermal sensitivity, excessive occlusal wear, tooth migration,
discomfort/pain on chewing, fractured teeth, radiographically widened periodontal
ligament space, root resorption, and hypercementosis (16)
• Primary occlusal trauma has been defined as injury resulting in tissue changes from
traumatic occlusal forces applied to a tooth or teeth with normal periodontal support
(16)
• Secondary occlusal trauma has been defined as injury resulting in tissue changes from
normal or traumatic occlusal forces applied to a tooth or teeth with reduced support
• Orthodontic forces: can affect the periodontium and result in recession, alveolar bone
loss, and pulpal disorders.
Workshop 3: Classification of factors related to teeth and
to dental prostheses that can affect periodontium
• The term “biologic width” was replaced by
“supracrestal attached tissues” =JE and the
supracrestal connective tissue attachment (16)
• Infringement with in the supracrestal
connective tissue attachment is associated
with inflammation and loss of periodontal
supporting tissue. Optimal restoration margins
located within the gingival sulcus don’t cause
gingival inflammation if good oral hygiene
measures are in place (16)
Workshop 4: Peri-Implant Disease
and Conditions
 Workshop 4: Implants

• Implant dentistry has become an important modality of treatment for

the replacement of absent or lost teeth since the last workshop in
1999 (18)
• Hard-tissue and soft-tissue implant site deficiencies (associated with
healing after tooth loss, extraction trauma, endodontic infections,
injury, and other causes) are also included (18)
Workshop 4: Peri-implant Health and Disease

• Peri-implant health is characterized by

the absence of erythema, BOP, swelling,
and suppuration (18)
• Peri-implant disease is an
encompassing term that includes
• Peri-implant mucositis
• Peri-implantitis
Workshop 4: Per-implant mucositis

• Presence of bleeding and/or

suppuration on gentle probing
with or without increased
probing depth compared to
previous examinations (18,28)
• Absence of bone loss beyond
crestal bone level changes
resulting from initial bone
remodeling (18,28)
Workshop 4: Peri-implantitis

• Presence of bleeding It is important to

and/or suppuration on assess BOP and
gentle probing (18) probing depth
• Presence of bone loss changes around peri-
beyond crestal bone level implant tissues and
changes resulting from for clinicians to
initial bone remodeling obtain baseline
• Increased probing depth radiographic and
compared to previous probing
exams (18) measurements (18)
Should classification systems
continue to change?
• The development of PD classification systems can be viewed as a
positive consequence as classification systems have progressed to
become more comprehensive and updated than previous ones, to
reflect advancements in technology and new knowledge of biology
and pathology which guides treatment for patients (11)
This would have not been possible if there was one agreed
system that has been used over time
• Thus, a classification system should not be regarded as a permanent
structure. It must be adaptable to change and evolve with the
development of new knowledge just as the TMN staging system for
cancer has continuously been updated (11)
 How will this new classification
system change patient care?
• The 2017 classification system is operational, as it
eliminates the ambiguity and vague constructs of the 1999
system. While this will lead to more accurate diagnoses
and better organization of patient information, it it may be
too complex and time-consuming for everyday practice (4)
• However, this will enable clinicians to individualize patient
treatment
• Information can be used to explain treatment needs to the
patient and insurance companies
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Thank you