0% found this document useful (0 votes)

45 views19 pages

Periodontology 2000 - 2023 - Salvi

This document provides a review of clinical periodontal diagnosis. It discusses how periodontal diagnosis is based on clinical signs and symptoms that may not accurately reflect active disease. Diagnosis can only be made after disease onset. The goals of periodontal therapy are to preserve sufficient tissue support and maintain a functional dentition through a combination of patient self-care and professional treatment. The review aims to present the subjective and objective criteria needed to classify periodontal health/disease and assign diagnoses to individual teeth.

Uploaded by

Consuelo Palma Huaroto

We take content rights seriously. If you suspect this is your content, claim it here.

Available Formats

Download as PDF, TXT or read online on Scribd

0% found this document useful (0 votes)

45 views19 pages

Periodontology 2000 - 2023 - Salvi

Uploaded by

Consuelo Palma Huaroto

We take content rights seriously. If you suspect this is your content, claim it here.

Available Formats

Download as PDF, TXT or read online on Scribd

You are on page 1/ 19

Received: 23 December 2022 | Revised: 16 February 2023 | Accepted: 14 March 2023

DOI: 10.1111/prd.12487

REVIEW ARTICLE

Clinical periodontal diagnosis

Giovanni E. Salvi1 | Andrea Roccuzzo1 | Jean-Claude Imber1 | Alexandra Stähli1 |

Björn Klinge2,3 | Niklaus P. Lang1
1
Department of Periodontology, School of Dental Medicine, University of Bern, Bern, Switzerland
2
Department of Periodontology, Faculty of Odontology, Malmö University, Malmö, Sweden
3
Division of Oral Diseases, Department of Dental Medicine, Karolinska Institute, Stockholm, Sweden

Correspondence
Giovanni E. Salvi, Department of Periodontology, School of Dental Medicine, University of Bern, Freiburgstrasse 7, Bern CH-3 010, Switzerland.
Email: [email protected]

1 | I NTRO D U C TI O N disease are lacking. Rather, periodontal diagnosis is based on clini-

cal and radiographic signs which may not reflect the presence of an
Periodontal diseases encompass pathological conditions of the active disease process but the sequelae of a previous pertubation of
tooth supporting structures initiated by the presence of bacterial the host defense mechanisms.
biofilms eliciting a host response.1–4 Following destruction of supra- Therefore knowledge of subclinical signs of disease activity and
crestal connective tissue, further loss of periodontal ligament fibers pathogenetic mechanisms also affect the interpretation of epide-
may result in loss of the alveolar bony support. From a clinical point miological data on the prevalence of periodontal diseases and their
of view, this condition may be recorded as loss of clinical attachment treatment modalities.
in relation to the cemento-enamel junction (CEJ) and be associated Despite all the limitations of contemporary diagnostic methods
with an inflammatory reaction in the gingiva clinically detectible as listed above, critical interpretation of clinical and radiographic pa-
erythema, swelling, and bleeding on probing (BoP). Additional signs rameters enable the clinician to routinely appraise the status of the
may include formation of periodontal pockets, recessions of the gin- periodontal patient.
gival margins, involvement of furcation areas, and, eventually, radio- More important to the patient, however, is the fact that clinical
graphic alveolar bone loss. Finally, patient-reported complaints such periodontal diagnosis requires the implementation of an appropriate
as increased mobility, tooth migration, and tilting may also be part of treatment strategy. In this respect, the consensus report of the 2017
the diagnostic process. World Workshop 4 guides the clinician in classifying the periodontal
Clinical periodontal diagnosis is based upon the recording and patient. In addition, a diagnosis for each individual tooth forms the
interpretation of the above-mentioned clinical signs and symptoms basis of a pretherapeutic prognosis and the establishment of a com-
in an attempt to establish extent and severity of the disease in the prehensive treatment plan for the individual patient.
entire dentition. lt should be realized, however, that based on clinical Eventually, the long-term goals of periodontal therapy focus on
parameters, periodontal diagnosis can only be established following the preservation of sufficient periodontal tissue support capable
the biological onset of the disease process. This means that clinical of maintaining a functional dentition for a lifetime. It is understood
onset of disease as well as periods of progression or remission at the that such treatment goals may only be achieved through the com-
tooth or site level may be unknown to the clinician. This is corrobo- bination of optimal self-administered biofilm control by the patient
rated by the fact that outcomes from preclinical and clinical studies and delivery of high-quality comprehensive therapy by dental
indicate that periodontitis progresses by periods of exacerbation professionals.
and remission.5,6 It is the aim of this review to present a summary of subjective
Today, routine clinical diagnostic methods aimed at detecting and objective criteria required to classify patients with periodontal
with high predictability periods of exacerbation or remission of health or disease as well as to assign a diagnosis to every single tooth.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in
any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
© 2023 The Authors. Periodontology 2000 published by John Wiley & Sons Ltd.

Periodontology 2000. 2023;00:1–19. wileyonlinelibrary.com/journal/prd | 1

16000757, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/prd.12487 by Cochrane Peru, Wiley Online Library on [06/09/2023]. 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
2 SALVI et al.

2 | G E N E R A L A N D D E NTA L H I S TO RY • Protection of the patient against systemic effects of routine

therapy
2.1 | Patient's chief complaint and expectations of • Control and/or knowledge of patient's modifiable and non-
treatment modifiable risk factors for successful comprehensive dental
treatment
Particular attention should be payed to the patient's chief complaint • Pain and anxiety control
and expectations of treatment. Such expectations have to be taken
seriously and must be incorporated in the evaluation of the clinical
situation. Patients, however, may express specific desires and ex- 2.4 | Assessment of family and social history
pectations regarding treatment outcomes that may be incongruent
with the true assessment by a dental professional with respect to Prior to a detailed assessment of the clinical condition, it is of para-
the clinical situation. Satisfactory treatment outcomes may only be mount importance to verify the patient's social environment and
achieved if the patient's expectations are in balance with the objec- to gain a sense for his/her priorities in life, including his/her expec-
tive evaluation of the extent and severity of the disease. tations and desires from both periodontal and implant therapy. In
addition, specific questions aimed at revealing the presence of peri-
odontitis (i.e., aggressive periodontitis; Stage II-IV, Grade C) within
2.2 | Patient's dental history and complaints the family should be always taken into consideration.

The assessment of complaints and symptoms of disease represent a

starting point and central part of the patient's dental history. These 2.5 | Assessment of oral hygiene habits, self-
aspects include an assessment of previous dental care and mainte- performed biofilm control, and smoking history
nance visits if not specified by the referring dentist. In this context,
information regarding signs and symptoms of periodontal diseases Due to the importance of self-performed biofilm control to success-
noted by the patient such as tooth migration or elongation and in- fully treat periodontitis, a concomitant accurate evaluation of pa-
creasing mobility, bleeding gums, food impaction, and impaired tient's routine dental care, including frequency and duration of daily
chewing ability should be evaluated. Outcomes from a recent ret- tooth-brushing procedures has to be performed. Moreover, patient's
rospective analysis, however, indicated that recognition of true peri- awareness of interdental cleansing devices, chemical supportive
odontal chief complaints by the patient such as bleeding gums, tooth agents, and regular utilization of fluorides should be evaluated.
mobility, and alterations in gingival color/shape was low.7 Since cigarette smoking has been documented to be the second
Improvements in chewing comfort including the need for tooth most important risk factor after inadequate self-performed bio-
replacement with removable or fixed dental prostheses should also film control in the etiopathogenesis of periodontal diseases,8 the
constitute an integral part of the comprehensive treatment plan. importance of smoking counseling should not be underestimated.
Furthermore, since cigarette smokers have been shown to be at
higher risk of developing peri-implant biological complications,9 im-
2.3 | Assessment of the medical history plant loss,10 and peri-implant marginal bone loss,11 proper assess-
ment of smoking history and habits should be performed for every
In order to make a personalized treatment plan for each patient, his candidate for implant therapy.12,13 Finally, it has be underlined that
or her medical history is of great importance. Prior to initial examina- the determination of smoking status should include detailed infor-
tion, a health questionnaire must be filled out and signed by every mation including exposure time and quantity.
patient. In order to evaluate the potential risk factors for routine
periodontal therapy, general medical conditions and medications
should be covered in this questionnaire. Moreover, an interview with 3 | S I G N S A N D S Y M P TO M S O F
the patient can give additional information regarding unclear risks PE R I O D O NTA L D I S E A S E S
or unknown conditons. Further uncertainties or missing information
which cannot be provided by the patient should be discussed with 3.1 | Extraoral features
the patient's physician. A written medical report from the physician
is very useful in patients with complex health conditions. The as- Dentists should be aware of the importance of an extraoral exami-
sessment of the medical history will help the clinician regarding the nation. The extraoral examination may include the assessment of
following important issues: skin, face, lymph nodes, odors from body and breath, and joints and
muscles of the head and neck region. The palpation of the cervical
• Protections of the dental team and other patients against infec- lymph nodes is recommended to identify possible lymphadenopa-
tious and contagious diseases thies. In a healthy status, lymph nodes are not palpable. If an ob-
• General risk assessment vious reason (e.g., acute infection) may cause the enlargement of
|

lymph nodes, the position, size, and mobility should be included in tissues may be the result of, for example, successful periodontal
the patient's history. A temporomandibular joint (TMJ) examination therapy with concomitant reduction in inflammation. Hence, it is ad-
is also important to detect parafunction. Possible extraoral findings visable to always evaluate PPD together with CAL in order to assess
for periodontal abscesses are facial swelling (3.6%), elevated body the periodontal condition in detail.
temperature, malaise, regional lymphadenopathy (7%–4 0%), or in-
creased blood leukocytes (31.6%).14 For necrotizing periodontal dis-
eases, typical extraoral signs are halitosis (84%–97%), adenopathy 3.3 | Clinical errors inherent to periodontal probing
(44%–61%), and/or fever (20%–39%).14 In case of persistence of the
enlargement or an unclear cause for swelling of the lymph nodes, the The determination of CAL and PPD is largely dependent on the
patient should be referred to his/her physician. instrument used for the examination and the technique applied to
assess the tissues. Clinical probing around teeth and implants is con-
sidered to be a fairly accurate clinical estimate for the evaluation of
3.2 | Assessment of pocket probing depth periodontal or peri-implant lesions, although some inherent inaccu-
racies in the evaluation have been recognized for many years.
The distance from the free gingival margin (FGM) to the bottom of The tip of the periodontal probe is considered to identify the most
the gingival/ periodontal pocket is termed pocket probing depth apical cell of the junctional (dento-gingival or implanto-mucosal) ep-
(PPD). Like clinical attachment level (CAL), PPD is assessed to the ithelium. Yet, research has indicated that this is rarely the case, and
nearest millimeter on all tooth surfaces by means of a standardized some inaccuracies are inherent to the probing procedure.17–24
and graduated periodontal probe. At least five factors may affect the readings of CAL and PPD: (i)
PPD should be assessed at all surfaces of all teeth present as well thickness of the probe at the tip, (ii) angulation and positioning of
as at existing implants in the oral cavity. PPD is the major contribu- the probe, (iii) graduation scale of the probe, (iv) pressure applied to
tor to the documentation of the periodontal lesions as depicted in a the probe, and (v) degree of inflammation of the periodontal tissues
periodontal chart. as an expression of the density of the collagenous tissue seal. It is
The periodontal chart represents the key diagnostic tool to be evident that only a histological examination will determine the ac-
used for an immediate evaluation of diseased sites from an extent curate anatomical level of the periodontal attachment and the apical
and severity perspective. The periodontal chart may also be used extension of the periodontal pocket.
in case presentations and discussions with the patient. Hence, it is Obviously, clinical assessments of CAL and PPD represent
a two-dimensional visualization of the health/disease status of the surrogate variables to the histologically documented situation.
periodontal tissues. Measurement errors depend up on factors like the thickness and
For convenience, the clinician is referred to a charting tem- taper of the probe, incorrect angulation or positioning of the probe,
plate offered free of charge by the University of Bern, Switzerland, and the graduation scale of the probe and may be minimized by
Department of Periodontology, with the following link: www.perio choosing standardized probes and careful examination techniques.
dontalchart-online.com. This site is available in 33 languages and Usually probes with a tip diameter of 0.4–0.5 mm are selected for
explains in detail how to perform a correct chart that may be down- assessment.
loaded for the patient record. Measurement errors as a consequence of variation in probing
Clinical probing of implant sites represents a sensitive diagnostic pressure and/or the variation in the extent of inflammatory infiltrate
procedure for the detection of peri-implant diseases. It has to be within the soft tissue seal are more difficult to control. Logically, the
realized that peri-implant probing is “a must” in monitoring implants higher the probing pressure applied, the deeper the probe will pene-
over time. The minor trauma left to the peri-implant soft tissue seal trate into the soft tissue seal. Studies performed to identify the vari-
after probing has been shown to completely repair with a new junc- ations in probing pressure (force) applied by clinicians have yielded
tional epithelium after 5–7 days following probing.15 Hence, there is probing pressures from 0.03–1.3 N. 25 Moreover, probing pressures
no adverse effect to the establishment of the soft tissue adhesion varied as much as 2:1 for single clinicians on repeated applications. 26
mechanism around implants. To minimize the errors encountered when applying various probing
PPD represents the severity and extent of the periodontal le- pressures, so-called pressure-sensitive probes have been proposed.
sions and is indirectly a measure of the inflammatory burden of the These probes are generally preset to a probing pressure of 0.3 N. 20,27
patient. Generally, PPD should be related to the reference of the Over- or underestimation of both PPD and CAL may occur as
attachment level, that is, the CEJ. Only by comparing PPD with CAL a result of the presence or absence of an inflammatory infiltrate
can an objective assessment of the extent and severity of periodon- subjacent to the junctional or pocket epithelium.17,20,21 When the
16
titis affected dentitions may be obtained. connective tissue subjacent to the pocket epithelium is infiltrated
It is evident that PPD is affected by the presence or absence of by inflammation, the periodontal probe will penetrate beyond the
inflammation within the tissues. Edema may cause swelling and a apical termination of the dento-gingival or implanto-mucosal epi-
coronal displacement of the gingival margin and result in the forma- thelium resulting in an overestimation of the “true” pocket depth.
tion of a pseudo-pocket. On the other hand, shrinkage of the gingival Conversely, for example, after successful periodontal therapy, when
|

