Received: 9 December 2017 Revised: 11 March 2018 Accepted: 12 March 2018

DOI: 10.1002/JPER.17-0719

2017 WORLD WORK SHOP

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. Chapple1 Brian L. Mealey2 Thomas E. Van Dyke3 P. Mark Bartold4
Henrik Dommisch5 Peter Eickholz6 Maria L. Geisinger7 Robert J. Genco8
Michael Glogauer9 Moshe Goldstein10 Terrence J. Griffin11 Palle Holmstrup12
Georgia K. Johnson13 Yvonne Kapila14 Niklaus P. Lang15 Joerg Meyle16
Shinya Murakami17 Jacqueline Plemons18 Giuseppe A. Romito19 Lior Shapira10
Dimitris N. Tatakis20 Wim Teughels21 Leonardo Trombelli22 Clemens Walter23
Gernot Wimmer24 Pinelopi Xenoudi25 Hiromasa Yoshie26
1 Periodontal Research Group, Institute of Clinical Sciences, College of Medical & Dental Sciences, University of Birmingham, UK

2 University of Texas Health Science Center at San Antonio, USA

3 The Forsyth Institute, Cambridge, MA, USA

4 School of Dentistry, University of Adelaide, Australia

5 Department of Periodontology and Synoptic Dentistry, Charité - Universitätsmedizin Berlin, Germany

6 Department of Periodontology, Center for Oral Medicine, Johann Wolfgang Goethe-University Frankfurt, Germany

7 Department of Periodontology, University of Alabama at Birmingham, USA

8 Department of Oral Biology, SUNY at Buffalo, NY, USA

9 Faculty of Dentistry, University of Toronto, Canada

10 Department of Periodontology, Faculty of Dental Medicine, Hebrew University-Hadassah Medical Center, Jerusalem, Israel

11 Periodontal Department, Tufts University School of Dental Medicine, Boston, MA, USA

12 Periodontology, Section 1, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark

13 Department of Periodontology, University of Iowa College of Dentistry, Iowa City, IA, USA

14 Orofacial Sciences, University of California San Francisco, USA

15 Department of Periodontology, University of Bern, Switzerland

16 Department of Periodontology, University of Giessen, Germany

17 Department of Periodontology, Graduate School of Dentistry, Osaka University, Japan

18 Department of Periodontics, Texas A&M College of Dentistry, Dallas, TX, USA

19 Division of Periodontology, Department of Stomatology, Dental School, University of São Paulo, Brazil

20 Division of Periodontology, College of Dentistry, Ohio State University, Columbus, OH, USA

21 Department of Oral Health Sciences, Periodontology, KU Leuven & Dentistry, University Hospitals Leuven, Belgium

22 Research Center for the Study of Periodontal and Peri-Implant Diseases, University of Ferrara, Italy

23 Department of Periodontology, Endodontology & Cariology, University Centre for Dental Medicine, University of Basel School of Dentistry, Switzerland

24 Department of Prosthodontics, School of Dentistry, Medical University Graz, Austria

25 Orofacial Sciences, School of Dentistry, University of California San Francisco, USA

26 Division of Periodontology, Niigata University Graduate School of Medical and Dental Sciences, Japan

© 2018 American Academy of Periodontology and European Federation of Periodontology

S74 wileyonlinelibrary.com/journal/jper J Periodontol. 2018;89(Suppl 1):S74–S84.

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CHAPPLE ET AL. S75

Correspondence
Dr. Iain Chapple
Abstract
Email: [email protected] Periodontal health is defined by absence of clinically detectable inflammation. There
Sources of Funding: The workshop was is a biological level of immune surveillance that is consistent with clinical gingival
planned and conducted jointly by the American
health and homeostasis. Clinical gingival health may be found in a periodontium that
Academy of Periodontology and the European
Federation of Periodontology with financial is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodon-
support from the American Academy of Peri- tium in either a non-periodontitis patient (e.g. in patients with some form of gingival
odontology Foundation, Colgate, Johnson
recession or following crown lengthening surgery) or in a patient with a history of
& Johnson Consumer Inc., Geistlich Bioma-
terials, SUNSTAR, and Procter & Gamble periodontitis who is currently periodontally stable. Clinical gingival health can be
Professional Oral Health. restored following treatment of gingivitis and periodontitis. However, the treated and
The proceedings of the workshop were stable periodontitis patient with current gingival health remains at increased risk of
jointly and simultaneously published in the
Journal of Periodontology and Journal of recurrent periodontitis, and accordingly, must be closely monitored.
Clinical Periodontology.
Two broad categories of gingival diseases include non-dental plaque biofilm–induced
gingival diseases and dental plaque-induced gingivitis. Non-dental plaque biofilm-
induced gingival diseases include a variety of conditions that are not caused by plaque
and usually do not resolve following plaque removal. Such lesions may be manifes-
tations of a systemic condition or may be localized to the oral cavity. Dental plaque-
induced gingivitis has a variety of clinical signs and symptoms, and both local pre-
disposing factors and systemic modifying factors can affect its extent, severity, and
progression. Dental plaque-induced gingivitis may arise on an intact periodontium
or on a reduced periodontium in either a non-periodontitis patient or in a currently
stable “periodontitis patient” i.e. successfully treated, in whom clinical inflammation
has been eliminated (or substantially reduced). A periodontitis patient with gingi-
val inflammation remains a periodontitis patient (Figure 1), and comprehensive risk
assessment and management are imperative to ensure early prevention and/or treat-
ment of recurrent/progressive periodontitis.