the inflammatory infiltrate is minimal or even absent, the newly This simple dichotomous score is preferred by the clinicians over
formed collagenous tissue in the area previously affected by the in- more elaborate and more accurate gingival indices.32
filtrate will result in a dento-gingival or implanto-mucosal unit that Usually, BoP is determined at four or six surfaces of all teeth and/
is more resistant to probe penetration; hence, the probing measure- or implants, and the mean percentage of BoP-positive sites for the
ments of PPD and CAL may underestimate the “true” histologically individual is calculated. While BoP-positive sites at teeth represent
defined levels. gingivitis, BoP-positive sites at implants reflect the presence of mu-
cositis. The higher the BoP score obtained, the more generalized the
inflammatory status becomes.
3.4 | Assessment of CAL Obviously, BoP represents a reversible inflammatory parameter
that may be affected by prophylactic measures, that is, oral hygiene and
CAL documents the extent and severity of the periodontal lesion. biofilm removal.33,34 As gingivitis represents a precursor for periodon-
The clinical attachment has been lost as a consequence of the mi- titis, mucositis represents the precursor for peri-implantitis (Figure 1).
crobial dysbiosis resulting in a host response that led to the loss of
connective tissue fiber attachment to the tooth. It is an irreversible
damage to the supporting apparatus of the tooth that, without any 3.6 | Assessment of furcation involvement
regenerative efforts, will be lost for the life of a tooth.
CAL is usually measured to the nearest millimeter applying a Periodontal pockets are usually defined as one-, two-, or three-wall
standardized and graduated periodontal probe. The reference is the bony pockets, the fourth wall being defined by the tooth surface. If the
CEJ as the apical extension of the junctional epithelium in a pris- disease has progressed into the furcation area of a multi-rooted tooth,
tine tooth without prior pathological tissue changes terminates at the roof of the furcation limits the lesion on three sides, and the alveo-
the CEJ. Consequently, the distance from the CEJ to the bottom of lar bone forms the lower limit of the lesion. Hence, a furcation involve-
the probable gingival/periodontal pocket is measured. The choice of ment (FI) represents a periodontal lesion oriented in a horizontal rather
the proper instrument is crucial in determining the accuracy of the than a vertical direction. As FI teeth are difficult to treat and maintain
clinical assessment. healthy by prophylactic measures, the identification of such teeth is of
To determine the CAL, it is necessary to provide two clinical utmost importance for the assessment of periodontal status.
measurements: (i) the distance from the FGM to the CEJ for each Furcation entrances of all molars and first premolars of the max-
tooth surface that is to be assessed, and (ii) the PPD, again, assessed illa should be assessed with a curved furcation probe (i.e., Nabers
to the nearest millimeter. CAL is calculated by subtracting the dis- furcation probe) usually with graduations at 3 and 5 mm. The hor-
tance of FGM-CEJ from PPD whenever the CEJ is covered by the izontal component of probing is graded (0–3) according to the fol-
soft tissue. In case of gingival or mucosal recessions, the distance lowing criteria:
from the FGM to the CEJ becomes negative; hence, the calculation
for CAL turns into an addition of this distance (FGM-CEJ) to the PPD.

3.5 | Assessment of BoP

BoP has been shown to represent a diagnostic clinical test to docu-

ment the inflammatory status of the dento-gingival or implanto-
mucosal unit.
A periodontal probe standardized for its dimensions and preferably
insertion pressure is inserted to the bottom of the gingival/periodon-
tal pocket by applying a light force.28 The force to be used has been
identified to be 0.2-0.3 N. This will avoid false positive readings and
identify the tissues bleeding due to the presence of inflammation and
not due to an applied trauma. The 0.3 N are to be applied both in pris-
tine and/or homeostatic tissues, that is, intact height of the periodon-
tium29 as well as in tissues that have experienced periodontitis and
were successfully treated, that is, a reduced periodontium.30
If bleeding is provoked by running a probe along the gingival
margin,31 the true tendency to bleed from the depth of the pocket
F I G U R E 1 Assessment of pocket probing depth in conjunction
is overlooked. with bleeding on probing. A graduated Michigan periodontal probe
If bleeding is provoked upon retrieval of the probe within 10 s, is inserted to the bottom of the periodontal pocket and is moved
the site is considered BoP-positive and, therefore, clinically inflamed. along the root surface.
|

Grade 0 = Furcation not probable. was electronically distributed to 2014 randomly selected dentists.
Grade 1 = Furcation with a horizontal component of probing The response rate was low (14.87%). In their clinical practice, the
≤3 mm. (superficial FI). responding dentists most often (52.45%) used articulation paper as
Grade 2 = Furcation with horizontal probing of >3 mm (at one en- an indicator for occlusion. Articulation foil was used by 26.22% and
trance of the furcation) (deep FI). articulation silk by 16.78%. The respondents expressed a growing
Grade 3 = Furcation with through and through opening (horizon- interest in using digital methods when (<0.2 mm) made available.45
tal probing of >3 mm from at least two entrances). The co-morbidity of periodontitis and rheumatoid arthritis
(RA) is well recognized, especially in recent scientific literature.46,47
The degree of the FI is charted using circles as a symbol. An open Temporo-mandibular disorders (TMDs) are a frequent finding in the
circle (o) (Grade 1), a semicircle (◒) (Grade 2), and a filled in circle (•) RA patient. Temporo-mandibular joint function was reported to be
(Grade 3). abnormal in 98.4% of the RA patients, and 62.9% of them presented
moderate or severe TMDs.47 Alertness of dental professionals to
TMD pain and periodontal inflammation is strongly recommended.
3.7 | Assessment of tooth mobility TMDs are a significant public health problem affecting approxi-
mately 5%–12% of the population. TMDs are the second most com-
In 1938, S.C. Miller developed the most commonly used clinical method mon musculoskeletal condition after chronic low back pain resulting
for determining tooth mobility (TM). Using his method, the tooth is held in pain and disability. Pain-related TMDs can impact the individual's
firmly between two instruments and moved back and forth and mobil- daily activities, psychosocial functioning, and quality of life (National
ity scored on a scale of 0 to 3. A score of 0 denotes no detectable move- Institute of Dental and Craniofacial Research).
ment when force is applied, other than what is considered normal (i.e.,
physiologic) motion (<0.2 mm). A score of 1 indicates mobility greater
than normal. Mobility of up to 1 mm in a buccolingual direction is scored 3.9 | Diagnostic criteria for TMDs
2. Movement of more than 1 mm in a buccolingual direction combined
with the ability to vertically depress the tooth is scored 3.35,36 The newly recommended diagnostic criteria for TMDs protocol in-
Methods for automatic simultaneous recording of tooth loading cludes both a valid screener for detecting any pain-related TMDs as
and subsequent displacement have been used to evaluate the ef- well as valid diagnostic criteria for differentiating the most common
fects on tooth mobility of various treatments of advanced periodon- pain-related TMD (sensitivity ≥0.86, specificity ≥0.98) and for one
titis, as exemplified by Grabec and co-workers.37 Their instrument intra-articular disorder (sensitivity of 0.80 and specificity of 0.97).48
included a pneumatically driven probe and incorporated sensors to The model has been adopted for general dentistry to identify, diag-
detect tooth mobility and loading force. However, in daily clinical nose, and treat patients for related orofacial pain. According to the
practice these more technically advanced and automated instru- Axis protocol, all patients being examined for the first time, or at
ments seem not as yet to have been widely adopted. follow-up examinations, are asked to answer three simple screening
In the literature following the 2017 World Workshop on the clas- questions (3Q/TMD): (1) Does it hurt once a week or more often
sification of periodontitis, in addition to stage III severity a high level in the temple, face, temporo-mandibular joint or jaws? (2) Does it
of tooth mobility (≥2) worsens the periodontitis to stage IV.38 hurt once a week or more often when you yawn or chew? (3) Do
Tooth splinting has been reported to be performed as an adjunc- you have locking or hooking in the temporo-mandibular joint once a
tive intervention for teeth with a progressive increase in tooth mo- week or more often? If the patient answers “Yes” to one or more of
39
bility in order to improve the patient's chewing capabilities. these questions, the patient should be offered a full examination and
In a recent systematic review, Helal and co-authors reported on subsequent treatment.
predictors for tooth loss in periodontitis patients.40 Among other
factors, tooth mobility was reported to be significantly associated
with tooth loss; however, the heterogeneity was high between the 3.10 | Radiographic analysis
four studies included for the analysis of tooth mobility.41–4 4
Without any doubt, the clinical periodontal examination provides the
clinician fundamental information with respect to PPDs, gingival reces-
3.8 | Assessment of static and dynamic sions, quantity and quality of attached gingiva, and FI. Nevertheless,
occlusion and temporo-mandibular disorders it cannot disclose the status of the alveolar bone which is of crucial
importance to precisely diagnose different periodontal conditions.
Static occlusion refers to the contacts between the teeth when the Among the available ionizing modalities, the use of periapical images
jaw is closed and stationary, whereas dynamic occlusion refers to oc- is by far the most commonly used non-invasive technique in dentistry
clusal contacts made when the mandible is moving. In an attempt to to inspect the alveolar bone. More specifically, periapical radiographs
report on the methods used by dentists for registration of occlusal provide relevant information including subgingival calculus deposits,
contacts, a survey was conducted and an anonymous questionnaire root morphology length and proximity, periapical lesions, and the
|

amount of alveolar bone destruction (Figure 2A,B).49 Furthermore, 4 | S I N G LE TO OTH D I AG N OS I S

to enable meaningful comparative analysis and increase reproduc-
ibility of the radiographs a long-cone paralleling technique is recom- Based on the clinical and radiographic conditions assessed through a
mended.50 However, clinicians should be aware of the limitations of comprehensive periodontal examination (i.e., periodontal chart and
2D radiographic images during the diagnostic phase such as: radiographs), five different diagnoses regarding the periodontal con-
dition may be given for every single tooth in the dentition.
• Lack of detection of periodontal pockets A correct diagnosis for every individual tooth should form the
• Lack of detection of tooth mobility basis for a pretherapeutic prognosis and the establishment of a com-
• Lack of discrimination between the buccal and lingual aspects of prehensive treatment plan of the individual patient.
tooth and bone
• Significant radiographic changes are visible only after advanced
clinical attachment loss 4.1 | Periodontal health
• Radiographic changes are visually detectable when 30%–50% of
the bone mineral content has been resorbed.51 According to the 2017 World Workshop on the Classification of
Periodontal Diseases and Conditions (Figure 4), four levels of peri-
In recent years, especially to overcome these limitations, utiliza- odontal health were proposed52:
tion of cone beam computed tomography (CBCT) has been rapidly
increasing. CBCT has become an integral tool for researchers and cli- 1. Pristine periodontal health characterized by a structurally sound
nicians, mostly applied to the implant field. As such, the use of CBCT and uninflamed periodontium
imaging for the diagnosis of periodontitis has also been evaluated. 2. Periodontal health characterized by a structurally and clinically
However, in 2017, the American Academy of Periodontology (AAP) intact periodontium
reported that, even though its use may be beneficial in selected 3. Periodontal disease stability on a reduced but healthy
cases, there is limited evidence to support the use of CBCT for the periodontium
different types of bony defects, and there are no guidelines for its 4. Periodontal disease remission/control on a reduced but healthy
application to periodontal treatment planning (Figure 3). periodontium.

F I G U R E 2 A, Radiographic scenario
of an infrabony defect on the mesial
aspect of tooth 46. B, Periapical
radiograph at the 12-month follow-up
examination following non-surgical
mechanical instrumentation documenting
radiographic bone fill.

F I G U R E 3 A–C , Clinical and

radiographic scenarios of a combined
infrabony and interradicular defect (i.e.,
increased pocket probing depth, furcation
involvement, bleeding on probing,
suppuration, and radiographic evidence of
alveolar bone destruction).
|

F I G U R E 4 A and B, Periodontal
health characterized by a clinically and
radiographically intact periodontium.

F I G U R E 5 Clinical signs of gingivitis.

A, Presence of supragingival biofilm and
calculus resulting in erythematous and
edematous gingival margin. B, Pocket
probing depth of 3 mm with bleeding on
probing.

4.2 | Gingivitis - tooth level mild–moderate periodontitis, horizontal as well as angular/vertical

alveolar bone loss are included in this diagnosis. The distinction be-
The diagnosis of gingivitis is applied to teeth displaying BoP without tween mild–moderate and severe periodontitis is solely based on
CAL loss. The sulcus depth usually ranges between 1 and 3 mm irre- increased PPD (Figure 7).
spective of the level of clinical attachment. So-called pseudopockets
may be present in cases of increased probing depth without con-
comitant loss of clinical attachment and alveolar bone and presence/ 4.5 | Interradicular periodontitis
absence of BoP. The diagnosis of gingivitis usually characterizes per-
iodontal lesions confined to the gingival margin (Figure 5). The adjunctive diagnosis of interradicular periodontitis may be given
to multirooted teeth with superficial or deep FI (Figure 8).
In the presence of necrotizing/ulcerative and acute (i.e., gingival
4.3 | Moderate periodontitis - tooth level and periodontal abscesses) lesions, these terms may be added to the
tooth-related diagnosis (Figure 9).
Gingivitis in combination with clinical attachment loss is termed
periodontitis. In cases of PPD ≤6 mm, a diagnosis of mild–
moderate periodontitis may be given irrespective of the mor- 5 | C LI N I C A L I N V E S TI G ATI O N S
phology of periodontal lesions. This diagnosis may, therefore, be
applied to teeth characterized by a horizontal pattern of alveolar 5.1 | Non-biofilm-induced gingival and periodontal
bone loss, thus representing suprabony lesions and/or to teeth conditions
characterized by an angular or vertical loss of alveolar bone, thus
representing infrabony lesions. Infrabony lesions include defects While biofilm-induced gingival and periodontal inflammatory lesions
with 1, 2, and 3 bony walls as well as craters between two adja- are very common, non-biofilm-induced gingival and periodontal
cent teeth (Figure 6). manifestations of systemic diseases are rather rare and often pre-
sent with both distinctive clinical features and characteristics in the
patient history. The diagnosis of these disorders is challenging as
4.4 | Severe periodontitis - tooth level many of them present with similar clinical findings. To succeed in
the diagnosis, a profound knowledge of clinical oral and systemic
In cases of PPD >6 mm, a diagnosis of severe periodontitis is characteristics of the respective disorder and an interdisciplinary ap-
given irrespective of the morphology of the osseous lesion. As for proach is often crucial.
|

F I G U R E 6 Clinical A and radiographic

B evidence of mild–moderate
periodontitis (i.e., presence of supra-and
subgingival calculus and radiographic
evidence of horizontal alveolar bone
destruction).

F I G U R E 7 Clinical A and radiographic

B evidence of severe periodontitis with
increased tooth mobility, tooth migration,
gingival recessions, and presence of
horizontal and angular alveolar bone
destruction.

F I G U R E 8 Clinical A and radiographic

B evidence of Grade 2 furcation
involvement at the distal aspect of tooth
16. Secondary caries on the mesial aspect
of 16 is also diagnosed.

One of the clinical hallmarks of non-biofilm-induced gingival and these the clinician needs to cast the net wider and understand the
periodontal conditions is that they do not resolve or not completely whole picture of the disease/condition.
after plaque control. Non-biofilm induced gingival and periodon-
tal lesions and systemic diseases that present in the periodontium
can have numerous causes, based on which a classification was 5.1.1 | Gingival diseases: non-biofilm-induced
established that was revised at the 2017 World Workshop on the
Classification of Periodontal Diseases organized by the American Non-biofilm-induced gingival diseases are limited to the gingiva and
Academy of Periodontology and the European Federation of have been listed at the 2017 World Workshop (Table 2).55
Periodontology.53,54 Most of these conditions are genetic, others are
acquired or inflammatory in nature (Tables 1 and 2). This review con- Hereditary gingival fibromatosis
centrates on clinical oral findings and investigations for non-plaque- Gingival overgrowth, also called gingival hyperplasia or gingival fi-
induced gingival and periodontal conditions. However, to recognize bromatosis is a well-known side effect of phenytoin, ciclosporine,
|

TA B L E 1 Overview of gingival and periodontal conditions as

they were classified at the 2017 World Workshop highlighting the
non-biofilm-induced conditions and manifestations of systemic
diseases.

Gingival and periodontal conditions

Periodontal health, gingival Periodontal health & gingival

diseases and conditions health
Gingivitis: Dental
biofilm-induced
Gingival diseases: Non-dental
biofilm-induced
Periodontitis Necrotizing periodontal diseases

F I G U R E 9 Clinical evidence of necrotizing periodontitis in the Periodontitis

upper and lower anterior areas with presence of supragingival Periodontitis as a manifestation
biofilm, calculus, and interproximal periodontal tissue destruction. of systemic disease
Other conditions affecting the Systemic diseases or conditions
periodontium affecting the periodontal
and with calcium channel blocker medication57; however, it can also supporting tissues
be of genetic origin and is then called hereditary gingival fibroma- Periodontal abscesses and
tosis (HGF). HGF can occur as an isolated phenomenon or as part endodontic-periodontal
of a syndrome including hypertrichosis, mental retardation, epilepsy, lesion

growth retardation, and abnormalities of the extremities.58 HGF pre- Mucogingival deformities and
conditions
sents with progressive slow, non-hemorrhagic, fibrous, albeit painless
Traumatic occlusal forces
growth of the gingival tissue and affects approximately 1 in 750,000
live births. 59
Hitherto the disorder has been mapped to five candi- Tooth and prosthesis related
factors
date genes including the Son of Sevenless genes, REST, ZnF862, Alk,
and CD36.60–62 One of the main pathogenic mechanisms results in
an excessive secretion of transforming growth factor-(TGF) β and an
extensive production of extracellular matrix proteins which clinically Clinical findings: These infections manifest as painful edema-
manifests as more or less severe enlargement of the gingiva; in severe tous ulcerations, as asymptomatic mucous patches, or atypically
cases, major parts of the tooth surface might be covered.63 as highly inflamed gingivitis or stomatitis. In cases of syphilis,
Clinical findings: The gingiva present with enlargement that multiple ulcerated lesions may appear on lips, tongue, or the hard
usually becomes obvious at the time of tooth eruption. In cases of palate. Some patients with undiagnosed syphilis may first pres-
early and severe manifestations, tooth eruption might be impacted. ent with oral lesions. 65 Oral tuberculous lesions have become very
Diastema, mispositioning of teeth, cross and open bites are frequent rare. 66 They appear mostly as secondary lesions often associated
observations. Due to the gingival enlargement, plaque accumulation with pulmonary disease. 67 Here oral lesions usually present as
may increase favoring gingival and periodontitis. Treatment consists single, painful, and irregular ulcers covered by inflammatory ex-
of good plaque control and gingivectomy. HGF cannot be cured and udate affecting most often the dorsum of the tongue. However,
64
often retreatment is required. they may also occur on any other site of the oral mucosa and in
Clinical investigations: HGF often accumulates within families. a variety of forms such as nodules, tuberculomas, and periapical
Therefore, a thorough patient and family history is mandatory. granulomas. 66,68,69
Histologic assessment of excised gingival tissue generally reveals Clinical investigations: A thorough patient history and clinical
increased an amount of collagen fibrils and significant epithelial rete evaluation is key. Biopsy and microbiologic assessment provide the
pegs. Blood tests are not indicated as no specific marker or gene conclusive evidence.
mutation is indicative for the disorder.54
Viral infections
Bacterial infections A variety of virus infections can present with lesions in the oral mu-
Non-biofilm-induced infections of gingival tissues are very rare and cosa and gingiva. Hand-foot-and-mouth disease caused by coxsackie
might affect immunocompromised individuals or individuals where viruses is one of those affecting mostly children under 10 years of
the homeostasis between host defense and non-plaque related age and often sweep through childcare units or schools.70,71
bacteria is disturbed. Acute infective gingivitis or stomatitis might Clinical findings: Children present with blisters in the mouth,
occur after infection with Neisseria gonorrhea, Treponema pallidum, mainly affecting the tongue, buccal mucosa, and the throat. Typical
Mycobacterium tuberculosis, or other pathogens. lesions can also be observed on the palms of the hands and around
|

TA B L E 2 Classification of non-plaque-induced gingival diseases and conditions according to Ref. [56].

Genetic/ developmental disorders Reactive processes

• Hereditary gingival fibromatosis • Epulides
Specific infections ◦ Fibrous epulis
• Bacterial origin ◦ Calcifying fibroblastic granuloma
◦ Neisseria gonorrhea ◦ Pyogenic granuloma (vascular epulis)
◦ Treponema pallidum ◦ Peripheral giant cell granuloma (or central)
◦ Mycobacterium tuberculosis Neoplasms
◦ Streptococcus gingivitis • Premalignant
• Viral origin ◦ Leukoplakia
◦ Coxsackie virus (hand-foot-and-mouth disease) ◦ Erythroplakia
◦ Herpes simplex virus types 1 and 2 • Malignant
◦ Varicella zoster virus (chicken pox or shingles affecting nerve V) ◦ Squamous cell carcinoma
◦ Molluscum contagiosum ◦ Leukemia
◦ Human papilloma virus ◦ Lymphoma
▪ Squamous cell papilloma Endocrine, nutritional, and metabolic diseases
▪ Condyloma acuminatum • Vitamin deficiencies
▪ Verruca bulgaris ◦ Vitamin C (scurvy)
▪ Focal epithelial hyperplasia Traumatic lesions
Inflammatory and immune conditions • Physical/mechanical insults
• Hypersensitivity reactions ◦ Frictional keratosis
◦ Contact allergy ◦ Mechanically induced gingival ulceration
◦ Plasma cell gingivitis ◦ Factitious injury
◦ Erythema multiforme • Chemical burn
• Autoimmune diseases of skin and mucous membranes ◦ Etching
◦ Pemphigus vulgaris ◦ Chlorhexidine
◦ Pemphigoid ◦ Acetylsalicylic acid
◦ Lichen planus ◦ Cocaine
◦ Lupus erythematosus ◦ Hydrogen
• Granulomatous inflammatory conditions (orofacial granulomatosis) ◦ Dentifrice detergents
◦ Crohn's disease ◦ Paraformaldehyde or calcium hydroxide
◦ Sarcoidosis • Thermal insult
◦ Burns to gingival mucosa
• Gingival pigmentation
◦ Melanoplakia
◦ Smoker's melanosis
◦ Drug-induced pigmentation
◦ Amalgam tattoo

the fingers and toes. Starting with red dots, the lesions develop into chain reaction. Alternatively, blood can be evaluated for antibody
vesicles that finally rupture.54 titers against HSV.
Infection with herpes simplex virus types 1 and 2 as well as vari-
cella zoster may pass asymptomatically but may also rarely be asso- Fungal infections
ciated with gingivostomatitis mostly occurring in infants when the Fungal infections comprise a variety of diseases such as aspergillosis,
viruses first hits.72 blastomycosis, candidosis, and histoplasmosis. The most common
Human papilloma virus (HPV): Only very few of the differ- fungal infection affecting the oral mucosa is caused by C. albicans.
ent subtypes can be found in the oral cavity, the squamous cell Infection with C. albicans has been associated with a reduced host
73,74
papilloma and verruca vulgaris are most common types. They response like immunodeficiency, reduced salivary flow, smoking,
appear as painless, small, whitish icicle-like or cauliflower-like removable prostheses, or treatment with corticosteroids or asthma
protrusions. sprays.75
Primary herpetic gingivostomatitis manifests as painful severe Clinical findings: Signs and symptoms include creamy white le-
gingivitis with general redness, or ulcerations and in case of stoma- sions mostly on the tongue, inner cheeks, on the palate, gingiva,
titis with edema. Often vesicles are first observed, which rupture and tonsils. Different types can be distinguished as pseudomembra-
and coalesce into fibrin-coated ulcers. Children might be feverish. nous, erythematous, plaque-like type, and nodular type of candido-
In adults, recurrent intraoral herpes lesions might be mistaken for sis. Unlike the pseudomembranous form that can be wiped off, the
aphthous ulcerations.72 plaque-like and nodular type are non-scrapable. Some of the lesions
Clinical investigations: Besides patient history and clinical exam- take on a cottage cheese-like appearance.76 Less commonly, they
ination, HSV from lesions can be sampled and tested by polymerase appear as a red area.
|