Precision dental medicine defines a patient-centered approach to care, and therefore,

creates differences in the way in which a “case” of gingival health or gingivitis is
defined for clinical practice as opposed to epidemiologically in population prevalence
surveys. Thus, case definitions of gingival health and gingivitis are presented for both
purposes. While gingival health and gingivitis have many clinical features, case defini-
tions are primarily predicated on presence or absence of bleeding on probing. Here we
classify gingival health and gingival diseases/conditions, along with a summary table
of diagnostic features for defining health and gingivitis in various clinical situations.

KEYWORDS
allergic reaction, amalgam tattoo, aspergillosis, biofilm, blastomycosis, calcifying fibroblastic granu-
loma, candidosis, chemical trauma, clinical health, coccidioidomycosis, condylomata acuminatum, con-
tact allergy, coxsackie virus, Crohn's disease, dental plaque-induced gingivitis, disease control, dis-
ease remission, disease stability, drug-induced gingival enlargement, drug-induced pigmentation, dys-
biosis, erythema multiforme, erythroplakia, factitious injury, fibrous epulis, focal epithelial hyperpla-
sia, frictional keratosis, geotricosis, gingival pigmentation, hand foot and mouth, hereditary gingival
fibromatosis, herpangina, herpes simplex, histoplasmosis, Hodgkin lymphoma, hyperglycemia, hyposali-
vation, intact periodontium, leukemia, leukoplakia, lichen planus, local risk factors, lupus erythemato-
sus, melanoplakia, Melkersson-Rosenthal, menstrual cycle, modifying factors, molluscum contagiosum,
mucormycosis, Mycobacterium tuberculosis, necrotizing periodontal diseases, Neisseria gonorrhoeae,
non–dental plaque-induced gingival conditions, non-Hodgkin lymphoma, oral contraceptive, orofacial
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.17-0719 by CAPES, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
S76 CHAPPLE ET AL.

granulomatosis, paracoccidioidomycosis, pemphigoid, pemphigus vulgaris, periodontal disease, periph-

eral giant cell granuloma, plasma cell gingivitis, predisposing factors, pregnancy, puberty, pyogenic granu-
loma, reduced periodontium, resolution of inflammation, restoration margins, sarcoidosis, scurvy, smoker's
melanosis, smoking, squamous cell carcinoma, squamous cell papilloma, stable periodontitis, streptocco-
cal gingivitis, symbiosis, systemic risk factors, thermal trauma, toothbrush trauma, Treponema pallidum,
varicella zoster, vascular epulis, verruca vulgaris

“Health is a state of complete physical, mental and social well- What is the spectrum of clinical periodontal
being and not merely the absence of disease or infirmity”.1 health at a site level?
Based upon this definition from the World Health Organi-
zation (WHO), it follows that periodontal health should be What is the biology of clinical gingival health?
defined as a state free from inflammatory periodontal dis- Clinical gingival health is generally associated with an
ease that allows an individual to function normally and avoid inflammatory infiltrate and a host response consistent with
consequences (mental or physical) due to current or past dis- homeostasis.
ease. Based upon this overall framework of health, periodon- On a site level, how do we classify clinical gingival health?
tal health should be predicated upon the absence of disease,
• Clinical gingival health on an intact periodontium
as assessed clinically, associated with gingivitis, periodonti-
tis, or other periodontal conditions, and may include patients • Clinical gingival health on a reduced periodontium
who have had a history of successfully treated gingivitis or ◦ Stable periodontitis patient
periodontitis, or other periodontal conditions, who have been ◦ Non-periodontitis patient (e.g. recession, crown length-
and are able to maintain their dentition without signs of clini- ening)
cal gingival inflammation. Additionally, clinical periodontal
What are the clinical features of gingival health on an intact
health embraces physiological immune surveillance involv-
periodontium?
ing levels of biological and inflammatory markers compati-
Clinical gingival health on an intact periodontium is char-
ble with homeostasis.2 Periodontitis is a chronic inflamma-
acterized by the absence of bleeding on probing, erythema
tory disease that currently can be successfully controlled, and
and edema, patient symptoms, and attachment and bone loss.
teeth can be retained for life. Periodontitis can remain stable
Physiological bone levels range from 1.0 to 3.0 mm apical to
(in remission) or enter periods of exacerbation. A stable peri-
the cemento-enamel junction.
odontitis patient remains at higher risk for recurrent disease
compared to a gingivitis patient or a healthy patient. There- What are the clinical features of gingival health on a reduced
fore, precision dental medicine requires ongoing, individual periodontium?
risk assessment as part of optimal patient management. Clinical gingival health on a reduced periodontium is char-
A definition of periodontal health and wellness is critical to acterized by an absence of bleeding on probing, erythema,
establish ideal and acceptable therapeutic end points to peri- edema and patient symptoms in the presence of reduced
odontal therapies, to systematically assess the biological bur- clinical attachment and bone levels. However, it should be
den of periodontal inflammation, to categorize gingival and recognized that successfully treated and stable periodontitis
periodontal disease prevalence in populations, and to evaluate patients remain at increased risk of recurrent progression of
individualized risk for future disease development. Periodon- periodontitis. In non-periodontitis patients, there is no current
tal health must be assessed and defined at both the patient and evidence for increased risk of periodontitis.
site level to achieve these goals. Furthermore, definitions of What are the clinical features of gingival health following
periodontal health that are used to inform treatment decisions treatment of gingivitis on an intact periodontium?
for individual patients may differ from those used in epidemi- Clinical gingival health following treatment of gingivitis
ological studies. on an intact periodontium is characterized by the absence of
bleeding on probing, erythema and edema, patient symptoms,
and attachment and bone loss.
Is there a level of gingival inflammation that is
What are the clinical features of gingival health following suc-
consistent with clinical periodontal health at a
cessful treatment of periodontitis?
site level?
Clinical gingival health following successful treatment of
There is a biological level of immune surveillance, manifest- periodontitis is characterized by an absence of bleeding on
ing as a predominantly neutrophilic infiltrate that is consistent probing, erythema, edema, and patient symptoms in the pres-
with clinical gingival health.2 ence of reduced clinical attachment and bone levels.
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.17-0719 by CAPES, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
CHAPPLE ET AL. S77

FIGURE 1 The transition from periodontal health to gingivitis is reversible following treatment that resolves gingival inflammation. The transi-
tion to periodontitis results in attachment loss which, at the present time is irreversible. More importantly, it signposts patients who are at lifelong high
risk of recurrent periodontitis. Optimal periodontal therapy can restore gingival health on a reduced periodontium, or may result in mild marginal gin-
gival inflammation at shallow probing pocket depths (≤ 3 mm). However, a history of periodontitis places patients at high risk of recurrent periodontitis
and such patients require careful site-specific monitoring during periodontal maintenance programs

CA S E DEFINI T I O N S FOR periodontal health may exhibit one or two sites with some evi-
PERIODONTA L HE A LT H A N D dence of clinical gingival inflammation. Moreover, localized
G I NGI V I T I S mild and delayed bleeding to probe at isolated sites is ubiqui-
tous, but may fall within the spectrum of “clinical health”.
Based on available methods to assess gingival inflamma- In clinical practice, a case of gingival health on an intact
tion, a gingivitis case can be simply, objectively and accu- periodontium would be a patient with no signs of gingivitis as
rately defined and graded using a bleeding on probing defined above.
score (BOP%),3 assessed as the proportion of bleeding sites In clinical practice, the goal of periodontal treatment on a
(dichotomous yes/no evaluation) when stimulated by a stan- reduced periodontium is a patient with no signs of gingivi-
dardized (dimensions and shape) periodontal probe with a tis as defined above. A case of gingival health on a reduced
controlled (∼0.25 N) force to the apical end of the sulcus at six periodontium in a stable periodontitis patient must be dis-
sites (mesio-buccal, buccal, disto-buccal, mesio-lingual, lin- tinguished from a case of periodontal health in a reduced
gual, disto-lingual) on all teeth present. Limitations of these periodontium in a non-periodontitis patient (recession, crown
clinical criteria arise from a lack of standardized periodon- lengthening), because there is a difference in risk for peri-
tal probes (e.g. probe dimensions, taper), examiner variability odontal disease progression.
(probe pressure, angle), patient related factors (biotype, med- Following treatment of periodontitis, periodontitis patients
ications, etc.) and smoking. may not attain a status of complete gingival health based on
In all references to an “intact periodontium” within this the above definition. However, evidence has demonstrated
consensus, an absence of detectable attachment and/or bone that a patient may achieve periodontal stability. Periodon-
loss is implicit. tal stability is characterized by successful treatment through
control of local and systemic risk factors, resulting in min-
imal (< 10% of sites4 ) BOP, no probing depths of 4 mm
How do we define a case of gingival health on
or greater that bleed on probing, optimal improvement in
an intact and a reduced periodontium for
other clinical parameters and lack of progressive periodon-
epidemiological purposes?
tal destruction.6 The treated and stable periodontitis patient
For an intact periodontium and a reduced and stable periodon- with current gingival health remains at increased risk of recur-
tium, gingival health is defined as < 10% bleeding sites4,5 with rent periodontitis and accordingly must be closely monitored.
probing depths ≤3 mm. Figure 1 summarizes the various scenarios that may arise fol-
lowing the transition from health, to gingivitis and ultimately
How do we define a case of gingival health on periodontitis.
an intact and a reduced periodontium for
clinical practice? How do we define gingivitis at a site level
Due to limitations in, and a lack of uptake of, standardized
(biological & clinical)?
ISO probes and techniques leading to inherent measurement Defining inflammation at a site level is quite distinct from
variability in the parameters of gingival health, a patient with defining a case of gingivitis. A universal case definition is
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.17-0719 by CAPES, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
S78 CHAPPLE ET AL.