Clinical investigations: A thorough patient history and clinical ex- occur. The diagnosis can be confirmed histologically by intraepithe-
aminations are the basis for identifying the infection. The diagnosis lial bulla formation.83 Blood serum reveals circulating autoantibody
54
can be accomplished by smear culture or biopsy. titers to desmoglein 1 and 3 that are detectable by enzyme-linked
immunosorbent assay mostly later than the initial stage.83,84

5.1.2 | Inflammatory and immune Pemphigoid

conditions and lesions Similarly to PV, pemphigoid is caused by autoantibodies but here
toward distinct components of the dermal-epidermal junction.
Hypersensitivity reactions and erythema multiforme Consequently, the epithelium detaches from the connective tissue.
Allergic reactions in the oral mucosa are rare. Reactions to restora- Pemphigoid so far describes eight disorders of which the targets all
tive materials may bear similarities with oral lichen planus lesion have been identified.81 Bullous pemphigoid (BP) is the most com-
or oral leukoplakia. Dentifrices, mouthwashes, or food ingredients mon type with an annual incidence of 2.4–21.7 new cases per million
might also give rise to type IV hypersensitivity reactions. population.85–87 It is mainly considered as a disease of the elderly
Erythema multiforme is a rare, self-limiting acute immune- and is rarely encountered in individuals younger than 50 years. One
inflammatory reaction of the oral mucosa with unknown etiology. type of pemphigoid, the mucous membrane pemphigoid (MMP) af-
It mostly affects young adults.54 Characteristically, swollen lips are fects mucous membranes, most commonly the oral mucosa, the ocu-
accompanied by heavy crust formation along the vermilion border. lar mucosa, oropharynx, larynx and the genital region.
Characteristically, at the buccal mucosa and the gingiva rupturing Clinical findings: Oral lesions are present in about 30% of the pa-
bullae appear leaving extensive ulcers.54 tients with BP and in about 40% with MMP. Oral lesions appear as
Clinical findings: The clinical manifestation of type IV hypersen- irregular diffuse ulcers, erosive patches with pseudomembranes, or
sitivity reactions occur within a timeframe of 48 h after exposure to generalized gingival erythema.
the allergen. Erythema multiforme displays swollen lips with severe Clinical investigation: Patient history and extra-and intraoral ex-
crust formation of the vermilion border and gingival or mucosal bul- amination might reveal the diagnosis. The ocular mucosal inspection
lae that rupture leaving extensive ruptures. Skin lesions are charac- should be inspected. With BP, the Nikolsky sign is mostly negative,
terized by an iris appearance with a central bulla surrounded by a while with MMP an induced trauma can elicit blisters and erosion
77
pale halo and an erythematous zone. (Nikolsky positive).88 Biopsy should involve perilesional tissue for
Clinical investigations: Allergy testing with skin patches might be histological and immunohistochemical examination that can distin-
considered. guish the different types of pemphigoid. Circulating antibodies in
the blood are not always detected.

5.1.3 | Autoimmune diseases Lichen planus

Oral lichen planus (OLP) is a recurrent mucocutaneous autoimmune
Pemphigus vulgaris disease displaying characteristic white lace-like lesions. It is a common
Pemphigus vulgaris (PV) is a rare immunoglobulin G (IgG) -mediated auto- disorder with a global prevalence of 1%89 to up to 2%90 with a female
immune disorder that is characterized by intraepithelial blistering in the preponderance. Erosive/ulcerative OLP has been classified as poten-
mouth and on the skin.78 These blisters are caused by auto-antibodies tially malignant disease. Tongue localization, presence of atrophic-
directed against epithelial desmosomal glycoproteins79,80 which result in erosive lesions, and alcohol consumption are risk factors for malignant
intraepithelial cleavage. The disease develops in middle aged or elderly transformation.91 Six types of OLP have been identified (papular, re-
individuals. The incidence varies between 0.5 and 6.1/100 000 in the ticular, plaque-type, erythematous, ulcerative, bullous). Basically, it has
population. Of note, Israeli and Ashkenazi Jewish women are more often been described as an inflammatory reaction against an unidentified
affected from PV than men and other populations.81 antigen in the basal epithelial layer/ within the basement membrane.
Clinical findings: Bulla formation are characteristic for the disease Approximately 15% of patients with OLP have also cutaneous lesions,
that may affect large areas of the skin. Often the disease presents first 20% also genital lesions.92
with oral lesions. Early lesions might bear resemblance with aphthous Clinical findings: OLP most commonly affects the buccal mu-
ulcers; later into the disease, widespread, painful desquamative lesions, cosa, tongue, and gingiva (Figure 10). It often shows a bilateral,
erosions, or ulcerations occur. The lesions heal without scarring, but symmetric distribution. Two or even more types of OLP can occur
bulla formation is recurrent. Other mucous membranes are involved. simultaneously (Figure 11). The reticular type displays characteristic
Clinical investigations: Patient history and clinical inspection are interlacing white lines (i.e., Wickham striae) and often manifests in
mandatory. A positive Nikolsky sign is characteristic for PV, which the posterior buccal areas.92 The papular type often appears con-
describes the formation of visible erosion and intraepithelial dis- currently with the reticular type. The erythematous type is charac-
ruption when applying lateral tension or friction by a finger on the terized by atrophic, erythematous lesions with radiating striae in the
skin.82 When PV is suspected, patients should be immediately re- periphery. The erythematous, ulcerative, and bullous types usually
ferred to the dermatologist as life-threatening complications can present with symptoms that require treatment.92
|

F I G U R E 1 0 Clinical frontal view of a young female patient with

generalized oral lichen planus lesions. Courtesy of PD Dr. V. Suter,
Department of Oral Surgery and Stomatology, University of Bern,
Bern, Switzerland.
F I G U R E 1 2 Squamous cell carcinoma in the retromolar region
of a 90-year-old patient.

Clinical findings: The typical lesion has a central atrophic area with
white dots surrounded by irradiating fine white striae. Characteristic
for DLE is a Bordeaux-colored, butterfly-shaped rash on the bridge
of the nose and the cheek consisting of photosensitive, scaly mac-
ules. Oral lesions can also ulcerate or resemble OLP lesions.
Clinical investigations: Patient history and clinical extra- and
intraoral inspection are the first pillars of the diagnosis. Further,
histopathological evaluation shows characteristic changes, that is,
hyperkeratosis, keratin plugging and variation in epithelial thickness,
liquefaction of basal cells, and increased width of the basement
membrane. Immunohistochemistry often reveals immunoglobulins,
C3, and fibrin along the basement membrane. Blood test may re-
veal lower numbers of erythrocytes, further antinuclear antibodies
(ANA) might be detected. Diagnosis of SLE might be challenging
F I G U R E 1 1 Combined reticular and ulcerative oral lichen planus
given the heterogeneity of the clinical features.
lesions in the posterior mandible of a 40-year-old female patient.
Courtesy of PD Dr. V. Suter, Department of Oral Surgery and
Stomatology, University of Bern, Bern, Switzerland. Reactive processes
Epulides describe very broadly exophytic processes originating
Clinical investigations: Patient history and clinical inspection is of from the gingiva. Usually, they are not accompanied with symptoms.
utmost importance. The diagnosis is based on the presence of bi- Several types can be distinguished, including the fibrous epulis, the
lateral papular-, reticular-t ype lesions. Histopathological evaluation calcifying fibroblastic granuloma, the pyogenic granuloma (i.e., vas-
reveals hyperkeratosis, degenerative changes of basal cells, and sub- cular epulis), and the peripheral giant cell granuloma.54
epithelial band-like accumulation of lymphocytes and macrophages Clinical findings: The fibrous epulis displays a smooth pink sur-
characteristic for a type IV hypersensitivity reaction.92 Given the face, the calcifying fibroblastic granuloma can reach larger sizes,
premalignant characteristics of certain OLPs, regular check-ups are although usually smaller than 1.5 cm, and can, if occurring inter-
recommended. dentally, separate adjacent teeth. The pyogenic granuloma often
develops during pregnancy. The peripheral giant cell granuloma is
Lupus erythematosus the most common reactive lesion and appears as swollen, sessile or
Lupus erythematosus (LE) is a group of autoimmune diseases that de- pedunculated, at times ulcerated process.54
velop autoantibodies against various cellular components including
nuclear and membrane components. Two forms are known: discoid LP Neoplasms
(DLE) and systemic LP (SLE), which may affect several organs. The annual Squamous cell carcinomas represent about 90% of intraoral carci-
incidence for SLE varies between 3.7 and 49 per 100 000 persons.93,94 nomas with a predilection for the posterior mandible96 (Figure 12).
For DLE, annual incidence estimates of about 0.5–6.5 per 100 000 indi- It is important to note that oral lesions can also be manifestations of
viduals have been published.95 Both forms are more common in women leukemias and non-Hodgkin lymphomas.
than men. DSE is chronic, although mostly shows a mild form affecting Clinical findings: The primary stage can be an ulcer or small nod-
the mucous membranes including the gingiva and oral mucosa. ules that might have an innocent appearance.
|

Clinical investigations: Biopsy is needed for diagnosis. Immediate Some of these diseases are innate, others are acquired later on
referral is of utmost importance because, when detected early, in life. Disorders that impair the immune response predispose these
oral squamous cell carcinomas can be cured in 89%–90% of cases, individuals to infections and also to a higher prevalence and severity
whereas later into the disease at stage 3 and 4, the survival rate de- of periodontal disease that depending on the severity of the impair-
creases to 20%.54 ment might already set in during adolescence. Genetic disorders de-
rive from gene mutations or chromosome aberrations. As individuals
Traumatic lesions with genetic disorders most often present with other systemic con-
Traumatic lesions of the gingiva can be found after physical/me- ditions, the genetic background is in most cases known before in-
chanical insults and may be induced by a traumatic tooth brushing dividuals seek dental care/treatment. Here, only the most common
technique or can be due to chemical insults including the use of chlo- disorders and conditions are discussed, while the full classification
rhexidine, acetylsalicylic acid, cocaine, hydrogen peroxide. Burns from the 2017 World Workshop is listed in Table 3.
caused by very hot food can further cause lesions.
Clinical findings and investigation: Patient history and clinical ex-
amination are important for the diagnosis. 5.2.1 | Systemic disorders with major impact on the
loss of periodontal tissues by influencing periodontal
inflammation
5.2 | Periodontitis as a manifestation of
systemic diseases Genetic disorders: Diseases affecting the immune response
Down syndrome. Despite significant improvements in prenatal
Several systemic diseases and medication have a severe impact on screening tests that are now able to detect chromosomal material
the periodontal tissues and may cause periodontal attachment loss from the fetus circulating in the maternal blood, Down syndrome
97,98
and bone loss or aggravate periodontal tissue loss. continues to be the most common disorder. In the United States,

TA B L E 3 Classification of diseases and conditions affecting the periodontal tissue according to References97,98.