essential to facilitate population surveillance, for clinicians What are the determinants of the rate of
setting therapeutic targets, and to enable assessment of the development of gingivitis, its severity and
efficacy of prevention and/or treatment regimes. extent?
There are broadly two categories of gingival disease:
The threshold of plaque accumulation necessary to induce
gingival inflammation and impact upon its rate of progres-
• Dental plaque biofilm-induced gingivitis sion at specific sites or at a whole mouth level varies between
individuals according to both local risk factors, known as pre-
• Non–dental plaque-induced gingival diseases
disposing factors, and systemic risk factors, referred to as
modifying factors, respectively.
Dental plaque biofilm-induced gingivitis is defined at
the site level as “an inflammatory lesion resulting from 1. Local risk factors (predisposing factors)
interactions between the dental plaque biofilm and the host's Local risk factors for gingivitis are those that encourage
immune-inflammatory response, which remains contained plaque accumulation at a specific site by either inhibiting
within the gingiva and does not extend to the periodontal its removal during daily oral hygiene practices, and/or cre-
attachment (cementum, periodontal ligament and alveolar ating a biological niche that encourages increased plaque
bone). Such inflammation remains confined to the gingiva accumulation.7 These include:
and does not extend beyond the mucogingival junction and is a. Dental plaque biofilm retention factors (including cer-
reversible by reducing levels of dental plaque at and apical tain tooth anatomical factors) – facilitate plaque accu-
to the gingival margin”. mulation at and apical to the gingival margin, enabling
Depending on whether dental plaque biofilm-induced gin- biofilm adherence and maturation and increasing the
gival inflammation occurs on an intact or reduced periodon- difficulty of mechanical plaque removal. Several clini-
tium, or in a patient diagnosed with periodontitis, gingivitis cal studies providing a moderate level of evidence have
can be further classified as: demonstrated that subgingival restoration margins may
be detrimental to gingival health.15,16
• Gingivitis on an intact periodontium b. Oral dryness is a clinical condition often associated
with symptoms of xerostomia. Oral dryness manifest-
• Gingivitis on a reduced periodontium in a non-periodontitis
ing as a lack of salivary flow, availability, or changes
patient (e.g., recession, crown lengthening)
in quality of saliva, leading to reduced cleansing of
• Gingival inflammation on a reduced periodontium in a suc- tooth surfaces is associated with reduced dental plaque
cessfully treated periodontitis patient (Note that recurrent biofilm removal and enhanced gingival inflammation.
periodontitis cannot be ruled out in this case) Common causes include medications that have anti-
parasympathetic action, Sjögrens syndrome when the
salivary acini are replaced by fibrosis following autoim-
Since the 1999 classification, there have been advances mune destruction, and mouth breathing in people who
in knowledge of the microbiome and the gingival tran- may have enhanced gingival display and/or an incom-
scriptome. Gingivitis is a non-specific inflammatory con- petent lip seal.17
dition and is therefore a consequence of sustained plaque
2. Systemic risk factors (modifying factors)
biofilm accumulation at and apical to the gingival margin.7
Systemic risk or modifying factors are those characteris-
Longitudinal studies have demonstrated that sites that do
tics present in an individual, which negatively influence the
not progress to attachment loss are characterized by less
gingival inflammation over time, whereas those sites that immune-inflammatory response to a given dental plaque
do progress have persistently greater levels of gingival biofilm burden, resulting in exaggerated or “hyper” inflam-
inflammation.8–14 Therefore, gingivitis is a major risk factor, mation. Examples include:
and a necessary pre-requisite, for periodontitis. The manage- a. Smoking – is one of the major lifestyle/behavioral risk
ment of gingivitis is thus a primary prevention strategy for factors for periodontitis, but which also has profound
periodontitis. effects upon the gingival tissues. Systemic circulatory
Periodontitis patients who are currently stable but develop uptake of components of cigarette smoke as well as
gingival inflammation at specific sites should remain on peri- local uptake are reported to induce microvascular vaso-
odontal maintenance and should be closely monitored during constriction and fibrosis. This can mask clinical signs
periodontal maintenance for any reactivation of periodonti- of gingivitis, such as bleeding on probing, despite a
tis. Such patients may not be managed in the same way as significant underlying pathological inflammatory cell
non-periodontitis patients with gingivitis. infiltrate.18
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.17-0719 by CAPES, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
CHAPPLE ET AL. S79

b. Metabolic factors – hyperglycemia in people with or Current epidemiological data on the prevalence of gingivi-
without diabetes. Excess glucose is toxic and directly tis suffer from the lack of a universally adopted case definition
induces mitochondrial stress and an enhanced res- and vary as widely as 6% to 94%, due to the use of indices
piratory burst in inflammatory cells that may acti- that measure gingival inflammation at individual sites rather
vate various proinflammatory mediator cascades. For- than considering the patient's mouth as a whole. Therefore,
mation of advanced glycation end-products (AGEs) mild localized clinical inflammation is reported to affect
may also result in AGE binding to its cell surface almost 95% of the population, a figure that would incorrectly
receptor (RAGE), which activates proinflammatory suggest gingivitis as being a variation of “normality” and thus
signaling cascades and downstream proinflammatory consistent with the spectrum of “clinical health” rather than
events.19 being a disease. By contrast, the more extensive the mani-
c. Nutritional factors – Severe Vitamin C deficiency, or festation of disease employed in a case definition, the lower
scurvy, results in compromised antioxidant micronu- the reported prevalence. A universally agreed case definition
trient defenses to oxidative stress and also negatively should be based upon a pragmatic appraisal of the evidence
impacts collagen synthesis, resulting in weakened base derived from longitudinal observation and intervention
capillary blood vessel walls and a consequent propen- studies.
sity to enhanced gingival bleeding.20
d. Pharmacological agents (prescription, non- Clinical, radiological, and biological signs and symptoms
prescription, and recreational agents) – can act 1. Gingivitis is a clinical diagnosis. While emerging tech-
via diverse mechanisms to increase susceptibility to nologies are starting to shed light on the microbiological,
gingivitis. This may include drugs that reduce salivary molecular, and pathophysiological characteristics of gin-
flow, drugs that impact endocrine function (see below), givitis, definitive knowledge is not sufficient to supersede
and drugs that may induce gingival enlargement and current clinical parameters.7
pseudo-pocketing. 2. The clinical signs of inflammation are erythema, edema,
e. Elevations in sex steroid hormones – at puberty, dur- pain (soreness), heat, and loss of function.
ing pregnancy, or following medication with first gen- 3. These may manifest clinically in gingivitis as:
eration oral contraceptives may modify the gingival
a. Swelling, seen as loss of knife-edged gingival margin
inflammatory response. Complex biological reactions
and blunting of papillae
within the gingival tissues result from such elevated sex
steroid levels and generate more than expected inflam- b. Bleeding on gentle probing
mation, in response to relatively small levels of plaque. c. Redness
However, modern oral contraceptive dosages have been d. Discomfort on gentle probing
reduced and there is little evidence for exaggerated 4. The symptoms a patient may report include:
gingival inflammatory responses to plaque with such
a. Bleeding gums (metallic/altered taste)
drugs.21
b. Pain (soreness)
f. Hematological conditions – particular blood malignan-
cies such as leukemia or pre-malignant conditions such c. Halitosis
as myelodysplasia are associated with signs of excess d. Difficulty eating
gingival inflammation in the absence of excessive e. Appearance (swollen red gums)
plaque biofilm accumulation. Signs include swollen,
f. Reduced oral health–related quality of life
purple or occasionally pale gingiva due to leukemic
cell infiltration, gingival bleeding that is inconsis- 5. Radiographs cannot be used to diagnose gingivitis.
tent with levels of dental plaque biofilm accumula-
tion, due to thrombocytopenia and/or clotting-factor
deficiencies.22 Should we classify dental plaque
biofilm-induced gingivitis?
There is utility in defining the severity of gingivitis as a patient
What are the diagnostic criteria for a gingivitis communication tool, but there are no objective clinical criteria
case? for defining severity. Thus, in this context alone, the extent of
Given the “spectrum” of presentation of gingival health and gingivitis can be used to communicate “mild, moderate, and
gingival inflammation in terms of severity and extent of gin- severe” gingivitis. Moreover, emerging evidence suggests that
gival involvement, it is important to define the features of a the contained gingivitis lesion may have systemic inflamma-
universally accepted case of gingivitis. tory consequences.23,24
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.17-0719 by CAPES, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
S80 CHAPPLE ET AL.