Systemic disorders that have a major impact on the loss Acquired immunodeficiency diseases
of periodontal tissue by influencing periodontal • Acquired neutropenia
inflammation: • HIV infection
Genetic disorders Inflammatory diseases
• Diseases associated with immunologic disorders • Epidermolysis bullosa acquisita
◦ Down syndrome • Inflammatory bowel disease
◦ Leukocyte adhesion deficiency syndromes • Arthritis (rheumatoid arthritis, osteoarthritis)
◦ Papillon-Lefèvre syndrome Other systemic disorders that influence the pathogenesis of periodontal disease:
◦ Haim-Munk syndrome • Emotional stress
◦ Chediak-Higashi syndrome • Smoking
◦ Severe neutropenia • Medications
▪ Congenital neutropenia Systemic diseases that can result in loss of periodontal tissue irrespective of
▪ Cyclic neutropenia periodontitis:
◦ Primary immunodeficiency diseases • Neoplasms
▪ Chronic granulomatous disease ◦ Primary neoplastic diseases of periodontal tissue
▪ Hyperimmunoglobulin E syndromes ▪ Oral squamous cell carcinoma
◦ Cohen syndrome ▪ Odontogenic tumors
• Diseases affecting the oral mucosa and gingival tissue ▪ Other primary neoplasms of periodontal tissue
◦ Epidermolysis bullosa ◦ Secondary metastatic neoplasms of periodontal tissue
▪ Dystrophic epidermolysis bullosa • Other disorders that may affect periodontal tissue
▪ Kindler syndrome ◦ Granulomatosis with polyangiitis
◦ Plasminogen deficiency ◦ Langerhans cell histiocytosis
• Diseases affecting connective tissues ◦ Giant cell granulomas
◦ Ehlers-Danlos syndrome (IV, VIII) ◦ Hyperparathyroidism
◦ Angioedema (C1-inhibitor deficiency) ◦ Systemic sclerosis (scleroderma)
◦ Systemic lupus erythematosus ◦ Vanishing bone disease (Gorham-Stout syndrome)
• Metabolic and endocrine disorders
◦ Glycogen storage disease
◦ Gaucher disease
◦ Hypophosphatasia
◦ Hypophosphatemic rickets
◦ Hajdu-Cheney syndrome
◦ Diabetes mellitus
◦ Obesity
◦ Osteoporosis
|

according to the Centers for Disease Control and Prevention (CDC), Clinical findings: LAD-1 individuals present with severe forms of
each year about 6000 babies are born with Down syndrome (DS) periodontal disease already during adolescence. Although tissues are
that is caused by a chromosome alteration resulting in three copies severely inflamed, LAD infections characteristically lack pus forma-
of all or part of chromosome 21. At birth, DS babies present with tion. LAD-I periodontitis is triggered by microbial biofilms and caused
certain physical traits such as low muscle tone, a single deep crease by deficient neutrophil surveillance and then by dysregulated IL-23/
across the palm of the hand, and an upward slant to the eyes, as IL-17 cytokine levels.109 Intriguingly, the LAD-I microbiome displays
well as pathological characteristics that often include congenital unique characteristics compared to healthy or periodontitis patients.
heart disease, gastrointestinal disease, mental retardation, and Clinical investigations: While the microbiome of periodontitis
other conditions like leukemia, epilepsy, and autoimmune diseases. patients exhibits an increased diversity and richness in subgingival
A karyotype confirms the diagnosis. Individuals are prone to a higher species in particular at inflamed sites, LAD-I periodontitis is charac-
susceptibility to infections which are caused by impaired phagocytotic terized by an increased bacterial load, but a decreased diversity of
function of polymorphonuclear leukocytes, agammaglobulinemia,99 species and a complete depletion of numerous bacterial species de-
alterations in T- and B-cell subpopulations,100 high levels of tumor tected in health, including Actinomyces or Streptococci.110,111 Patients
necrosis factor (TNF)-α and interferon (IFN)γ,101 to increased with moderate deficiency are diagnosed later in life. Although they
immunoactivity, and altered ratios of CD8+-, CD4 +-, and CD56+ may have fewer severe infections when compared to severe forms
natural killer (NK) cells.102 of LAD, they present with leukocytosis, delayed wound healing, and
Clinical findings: Down syndrome is characterized by mid-facial moderate periodontal disease. The diagnosis is based on clinical
growth deficiency and Class III malocclusion. A generalized orofacial evaluation, detailed patient history, and confirmed by a high white
muscles hypotonia results in poor oral muscle seal, poor suck, and cell count and finally molecular genetic testing.
poor tongue control.103 The lower lip is thick and everted, the mouth
angles are pulled downward, and the mouth stays mostly often due Papillon-Lefèvre syndrome. Papillon-Lefèvre syndrome (PLS) is
to the relatively large tongue. In children with DS, frequent orolabial an autosomal recessive inherited disorder that presents with dry
lesions occur, such as fissured tongue (78%), lip fissures (64%), angu- scaly patches at the palm of hands and feet as well as a severe
lar cheilitis (38%), and cheilitis (14%).104 Microdontia of permanent form of early-onset periodontitis affecting both primary and
teeth, altered crown morphology, taurodontism, hypodontia and permanent teeth.112 The underlying mechanism is the deficiency
supernumerary teeth, delayed and asymmetric eruption are com- of cathepsin C that results in a lack of serine protease activity and
mon characteristics.103 The mucosal lining of the oral cavity is gen- a dysregulated host response.113,114 The incidence lies around 1–4
erally thin due to the reduced salivary flow. DS individuals generally per million. The pathobiology of the disease was recently shown to
present with poor oral hygiene which together with a compromised be due to relentless recruitment of hyper-responsive neutrophils
immune response manifests as marginal gingival inflammation. DS to periodontal tissues following failed clearance of pathogens.114
individuals show increased prevalence and severity of periodontal PLS becomes evident by 2–3 years of age when deciduous teeth
diseases which often sets in by mid to late teen years.105–108 present with periodontal infections leading to premature shedding
Clinical investigations: Dental treatment should follow an inter- of the primary teeth. Some of the PLS individuals are susceptible to
disciplinary approach. A thorough clinical and radiographic examina- other infections than periodontitis.115
tion should be preceded by consultation of treating physicians and Clinical findings: Individuals with PLS present with two cardinal
cardiologists as often congenital heart malformations occur and a features, namely palmoplantar keratosis and rapid periodontal de-
high percentage develop mitral valve prolapse later on that might struction affecting both dentitions.
not have been discovered yet. A thorough medical history and a Clinical investigations: Patient history and clinical inspection includ-
medical check-up including blood testing of immune cells and glu- ing palms of hands and/or feet. Diagnostic tests involve genetic test
cose levels cannot be over-emphasized. for mutations of cathepsin C gene on chromosome 11q14. Further, a
test is available for testing cathepsin C deficiency in the urine.
Leukocyte adhesion deficiency. Leukocyte adhesion deficiency
(LAD) is a rare syndrome affecting 1 out of 100 000 births. It is Severe neutropenia. Congenital neutropenia (e.g., Kostmann
characterized by an autosomal recessive mutation on the CD18 syndrome) comprises a group of hematological diseases that result
subunit of β2 integrins or other adhesion molecules. Three types in impaired maturation of neutrophil granulocytes. Individuals
are known (LAD-I, II, and III), whereby LAD-I is the most common with congenital neutropenia commonly suffer from recurrent
one. Given the lack of adhering molecules, neutrophils cannot infections beginning by 2–3 months after birth. Later on, periodontal
adhere to endothelial cells and extravasate to sites of infection or inflammation and tissue destruction are common (Figure 13).116 The
inflammation. Infants with LAD present with a delayed detachment Kostmann syndrome occurs in 3–10 individuals out of 1 million.114
of the umbilical cord stump as one of the first signs, then develop Mutations in the ELANE genes encoding for neutrophil elastase
severe bacterial infections and inflammations in particular affecting seem to be crucially involved in the pathogenesis of periodontitis in
the skin, mucous membranes, lungs, and gingival tissues and usually patients with congenital neutropenia.117,118 Neutropenia can further
lose their primary dentition. be the result of cancer treatment.
|

Clinical findings: Individuals with severe forms of neutropenia present with recurrent blister formation on the skin, the oral mu-
struggle with recurrent infections. Periodontal inflammation and tis- cosa, and with severe loss of keratinized tissue and of periodontal
sue destruction are common in these individuals. tissues as clinical findings.119–121
Clinical investigations: Patient history and clinical diagnosis in Clinical investigations: Genetic testing confirms the diagnosis.
most cases depict a clear picture of the disease. The initial diagnosis
is based on blood examination and neutrophil count as well as ge- Metabolic or endocrine disorders
netic testing for mutations in ELANE. Diabetes mellitus (DM) refers to a group of disorders affecting the
insulin-glucose system resulting in chronic hyperglycemia. It is one
Diseases affecting the gingival tissue, mucosa, and connective of the most important global health threats of the 21th century with
tissue significantly growing numbers over the past 20 years. According
Mutations in genes relevant for the functioning of the basement to the World Health Organizataion (WHO) an estimated 422 mil-
membrane (e.g., Kindler syndrome) or in collagen chains like in dys- lion people globally suffer from DM122 mainly type II. An insulin-
trophic epidermolysis bullosa or Ehlers-Danlos syndrome usually dependent (type I) (Figure 14) and a non-insulin-dependent (type II)

F I G U R E 1 3 Periodontal disease and massive gingival hyperplasia in a patient diagnosed with acquired neutropenia, polyneuropathy,
Cushing-syndrome, glomerulonephritis, and hypertensive heart valve disease. The 58-year-old patient took immunosuppressants and
calcium antagonists. Periodontal therapy was performed after consultation with the hematologist.

F I G U R E 1 4 Clinical and radiographic

overviews of a 28-year-old patient with
type I diabetes mellitus and severe
periodontitis.
|

one can be distinguished. Increasing protein glycation and accumu- • Assessment of clinical and radiographic parameters prior to
lation of advanced glycation end (AGE) products activate numer- therapy and during long-term supportive care is of paramount
ous intracellular pathways via binding to transmembrane receptors importance.
(RAGE) leading to development of DM sequelae over time123 includ- • Clinical and radiographic diagnostic parameters should be as-
ing retinopathy, nephropathy, or atherosclerosis. sessed at the patient, tooth and site level.
It is well-established that DM type II and in particular when • Continuous monitoring of periodontal conditions following each
it is uncontrolled, is a considerable risk factor for periodonti- therapeutic step should guide dental professionals on the need
tis,124,125 and, vice versa, periodontitis can exacerbate the diabetic for additional treatment measures.
development.126,127 • Cost–benefit aspects and added values of new diagnostic tech-
Clinical findings: A thorough patient history and clinical history nologies should be carefully evaluated.
are important. While in type I DM, symptoms occur quickly within
days or weeks, in type II DM symptoms such as fatigue, numb- AC K N OW L E D G M E N T S
ness, pruritus, drowsiness, increased thirst, frequent urination, and Open access funding provided by Universitat Bern.
depression often slowly develop or might be veiled by other con-
ditions like aging or being overweight. Intraorally, no hyperglycemia- DATA AVA I L A B I L I T Y S TAT E M E N T
associated lesions or periodontitis patterns are reported. Individuals Data sharing is not applicable to this article as no new data were cre-
with DM have a higher prevalence and severity of periodontitis. ated or analyzed in this study.
Poor glycemic control was further associated with symptoms of xe-
rostomia, burning mouth, coated fissured tongue, oral candidiasis, REFERENCES
increased caries activity, and delayed wound healing.128 1. Chapple ILC, Mealey BL, Van Dyke TE, et al. Periodontal health
Clinical investigations: A thorough patient history and clinical and gingival diseases and conditions on an intact and a reduced
periodontium: consensus report of workgroup 1 of the 2017
examination are important. Patients with diabetes or diabetes-
World Workshop on the Classification of Periodontal and Peri-
like symptoms or, in general, being overweight should be sent to a Implant Diseases and Conditions. J Clin Periodontol. 2018;45 Suppl
physician for blood testing (i.e., assessment of fasting plasma glu- 20:S68-S77.
cose level). Glycosylated hemoglobin (HbA1c) should be monitored 2. Lang NP, Bartold PM. Periodontal health. J Clin Periodontol.
2018;45(Suppl 20):S9-s16.
every 3 months since the lifespan of erythrocytes is about 120 days.
3. Murakami S, Mealey BL, Mariotti A, Chapple ILC. Dental plaque-
The percentage of HbA1c mirrors the glucose level over the last induced gingival conditions. J Clin Periodontol. 2018;45(Suppl
3 months; it is around 5% in healthy individuals and should not ex- 20):S17-S27.
ceed 7.0%–7.5% despite DM.129 4. Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: con-
sensus report of workgroup 2 of the 2017 World Workshop on
the Classification of Periodontal and Peri-Implant Diseases and
Other systemic disorders influencing the pathogenesis of Conditions. J Clin Periodontol. 2018;45(Suppl 20):S162-S170.
periodontal diseases 5. Ebersole JL, Nagarajan R, Kirakodu S, Gonzalez OA. Transcriptomic
Medications. Some medications severely impair the host's immune phases of periodontitis lesions using the nonhuman primate model.
response such as certain cytotoxic chemotherapeutics, others again Sci Rep. 2021;11(1):9282.
6. Socransky SS, Haffajee AD, Goodson JM, Lindhe J. New con-
have an impact about gingival tissue resulting in gingiva hyperplasia
cepts of destructive periodontal disease. J Clin Periodontol.
or synonymously called gingival overgrowth (Figure 13). Drug-induced 1984;11(1):21-32.
gingival overgrowth is a frequent adverse reaction to a certain category 7. Abdulkareem AA, Imran NK, Abdulraheam RH, Gul SS.
of immunosuppressants (ciclosporin), anticonvulsants (Dilantin’s Prevalence and factors influencing reporting of true periodon-
tal chief complaints: a retrospective analysis. Clin Exp Dent Res.
e.g., phenytoin), and calcium channel blockers (e.g., nifedipine).130
2021;7(4):443-4 49.
Clinical findings: More or less prominent gingival enlargement is 8. Darby I. Risk factors for periodontitis & peri-implantitis. Periodontol
obvious affecting mostly the frontal region. In severe cases, gingival 2000. 2022;90(1):9-12.
hyperplasia might cover nearly completely the clinical crowns and 9. Roccuzzo A, Imber JC, Marruganti C, Salvi GE, Ramieri G, Roccuzzo
M. Clinical outcomes of dental implants in patients with and with-
severely impair oral hygiene (Figure 13).
out history of periodontitis: a 20-year prospective study. J Clin
Clinical investigations: A thorough patient history reveals the un- Periodontol. 2022;49(12):1346-1356.
derlying cause. 10. Chrcanovic BR, Albrektsson T, Wennerberg A. Smoking and
dental implants: a systematic review and meta-analysis. J Dent.
2015;43(5):487-498.
11. French D, Grandin HM, Ofec R. Retrospective cohort study of
6 | CO N C LU S I O N S 4,591 dental implants: analysis of risk indicators for bone loss
and prevalence of peri-implant mucositis and peri-implantitis. J
• Discrimination between periodontal health or disease should Periodontol. 2019;90(7):691-700.
12. Heitz-Mayfield LJ, Huynh-Ba G. History of treated periodonti-
form the basis for a pretherapeutic prognosis and a comprehen-
tis and smoking as risks for implant therapy. Int J Oral Maxillofac
sive treatment plan. Implants. 2009;24 Suppl:39-68.
|

13. Strietzel FP, Reichart PA, Kale A, Kulkarni M, Wegner B, Küchler 35. Miller SC. Textbook of Periodontics. The Blakestone Company;
I. Smoking interferes with the prognosis of dental implant treat- 1938:125.
ment: a systematic review and meta-analysis. J Clin Periodontol. 36. Miller SC. Textbook of Periodontia Oral Medicine. 3d ed. The
2007;34(6):523-544. Blakestone Company; 1950.
14. Herrera D, Retamal-Valdes B, Alonso B, Feres M. Acute periodon- 37. Grabec I, Groselj D. Detection and prediction of tooth mobility
tal lesions (periodontal abscesses and necrotizing periodontal dis- during the periodontitis healing process. Comput Methods Biomech
eases) and endo-periodontal lesions. J Clin Periodontol. 2018;45 Biomed Engin. 2003;6(5–6):319-328.
Suppl 20:S78-s94. 38. Sanz M, Herrera D, Kebschull M, et al. Treatment of stage I-III
15. Etter TH, Håkanson I, Lang NP, Trejo PM, Caffesse RG. Healing periodontitis–the EFP S3 level clinical practice guideline. J Clin
after standardized clinical probing of the perlimplant soft tissue Periodontol. 2020;47 Suppl 22:4-60.
seal: a histomorphometric study in dogs. Clin Oral Implants Res. 39. Dommisch H, Walter C, Difloe-G eisert JC, Gintaute A, Jepsen S,
2002;13(6):571-580. Zitzmann NU. Efficacy of tooth splinting and occlusal adjust-
16. Listgarten MA. Periodontal probing: what does it mean? J Clin ment in patients with periodontitis exhibiting masticatory dys-
Periodontol. 1980;7(3):165-176. function: a systematic review. J Clin Periodontol. 2022;49 Suppl
17. Armitage GC, Svanberg GK, Löe H. Microscopic evaluation of clin- 24:149-166.
ical measurements of connective tissue attachment levels. J Clin 40. Helal O, Göstemeyer G, Krois J, Fawzy El Sayed K, Graetz C,
Periodontol. 1977;4(3):173-190. Schwendicke F. Predictors for tooth loss in periodontitis pa-
18. Listgarten MA, Mao R, Robinson PJ. Periodontal probing and the tients: systematic review and meta-analysis. J Clin Periodontol.
relationship of the probe tip to periodontal tissues. J Periodontol. 2019;46(7):699-712.
1976;47(9):511-513. 41. Faggion CM Jr, Petersilka G, Lange DE, Gerss J, Flemmig TF.
19. Magnusson I, Listgarten MA. Histological evaluation of prob- Prognostic model for tooth survival in patients treated for peri-
ing depth following periodontal treatment. J Clin Periodontol. odontitis. J Clin Periodontol. 2007;34(3):226-231.
1980;7(1):26-31. 42. Graetz C, Schützhold S, Plaumann A, et al. Prognostic factors for
20. Polson AM, Caton JG, Yeaple RN, Zander HA. Histological deter- the loss of molars –an 18-years retrospective cohort study. J Clin
mination of probe tip penetration into gingival sulcus of humans Periodontol. 2015;42(10):943-950.
using an electronic pressure-sensitive probe. J Clin Periodontol. 43. Martinez-C anut P. Predictors of tooth loss due to periodontal dis-
1980;7(6):479-488. ease in patients following long-term periodontal maintenance. J
21. Robinson PJ, Vitek RM. The relationship between gingival inflam- Clin Periodontol. 2015;42(12):1115-1125.
mation and resistance to probe penetration. J Periodontal Res. 44. Muzzi L, Nieri M, Cattabriga M, Rotundo R, Cairo F, Pini Prato
1979;14(3):239-243. GP. The potential prognostic value of some periodontal factors
22. Saglie R, Johansen JR, Flotra L. The zone of completely and par- for tooth loss: a retrospective multilevel analysis on periodon-
tially destructed periodontal fibres in pathological pockets. J Clin tal patients treated and maintained over 10 years. J Periodontol.
Periodontol. 1975;2(4):198-202. 2006;77(12):2084-2089.
23. Spray JR, Garnick JJ, Doles LR, Klawitter JJ. Microscopic demon- 45. Bozhkova T, Musurlieva N, Slavchev D, Dimitrova M, Rimalovska S.
stration of the position of periodontal probes. J Periodontol. Occlusal indicators used in dental practice: a survey study. Biomed
1978;49(3):148-152. Res Int. 2021;2021:2177385.
24. van der Velden U. Probing force and the relationship of the probe 46. dePablo P, Chapple ILC, Buckley CD, Dietrich TD. Periodontitis in
tip to the periodontal tissues. J Clin Periodontol. 1979;6(2):106-114. systemic rheumatic diseases. Nat Rev Rheumatol. 2009;5:218-224.
25. Hassell TM, Germann MA, Saxer UP. Periodontal probing: interin- 47. González-Chávez SA, Pacheco-Tena C, de Jesús Caraveo-Frescas
vestigator discrepancies and correlations between probing force T, Quiñonez-Flores CM, Reyes-Cordero G, Campos-Torres RM.
and recorded depth. Helv Odontol Acta. 1973;17(1):38-42. Oral health and orofacial function in patients with rheumatoid ar-
26. Gabathuler H, Hassell T. A pressure-sensitive periodontal probe. thritis. Rheumatol Int. 2020;40(3):445-453.
Helv Odontol Acta. 1971;15(2):114-117. 48. Schiffman E, Ohrbach R, Truelove E, et al. Diagnostic Criteria
27. van der Velden U, de Vries JH. Introduction of a new periodontal for Temporomandibular Disorders (DC/TMD) for Clinical and
probe: the pressure probe. J Clin Periodontol. 1978;5(3):188-197. Research Applications: recommendations of the International
28. Lang NP, Joss A, Orsanic T, Gusberti FA, Siegrist BE. Bleeding on RDC/TMD Consortium Network* and Orofacial Pain Special
probing. A predictor for the progression of periodontal disease? J Interest Group†. J Oral Facial Pain Headache. 2014;28(1):6-27.
Clin Periodontol. 1986;13(6):590-596. 49. Lang NP, Hill RW. Radiographs in periodontics. J Clin Periodontol.
29. Lang NP, Nyman S, Senn C, Joss A. Bleeding on probing as it re- 1977;4(1):16-28.
lates to probing pressure and gingival health. J Clin Periodontol. 50. Updegrave WJ. The paralleling extension-cone technique in
1991;18(4):257-261. intraoral dental radiography. Oral Surg Oral Med Oral Pathol.
30. Karayiannis A, Lang NP, Joss A, Nyman S. Bleeding on probing 1951;4(10):1250-1261.
as it relates to probing pressure and gingival health in patients 51. Ortman LF, McHenry K, Hausmann E. Relationship between al-
with a reduced but healthy periodontium. A clinical study. J Clin veolar bone measured by 125I absorptiometry with analysis
Periodontol. 1992;19(7):471-475. of standardized radiographs: 2. Bjorn technique. J Periodontol.
31. Ainamo J, Bay I. Problems and proposals for recording gingivitis 1982;53:311-314. doi:10.1902/jop.1982.53.5.311
and plaque. Int Dent J. 1975;25(4):229-235. 52. Lang NP, Bartold PM. Periodontal health. J Periodontol. 2018;89
32. Loe H, Silness J. Periodontal disease in pregnancy I. Prevalence Suppl 1:S9-S16. doi:10.1002/JPER.16-0517
and severity. Acta Odontol Scand. 1963;21:533-551. 53. Albandar JM, Susin C, Hughes FJ. Manifestations of systemic
33. Loe H, Theilade E, Jensen SB. Experimental gingivitis in man. J diseases and conditions that affect the periodontal attachment
Periodontol. 1930;1965(36):177-187. apparatus: case definitions and diagnostic considerations. J Clin
34. Salvi GE, Aglietta M, Eick S, Sculean A, Lang NP, Ramseier CA. Periodontol. 2018;45 Suppl 20:S171-S189.
Reversibility of experimental peri-implant mucositis compared 54. Chapple ILC, Mealey BL, Van Dyke TE, et al. Periodontal health
with experimental gingivitis in humans. Clin Oral Implants Res. and gingival diseases and conditions on an intact and a reduced
2012;23(2):182-190. periodontium: consensus report of workgroup 1 of the 2017
|