TABLE 1 Diagnostic look-up table for gingival health or dental plaque-induced gingivitis in clinical practice
Intact periodontium Health Gingivitis
Probing attachment loss No No
Probing pocket depths (assuming no pseudo pockets)a ≤3 mm ≤3 mm
Bleeding on probinga <10% Yes (≥ 10%)
Radiological bone loss No No
Reduced periodontium
Non-periodontitis patient Health Gingivitis
Probing attachment loss Yes Yes
Probing pocket depths (all sites & assuming no pseudo ≤3 mm ≤3 mm
pockets)a
Bleeding on probinga <10% Yes (≥ 10%)
Radiological bone loss Possible Possible
NB: In conditions where there is treatment but not cure, e.g. rheumatoid arthritis, periodontitis, the post-treatment parameters that define
stability/health or gingivitis may differ from the parameters for health/gingivitis in a non-periodontitis patient. The threshold for “clinical health”
in a treated and stable periodontitis patient is therefore set at ≤ 4 mm.
Gingivitis in a patient with
Successfully treated stable periodontitis patient Health a history of periodontitis
Probing attachment loss Yes Yes
Probing pocket depths (all sites & assuming no pseudo ≤4 mm (no site ≥ 4 mm ≤3 mm
pockets)a with BOP)b
Bleeding on probinga <10% Yes (≥ 10%)
Radiological bone loss Yes Yes
NB: 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. Therefore, gingivitis is defined as bleeding at a shallow site of ≤ 3 mm rather than ≤ 4 mm, as is the case in
gingival heath. Where the probing depth is 4 mm or higher with bleeding, this is no longer a “closed pocket.”21,25
a Assumes a light probing pressure of 0.2 to 0.25 N.
b There was a rational minority view expressed that the threshold for defining a clinical case of health in a successfully treated periodontitis patient should be set at ≤ 3 mm
with no BOP to acknowledge the elevated risk of recurrent disease. However, the counter and majority view was that the ≤ 3 mm threshold is rarely achieved at 100% of
treated sites and could lead to over-treatment, since any non-bleeding site > 3 mm would not be classified as “health” and thus open to further invasive treatment, rather
than monitoring and supportive care. The threshold was therefore set at ≤ 4 mm acknowledging that post-treatment clinical phenotypes need to be considered differently
to pre-treatment phenotypes.

There is no robust evidence to clearly differentiate mild, gingivitis is defined as 10%-30% bleeding sites; generalized
moderate, and severe gingivitis, and definitions remain a gingivitis is defined as > 30% bleeding sites.
matter of professional opinion. Methods of defining gingivitis For epidemiological purposes alone, a periodontitis case
may include: cannot simultaneously be defined as a gingivitis case. There-
Defining percentages (e.g. mild = < 10%, moderate = 10%- fore, a patient with a history of periodontitis, with gingival
30%, severe = > 30% sites) inflammation is still a periodontitis case.
Grading (e.g. grade 1 to 5 in 20% quintiles for % sites bleeding
on probing).
How do we classify a patient with dental
plaque-induced gingivitis on an intact and a
How do we define a case of dental reduced periodontium for clinical practice?
plaque-induced gingivitis on an intact and a In clinical practice, a case of gingivitis on an intact
reduced periodontium for epidemiological periodontium, or a reduced periodontium in a patient
purposes? without a history of periodontitis, would be a patient
For epidemiological purposes, gingivitis on an intact peri- with signs of gingival inflammation as defined above
odontium and gingivitis on a reduced periodontium in a (Table 1).
patient without a history of periodontitis, is defined as ≥10% In clinical practice, periodontitis patients, if successfully
bleeding sites4,5 with probing depths ≤3 mm. Localized treated can achieve a reduced and stable periodontium where
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.17-0719 by CAPES, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
CHAPPLE ET AL. S81

probing pocket depths are ≤4 mm25 and there is an absence of TABLE 2 Classification of gingival health and gingival dis-
clinical inflammation (bleeding on probing). Gingival inflam- eases/conditions
mation may arise at specific sites, and where probing depths
are ≤ 3 mm is termed gingival inflammation in a stable 1. Periodontal health2
periodontitis patient. However, such patients remain at high A. Clinical health on an intact periodontium
risk of recurrent periodontitis and require close monitoring B. Clinical gingival health on a reduced periodontium
as such sites are at high risk of reverting to periodontitis (i) Stable periodontitis patient
(Table 1). (ii) Non-periodontitis patient
2. Gingivitis – dental plaque-induced: intact periodontium;
reduced periodontium in non-periodontitis patient; reduced
periodontium in successfully treated periodontitis patient.7