World Workshop on the Classification of Periodontal and Peri- 77. Wolf R, Lipozencic J. Shape and configuration of skin lesions:
Implant Diseases and Conditions. J Periodontol. 2018;89 Suppl targetoid lesions. Clin Dermatol. 2011;29(5):504-508.
1:S74-S 84. 78. Ormond M, McParland H, Donaldson ANA, et al. An oral disease
55. Holmstrup P, Plemons J, Meyle J. Non-plaque-induced gingival dis- severity score validated for use in oral pemphigus vulgaris. Br J
eases. J Periodontol. 2018;89 Suppl 1:S28-s 45. Dermatol. 2018;179(4):872-881.
56. Holmstrup P, Jontell M. Non-plaque induced gingival diseases. In: 79. Tsunoda K, Ota T, Saito M, et al. Pathogenic relevance of IgG and
Berglund T, Giannobile WV, Sanz M, Lang NP, eds. Lindhe's Clnical IgM antibodies against desmoglein 3 in blister formation in pem-
Periodontology and Implant Dentistry. Vol 1. 7th ed. John Wiley& phigus vulgaris. Am J Pathol. 2011;179(2):795-8 06.
Sons; 2021:331-367. 80. Kridin K. Pemphigus group: overview, epidemiology, mortality,
57. Marshall RI, Bartold PM. Medication induced gingival overgrowth. and comorbidities. Immunol Res. 2018;66(2):255-270.
Oral Dis. 1998;4(2):130-151. 81. Kridin K, Zelber-Sagi S, Khamaisi M, Cohen AD, Bergman R.
58. Horning GM, Fisher JG, Barker BF, Killoy WJ, Lowe JW. Gingival Remarkable differences in the epidemiology of pemphigus among
fibromatosis with hypertrichosis. A case report. J Periodontol. two ethnic populations in the same geographic region. J Am Acad
1985;56(6):344-3 47. Dermatol. 2016;75(5):925-930.
59. Machado RA, de Andrade RS, Pêgo SPB, Krepischi ACV, Coletta 82. Moss C, Gupta E. The Nikolsky sign in staphylococcal scalded skin
RD, Martelli-Júnior H. New evidences of genetic heterogeneity syndrome. Arch Dis Child. 1998;79(3):290.
of causing hereditary gingival fibromatosis and ALK and CD36 as 83. Manocha A, Tirumalae R. Histopathology of pemphigus vulgaris
new candidate genes. J Periodontol. 2022;94:108-118. revisited. Am J Dermatopathol. 2021;43(6):429-437.
60. Hart TC, Zhang Y, Gorry MC, et al. A mutation in the SOS1 gene 84. Belloni-Fortina A, Faggion D, Pigozzi B, et al. Detection of auto-
causes hereditary gingival fibromatosis type 1. Am J Hum Genet. antibodies against recombinant desmoglein 1 and 3 molecules in
2002;70(4):943-954. patients with pemphigus vulgaris: correlation with disease extent
61. Wu J, Chen D, Huang H, et al. A novel gene ZNF862 causes hered- at the time of diagnosis and during follow-up. Clin Dev Immunol.
itary gingival fibromatosis. Elife. 2022;11:e66646. 2009;2009:187864.
62. Gawron K, Bereta G, Nowakowska Z, et al. Analysis of mutations 85. Bernard P, Vaillant L, Labeille B, et al. Incidence and distribution of
in the SOS-1 gene in two Polish families with hereditary gingival subepidermal autoimmune bullous skin diseases in three French
fibromatosis. Oral Dis. 2017;23(7):983-989. regions. Bullous Diseases French Study Group. Arch Dermatol.
63. Quarto N, Tajana GF, D'Alessio G. Synthesis of seminal ribonu- 1995;131(1):48-52.
clease in isolated lobules of bull seminal vesicles. J Reprod Fertil. 86. Marazza G, Pham HC, Scharer L, et al. Incidence of bullous pem-
1987;80(1):81-89. phigoid and pemphigus in Switzerland: a 2-year prospective study.
64. Pego SP, Coletta RD, Mendes DC, et al. Hereditary gingival fibro- Br J Dermatol. 2009;161(4):861-868.
matosis: clinical and ultrastructural features of a new family. Med 87. Baican A, Baican C, Chiriac G, et al. Pemphigus vulgaris is the most
Oral Patol Oral Cir Bucal. 2015;20(2):e150-e155. common autoimmune bullous disease in Northwestern Romania.
65. Smith MH, Vargo RJ, Bilodeau EA, et al. Oral manifestations of Int J Dermatol. 2010;49(7):768-774.
syphilis: a review of the clinical and histopathologic characteristics 88. Goldberg SH, Branson D. Blistering diseases. Postgrad Med.
of a reemerging entity with report of 19 new cases. Head Neck 1991;89(2):159-162.
Pathol. 2021;15(3):787-795. 89. Gonzalez-Moles MA, Warnakulasuriya S, Gonzalez-Ruiz I, et al.
66. Eng HL, Lu SY, Yang CH, Chen WJ. Oral tuberculosis. Oral Surg Oral Worldwide prevalence of oral lichen planus: a systematic review
Med Oral Pathol Oral Radiol Endod. 1996;81(4):415-420. and meta-analysis. Oral Dis. 2021;27(4):813-828.
67. Krawiecka E, Szponar E. Tuberculosis of the oral cavity: an 90. McCartan BE, Healy CM. The reported prevalence of oral lichen pla-
uncommon but still a live issue. Postepy Dermatol Alergol. nus: a review and critique. J Oral Pathol Med. 2008;37(8):447-453.
2015;32(4):302-3 06. 91. Gonzalez-Moles MA, Ruiz-Avila I, Gonzalez-Ruiz L, Ayen A, Gil-
68. Pekiner FN, Erseven G, Borahan MO, Gümrü B. Natural barrier Montoya JA, Ramos-Garcia P. Malignant transformation risk of
in primary tuberculosis inoculation: oral mucous membrane. Int J oral lichen planus: a systematic review and comprehensive meta-
Tuberc Lung Dis. 2006;10(12):1418. analysis. Oral Oncol. 2019;96:121-130.
69. Sierra C, Fortún J, Barros C, et al. Extra-laryngeal head and neck 92. Chiang CP, Yu-Fong Chang J, Wang YP, Wu YH, Lu SY, Sun A.
tuberculosis. Clin Microbiol Infect. 2000;6(12):644-6 48. Oral lichen planus – differential diagnoses, serum autoantibod-
70. Esposito S, Principi N. Hand, foot and mouth disease: current ies, hematinic deficiencies, and management. J Formos Med Assoc.
knowledge on clinical manifestations, epidemiology, aetiology and 2018;117(9):756-765.
prevention. Eur J Clin Microbiol Infect Dis. 2018;37(3):391-398. 93. Li S, Gong T, Peng Y, Nieman KM, Gilbertson DT. Prevalence
71. Aswathyraj S, Arunkumar G, Alidjinou EK, Hober D. Hand, foot and and incidence of systemic lupus erythematosus and associated
mouth disease (HFMD): emerging epidemiology and the need for a outcomes in the 2009-2016 US Medicare population. Lupus.
vaccine strategy. Med Microbiol Immunol. 2016;205(5):397-4 07. 2020;29(1):15-26.
72. Huang CW, Hsieh CH, Lin MR, Huang YC. Clinical features of gin- 94. Ungprasert P, Sagar V, Crowson CS, et al. Incidence of systemic
givostomatitis due to primary infection of herpes simplex virus in lupus erythematosus in a population-based cohort using revised
children. BMC Infect Dis. 2020;20(1):782. 1997 American College of Rheumatology and the 2012 Systemic
73. Soheili M, Keyvani H, Soheili M, Nasseri S. Human papilloma virus: Lupus International Collaborating Clinics classification criteria.
a review study of epidemiology, carcinogenesis, diagnostic meth- Lupus. 2017;26(3):240-247.
ods, and treatment of all HPV-related cancers. Med J Islam Repub 95. Izmirly P, Buyon J, Belmont HM, et al. Population-based preva-
Iran. 2021;35:65. lence and incidence estimates of primary discoid lupus erythema-
74. Garlick JA, Taichman LB. Human papillomavirus infection of the tosus from the Manhattan Lupus Surveillance Program. Lupus Sci
oral mucosa. Am J Dermatopathol. 1991;13(4):386-395. Med. 2019;6(1):e000344.
75. Tsui C, Kong EF, Jabra-Rizk MA. Pathogenesis of Candida albicans 96. Johnson NW, Jayasekara P, Amarasinghe AA. Squamous cell car-
biofilm. Pathog Dis. 2016;74(4):ftw018. cinoma and precursor lesions of the oral cavity: epidemiology and
76. Patil S, Rao RS, Majumdar B, Anil S. Clinical appearance of oral aetiology. Periodontol 2000. 2011;57(1):19-37.
candida infection and therapeutic strategies. Front Microbiol. 97. Jepsen S, Caton JG, Albandar JM, et al. Periodontal manifesta-
2015;6:1391. tions of systemic diseases and developmental and acquired
|

conditions: consensus report of workgroup 3 of the 2017 115. Haneke E, Hornstein OP, Lex C. Increased susceptibility to in-
World Workshop on the Classification of Periodontal and Peri- fections in the Papillon-Lefèvre syndrome. Dermatologica.
Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1975;150(5):283-286.
1):S237-S248. 116. Carlsson G, Wahlin YB, Johansson A, et al. Periodontal disease in
98. Albandar JM, Susin C, Hughes FJ. Manifestations of systemic dis- patients from the original Kostmann family with severe congenital
eases and conditions that affect the periodontal attachment appa- neutropenia. J Periodontol. 2006;77(4):744-751.
ratus: case definitions and diagnostic considerations. J Periodontol. 117. Acar B, Cagdas D, Tan C, et al. Evaluation of periodontal status and
2018;89 Suppl 1:S183-S203. cytokine/chemokine profile of GCF in patients with severe con-
99. Bruton OC. Agammaglobulinemia. Pediatrics. 1952;9(6):722-728. genital neutropenia. Odontology. 2021;109(2):474-482.
100. Levin S. The immune system and susceptibility to infections in 118. Nishi H, Ohta K, Kuramoto Y, et al. Periodontal inflamed surface
Down's syndrome. Prog Clin Biol Res. 1987;246:143-162. area in oral cavity associated with febrile neutropenia in patients
101. Tsilingaridis G, Yucel-Lindberg T, Modéer T. T-helper-related cy- with hematologic malignancy undergoing chemotherapy. Sci Rep.
tokines in gingival crevicular fluid from adolescents with Down 2022;12(1):2483.
syndrome. Clin Oral Investig. 2012;16(1):267-273. 119. Wiebe CB, Petricca G, Häkkinen L, Jiang G, Wu C, Larjava HS.
102. Tsilingaridis G, Yucel-Lindberg T, Concha Quezada H, Modéer Kindler syndrome and periodontal disease: review of the literature
T. The relationship between matrix metalloproteinases (MMP- and a 12-year follow-up case. J Periodontol. 2008;79(5):961-966.
3, -8, -9) in serum and peripheral lymphocytes (CD8+, CD56+) 120. Gurevich I, Agarwal P, Zhang P, et al. In vivo topical gene therapy
in Down syndrome children with gingivitis. J Periodontal Res. for recessive dystrophic epidermolysis bullosa: a phase 1 and 2
2014;49(6):742-750. trial. Nat Med. 2022;28(4):780-788.
103. Desai SS. Down syndrome: a review of the literature. Oral Surg 121. Vanden Oever M, Twaroski K, Osborn MJ, Wagner JE, Tolar J.
Oral Med Oral Pathol Oral Radiol Endod. 1997;84(3):279-285. Inside out: regenerative medicine for recessive dystrophic epider-
104. Al-Maweri SA, Tarakji B, Al-Sufyani GA, Al-Shamiri HM, Gazal G. molysis bullosa. Pediatr Res. 2018;83(1–2):318-324.
Lip and oral lesions in children with Down syndrome. A controlled 122. Collaboration NCDRF. Worldwide trends in diabetes since 1980:
study. J Clin Exp Dent. 2015;7(2):e284-e288. a pooled analysis of 751 population-based studies with 4.4 million
105. Shaw L, Saxby MS. Periodontal destruction in Down's syndrome participants. Lancet. 2016;387(10027):1513-1530.
and in juvenile periodontitis. How close a similarity? J Periodontol. 123. Mengstie MA, Chekol Abebe E, Behaile Teklemariam A,
1986;57(11):709-715. et al. Endogenous advanced glycation end products in the
106. Sakellari D, Arapostathis KN, Konstantinidis A. Periodontal con- pathogenesis of chronic diabetic complications. Front Mol Biosci.
ditions and subgingival microflora in Down syndrome patients. A 2022;9:1002710.
case-control study. J Clin Periodontol. 2005;32(6):684-690. 124. Nelson RG, Shlossman M, Budding LM, et al. Periodontal disease
107. López-Pérez R, Borges-Yáñez SA, Jiménez-García G, Maupomé G. and NIDDM in Pima Indians. Diabetes Care. 1990;13(8):836-8 40.
Oral hygiene, gingivitis, and periodontitis in persons with Down 125. Chiu CJ, Chang ML, Kantarci A, Van Dyke TE, Shi W. Exposure to
syndrome. Spec Care Dentist. 2002;22(6):214-220. Porphyromonas gingivalis and modifiable risk factors modulate risk
108. Søhoel DC, Johannessen AC, Kristoffersen T, Nilsen R. Expression for early diabetic retinopathy. Transl Vis Sci Technol. 2021;10(2):23.
of HLA class II antigens in marginal periodontitis of patients with 126. Xu R, Zeng G, Wang S, et al. Periodontitis promotes the diabetic
Down's syndrome. Eur J Oral Sci. 1995;103(4):207-213. development of obese rat via miR-147 induced classical macro-
109. Moutsopoulos NM, Konkel J, Sarmadi M, et al. Defective neutro- phage activation. Biomed Pharmacother. 2016;83:892-897.
phil recruitment in leukocyte adhesion deficiency type I disease 127. Wang F, Peng L, Gu F, et al. Circulating small extracellular vesicles
causes local IL-17-driven inflammatory bone loss. Sci Transl Med. from patients with periodontitis contribute to development of in-
2014;6(229):229ra240. sulin resistance. J Periodontol. 2022;93:1902-1915.
110. Hajishengallis G, Moutsopoulos NM. Role of bacteria in leuko- 128. Rohani B. Oral manifestations in patients with diabetes mellitus.
cyte adhesion deficiency-associated periodontitis. Microb Pathog. World J Diabetes. 2019;10(9):485-489.
2016;94:21-26. 129. Chee B, Park B, Bartold PM. Periodontitis and type II diabetes: a
111. Moutsopoulos NM, Chalmers NI, Barb JJ, et al. Subgingival mi- two-way relationship. Int J Evid Based Healthc. 2013;11(4):317-329.
crobial communities in Leukocyte Adhesion Deficiency and 130. Zhang R, Wu J, Zhu J, Wang X, Song J. Bibliometric analysis of
their relationship with local immunopathology. PLoS Pathog. research trends and characteristics of drug-induced gingival over-
2015;11(3):e1004698. growth. Front Public Health. 2022;10:979861.
112. Hart TC, Shapira L. Papillon-Lefèvre syndrome. Periodontol 2000.
1994;5:88-100.
113. Wani AA, Devkar N, Patole MS, Shouche YS. Description of two
new cathepsin C gene mutations in patients with Papillon-Lefèvre
How to cite this article: Salvi GE, Roccuzzo A, Imber J-C,
syndrome. J Periodontol. 2006;77(2):233-237.
114. Roberts H, White P, Dias I, McKaig S, Veeramachaneni R, Thakker Stähli A, Klinge B, Lang NP. Clinical periodontal diagnosis.
N, Grant M, Chapple I. Characterisation of neutrophil function in Periodontol 2000. 2023;00:1-19. doi:10.1111/prd.12487
Papillon-Lefevre Syndrome. J Leukoc Biol. 2016;100:433-4 44.