How do we classify non–dental plaque-induced A. Associated with biofilm alone

gingival conditions? B. Mediated by systemic or local risk factors
i. Systemic risk factors (modifying factors)
Although oral health and systemic health are frequently con-
sidered as separate entities, both are strongly interrelated. (a) Smoking

There are numerous examples of how oral diseases may (b) Hyperglycemia
impact systemic health and how the oral cavity may be a (c) Nutritional factors
window to general health. Consequently, it is crucial for all (d) Pharmacological agents (prescription,
health-care providers to understand these interrelationships, non-prescription and recreational)
inform patients of such conditions, and make appropriate (e) Sex steroid hormones
referrals. Puberty
Non-dental plaque-induced gingival conditions encompass Menstrual cycle
a variety of conditions that are not caused by plaque and Pregnancy
usually do not resolve following plaque removal. Such lesions Oral contraceptives
may be manifestations of a systemic condition or may be (f) Hematological conditions
localized to the oral cavity.26 Although these lesions are not ii. Local risk factors (predisposing factors)
caused by the dental plaque biofilm, the severity of the clini- (a) Dental plaque biofilm retention factors (e.g.,
cal manifestations often depends on plaque accumulation and prominent restoration margins)
subsequent gingival inflammation.27 (b) Oral dryness
The proposed classification considers those conditions C. Drug-influenced gingival enlargement
listed in Table 2. 3. Gingival diseases – non–dental plaque-induced26
A. Genetic/developmental disorders
i. Hereditary gingival fibromatosisa
B. Specific infections
Which non–dental plaque-induced gingival i. Bacterial origin
conditions may have associated systemic (a) Neisseria gonorrhoeaea
involvement and how does that impact upon
(b) Treponema palliduma
patient-centered care pathways?
(c) Mycobacterium tuberculosisa
In recent years, the traditional treatment model in which the (d) Streptococcal gingivitis
patient was a passive receiver of care is changing toward
ii. Viral origin
patient-centered care in precision dental medicine (PDM).
(a) Coxsackie virus (hand-foot-and-mouth disease)a
In PDM, an individual's specific health needs and desired
(b) Herpes simplex I & II (primary or recurrent)a
health outcomes are the driving force behind all health-care
decisions and quality measurements. One of the elements (c) Varicella zoster (chicken pox & shingles – V
nerve)a
in PDM is that care is collaborative, coordinated, and
accessible. The right care is provided at the right time and (d) Molluscum contagiosuma
the right place. Considering that the conditions marked (e) Human papilloma virus (squamous cell
with an “a.” (Table 2) have associated systemic involvement papilloma; condyloma acuminatum; verruca
vulgaris; focal epithelial hyperplasia)
or are oral manifestations of systemic conditions, other
health-care providers may be involved in diagnosis and
(Continues)
treatment.
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S82 CHAPPLE ET AL.

TABLE 2 (Continued) TABLE 2 (Continued)

iii. Fungal origin H. Gingival pigmentation

(a) Candidosis i. Melanoplakiaa
(b) Other mycoses, e.g., histoplasmosis, aspergillosis ii. Smoker's melanosis
C. Inflammatory and immune conditions iii. Drug-induced pigmentation (antimalarials,
i. Hypersensitivity reactions minocycline)
(a) Contact allergya iv. Amalgam tattoo
(b) Plasma cell gingivitisa
a Conditions marked with an “a” have associated systemic involvement or are oral
(c) Erythema multiformea
manifestations of systemic conditions; therefore, other health-care providers may
ii. Autoimmune diseases of skin and mucous membranes be involved in diagnosis and treatment.

(a) Pemphigus vulgarisa

(b) Pemphigoida FUTURE RESEARCH NEEDS
a
(c) Lichen planus
(d) Lupus erythematosusa Regarding classification and diagnosis of periodontal health
and gingival diseases/conditions, future research is needed on
Systemic lupus erythematosis
Discoid lupus erythematosis the:
iii. Granulomatous inflammatory lesions (orofacial
• development and validation of non-invasive diagnostic
granulomatoses)
tools (e.g., saliva-based diagnostics), especially as they
(a) Crohn's diseasea
relate to detection of gingival inflammation;
(b) Sarcoidosisa
• identification of the characteristics (e.g., genetic factors)
D. Reactive processes
that distinguish persons who are resistant to the develop-
i. Epulides ment of dental plaque biofilm-induced or non-dental plaque
(a) Fibrous epulis biofilm–induced gingival diseases from those who are sus-
(b) Calcifying fibroblastic granuloma ceptible;
(c) Vascular epulis (pyogenic granuloma) • expansion of our limited knowledge of the determinants
(d) Peripheral giant cell granulomaa that affect the reliability of currently available diagnostic
E. Neoplasms tools (e.g., effects of probe design on bleeding on probing
i. Premalignancy responses);
(a) Leukoplakia • characterization of the possible differences (e.g., molecular
(b) Erythroplakia determinants) between gingivitis on an intact periodontium
ii. Malignancy
and other forms of gingival inflammatory disease.
(a) Squamous cell carcinomaa Regarding the current primary periodontal diagnostic tool,
(b) Leukemic cell infiltrationa the graduated periodontal measuring probe, the following are
(c) Lymphomaa recommendations for an ISO periodontal probe:
Hodgkin
The reliability and reproducibility of any case definition
Non-Hodgkin for health, gingival or periodontal conditions relies upon stan-
F. Endocrine, nutritional & metabolic diseases
dardization of probing protocols, which is only possible with
the implementation of an ISO probe. The current Interna-
i. Vitamin deficienciesa
tional Organization for Standardization (ISO) for periodontal
(a) Vitamin C deficiency (scurvy)
probes is – ISO 21672, but requires updating in order to define
G. Traumatic lesions the features of a global standard periodontal probe. These
i. Physical/mechanical trauma characteristics are:
(a) Frictional keratosis
1. Tip diameter 0.5 mm
(b) Mechanically induced gingival ulceration
2. Cylindrical tine structure
(c) Factitious injury (self-harm)
3. Constant force limiter of 0.25 N
ii. Chemical (toxic) burn
iii. Thermal insults 4. 15-mm scale with precise individual or banded millimeter
markings
(a) Burns to gingiva
(Continues) 5. A taper of 1.75◦
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.17-0719 by CAPES, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
CHAPPLE ET AL. S83

ACKNOW LEDGMENTS AND DISCLOSURES 10. Clerehugh V, Worthington HV, Lennon MA, Chandler R. Site pro-
gression of loss of attachment over 5 years in 14- to 19-year-old
Workshop participants filed detailed disclosure of potential
adolescents. J Clin Periodontol. 1995;22:15–21.
conflicts of interest relevant to the workshop topics, and
11. Albandar JM, Kingman A, Brown LJ, Löe H. Gingival inflammation
these are kept on file. The authors receive, or have received,
and subgingival calculus as determinants of disease progression in
research funding, consultant fees, and/or lecture compensa-
early-onset periodontitis. J Clin Periodontol. 1998;25:231–237.
tion from the following companies: 3D Matrix, BioGaia AB,
12. Schätzle M, Löe H, Bürgin W, Anerud A, Boysen H, Lang NP.
BioHorizons, Boehringer Ingleheim, CALCIVIS, Cigna, Col-
Clinical course of chronic periodontitis. I. Role of gingivitis.
gate, CP GABA, Dentaid, Dentsply Sirona, Dexcel Pharma, J Clin Periodontol. 2003;30:887–901. Erratum in: J Clin Periodon-
EMS Dental, GC Corporation, Geistlich, GlaxoSmithK- tol 2004;31:813.
line, Hain Lifescience, Intra-Lock, ISOThrive, ITI Foun- 13. Ramseier CA, Ånerud A, Dulac M, et al. Natural history of
dation, Ivoclar-Vivadent, Johnson & Johnson, Kaken Phar- periodontitis: disease progression and tooth loss over 40 years.
maceutical, Kulzer Dental, Lion Corporation, Millennium J Clin Periodontol. 2017;44:1182–1191.
Dental Technologies, MIS Implants, Mitsubishi Chemical, 14. Tanner ACR, Kent R, Jr, Kanasi E, et al. Clinical characteristics
National Safety Associates, Nobel Biocare, Noveome Bio- and microbiota of progressing slight chronic periodontitis in adults.
therapeutics, OraPharma, Osteogenics Biomedical, Philips, J Clin Periodontol. 2007;34:917–930.
Procter & Gamble, Reminova, Schülke & Mayr, Strau- 15. Lang NP, Kiel RA, Anderhalden K. Clinical and microbiological
mann, SUNSTAR, Thommen Medical, TRISA, Unilever, and effects of subgingival restorations with overhanging or clinically
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