DR Ehsan Lectures Periodontology Osce
No ratings yet
DR Ehsan Lectures Periodontology Osce
38 pages
Conventional Diagnostic Criteria For Periodontal D
No ratings yet
Conventional Diagnostic Criteria For Periodontal D
10 pages
313 Classification of Periodontal and Peri-Implant Diseases and Conditions 2020 - Part II
100% (1)
313 Classification of Periodontal and Peri-Implant Diseases and Conditions 2020 - Part II
52 pages
Diagnosis and Treatment Planning
No ratings yet
Diagnosis and Treatment Planning
64 pages
Mock Answers PDF
100% (1)
Mock Answers PDF
19 pages
Strategies For Periodontal Disease Prevention and Treatment: Comprehensive Guide
No ratings yet
Strategies For Periodontal Disease Prevention and Treatment: Comprehensive Guide
78 pages
Presentation Perio 12
No ratings yet
Presentation Perio 12
47 pages
Jper 19-0557
No ratings yet
Jper 19-0557
21 pages
2017 Classification of Periodontitis and It's Application in Clinical Practice 2
No ratings yet
2017 Classification of Periodontitis and It's Application in Clinical Practice 2
33 pages
Background: Staging and Grading of Periodontitis: Framework and Proposal of A New Classi!cation and Case De!nition
No ratings yet
Background: Staging and Grading of Periodontitis: Framework and Proposal of A New Classi!cation and Case De!nition
37 pages
Diagnosis of Gingivitis and Periodontitis
No ratings yet
Diagnosis of Gingivitis and Periodontitis
84 pages
Periodontal Considerations Semester 10 Fixed 6 Date 24-3-2020
No ratings yet
Periodontal Considerations Semester 10 Fixed 6 Date 24-3-2020
54 pages
Diagnosis and Prognosis of Periodontal Diseases
No ratings yet
Diagnosis and Prognosis of Periodontal Diseases
87 pages
2017 Staging Grading Perio
No ratings yet
2017 Staging Grading Perio
48 pages
Classification of Periodontal Disease - PPTX - Last Saved by User
No ratings yet
Classification of Periodontal Disease - PPTX - Last Saved by User
46 pages
2017 Classification of Periodontal and Peri-Implant Diseases and Conditions. Decision Making Algorithms For Clinical Practice
100% (1)
2017 Classification of Periodontal and Peri-Implant Diseases and Conditions. Decision Making Algorithms For Clinical Practice
40 pages
Journal of Periodontology - 2018 - Papapanou - Periodontitis Consensus Report of Workgroup 2 of The 2017 World Workshop On
No ratings yet
Journal of Periodontology - 2018 - Papapanou - Periodontitis Consensus Report of Workgroup 2 of The 2017 World Workshop On
10 pages
Periodental
No ratings yet
Periodental
53 pages
Journal of Periodontology - 2018 - Tonetti - Staging and Grading of Periodontitis Framework and Proposal of A New
No ratings yet
Journal of Periodontology - 2018 - Tonetti - Staging and Grading of Periodontitis Framework and Proposal of A New
14 pages
Periodontitis- Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and Conditions - Papapanou - 2018 - Journal of Periodontology - Wiley Online Library
No ratings yet
Periodontitis- Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and Conditions - Papapanou - 2018 - Journal of Periodontology - Wiley Online Library
17 pages
Examination of Patients: Chapter 22
No ratings yet
Examination of Patients: Chapter 22
16 pages
'H' Periodontal Health and Disease Nehal
No ratings yet
'H' Periodontal Health and Disease Nehal
12 pages
Diagnosis 23 New
No ratings yet
Diagnosis 23 New
11 pages
Journal of Dental Education - 2022 - Gandhi - Diagnosis and Treatment Planning Using The 2017 Classification of Periodontal
No ratings yet
Journal of Dental Education - 2022 - Gandhi - Diagnosis and Treatment Planning Using The 2017 Classification of Periodontal
8 pages
Art Periodoncia 2
No ratings yet
Art Periodoncia 2
7 pages
Tonetti 2019
No ratings yet
Tonetti 2019
18 pages
Journal of Periodontology - 2018 - Papapanou - Periodontitis Consensus Report of Workgroup 2 of The 2017 World Workshop On
No ratings yet
Journal of Periodontology - 2018 - Papapanou - Periodontitis Consensus Report of Workgroup 2 of The 2017 World Workshop On
10 pages
Ravida - The Correlation Between History of Periodontitis According To Staging and
No ratings yet
Ravida - The Correlation Between History of Periodontitis According To Staging and
14 pages
Perio Logbook
100% (2)
Perio Logbook
19 pages
Periodontology 2000 - 2024 - Heitz Mayfield - Conventional Diagnostic Criteria For Periodontal Diseases Plaque Induced
No ratings yet
Periodontology 2000 - 2024 - Heitz Mayfield - Conventional Diagnostic Criteria For Periodontal Diseases Plaque Induced
10 pages
Reading Material
No ratings yet
Reading Material
8 pages
Artículo Perio Inglés
No ratings yet
Artículo Perio Inglés
9 pages
Point of Care-A Novel Approach To Periodontal Diagnosis-A Review
No ratings yet
Point of Care-A Novel Approach To Periodontal Diagnosis-A Review
6 pages
Tonetti Et Al-2018-Journal of Periodontology T
No ratings yet
Tonetti Et Al-2018-Journal of Periodontology T
14 pages
Sara Pavlović Marko Pongrac
No ratings yet
Sara Pavlović Marko Pongrac
34 pages
٨-٧ ﻲﺒﻫﺬﻟا ﻒﻠﻤﻟا Cerrected by yes we can 2021
No ratings yet
٨-٧ ﻲﺒﻫﺬﻟا ﻒﻠﻤﻟا Cerrected by yes we can 2021
60 pages
Calculus As A Risk Factor For Periodontal Disease Narrative
No ratings yet
Calculus As A Risk Factor For Periodontal Disease Narrative
8 pages
Periodontitis - Clinical
No ratings yet
Periodontitis - Clinical
20 pages
FinalOD April 2019 Clinical-New Disease
No ratings yet
FinalOD April 2019 Clinical-New Disease
6 pages
Annals 1384 028
No ratings yet
Annals 1384 028
22 pages
Dental Clinics of North America
No ratings yet
Dental Clinics of North America
204 pages
Basic Perio
No ratings yet
Basic Perio
18 pages
Ctiterios Diagnosticos para Gingivitis y Periodontitis Inducida Por Placa 2024
No ratings yet
Ctiterios Diagnosticos para Gingivitis y Periodontitis Inducida Por Placa 2024
10 pages
Biomedicines 10 02659 v2
No ratings yet
Biomedicines 10 02659 v2
18 pages
Carranza Chapter 27
No ratings yet
Carranza Chapter 27
14 pages
Adj 12440
No ratings yet
Adj 12440
9 pages
New Protocol 2017
No ratings yet
New Protocol 2017
13 pages
8
No ratings yet
8
7 pages
Overview of Periodontal Disease, Etiology, Pathogenesis, Diagnosis and Treatment Therapy
No ratings yet
Overview of Periodontal Disease, Etiology, Pathogenesis, Diagnosis and Treatment Therapy
9 pages
Critical Mass Theory in Periodontics
No ratings yet
Critical Mass Theory in Periodontics
12 pages
Clinical Application of The New Classification of PD
No ratings yet
Clinical Application of The New Classification of PD
10 pages
Trombelli Et Al-2017-Journal of Clinical Periodontology
No ratings yet
Trombelli Et Al-2017-Journal of Clinical Periodontology
7 pages
Artículo Perio
No ratings yet
Artículo Perio
5 pages
Journal of Periodontology - 2018 - Tonetti - Staging and Grading of Periodontitis Framework and Proposal of A New
No ratings yet
Journal of Periodontology - 2018 - Tonetti - Staging and Grading of Periodontitis Framework and Proposal of A New
14 pages
Classification of Periodontal Disease
No ratings yet
Classification of Periodontal Disease
6 pages
Neet Mds Dec 2021 Recall 1-80 Questions - Meriters Strikes
No ratings yet
Neet Mds Dec 2021 Recall 1-80 Questions - Meriters Strikes
298 pages
Risk Management in Clinical Practice. Part 10. Periodontology
No ratings yet
Risk Management in Clinical Practice. Part 10. Periodontology
9 pages
Strategies For Periodontal Risk Assessment and Prognosis
No ratings yet
Strategies For Periodontal Risk Assessment and Prognosis
12 pages
Impact of Different Periodontitis Case Definitions On Periodontal Research
No ratings yet
Impact of Different Periodontitis Case Definitions On Periodontal Research
8 pages
Wadia 2019 The Updated Periodontal Classification
No ratings yet
Wadia 2019 The Updated Periodontal Classification
4 pages
Diagnosis of Periodontal Diseases
No ratings yet
Diagnosis of Periodontal Diseases
11 pages
Preface
No ratings yet
Preface
2 pages
Radiology in Periodontics PDF
No ratings yet
Radiology in Periodontics PDF
7 pages
Clinical Judgement Protocol 2013 Final
100% (1)
Clinical Judgement Protocol 2013 Final
12 pages
The Impact of Coronal Flaring Files On Pericervica
No ratings yet
The Impact of Coronal Flaring Files On Pericervica
6 pages
Periodontology - 4th Edition Updated Edition Download
100% (15)
Periodontology - 4th Edition Updated Edition Download
16 pages
Oral Radiology Principles and Interpretation Part2
No ratings yet
Oral Radiology Principles and Interpretation Part2
376 pages
Furcation Involvement and Treatment
No ratings yet
Furcation Involvement and Treatment
38 pages
Endodontic Diagnosis & Treatment Planning
No ratings yet
Endodontic Diagnosis & Treatment Planning
48 pages
CAL, Furcation & Mobility
No ratings yet
CAL, Furcation & Mobility
45 pages
ACJ 2017 Protocol
No ratings yet
ACJ 2017 Protocol
17 pages
Examination Periodontal Disease
No ratings yet
Examination Periodontal Disease
20 pages
Case Study F Group B
No ratings yet
Case Study F Group B
28 pages
Principios Periodontales Usta
No ratings yet
Principios Periodontales Usta
29 pages
Newman and Carranza's Clinical Periodontology-Chapter 33 Radiographic Aids in The Diagnosis of Periodontal Disease
No ratings yet
Newman and Carranza's Clinical Periodontology-Chapter 33 Radiographic Aids in The Diagnosis of Periodontal Disease
20 pages
Perio Study Guide
No ratings yet
Perio Study Guide
8 pages
Periodontology 2000 - 2023 - Salvi
No ratings yet
Periodontology 2000 - 2023 - Salvi
19 pages
Perio 2
No ratings yet
Perio 2
12 pages
Chapter 62
No ratings yet
Chapter 62
5 pages
Furcation Involvement
No ratings yet
Furcation Involvement
21 pages
Jode 8 41
No ratings yet
Jode 8 41
6 pages
Vrushali Bhor Resume 2021
No ratings yet
Vrushali Bhor Resume 2021
2 pages
Mecânica para Verticalização de Molar
No ratings yet
Mecânica para Verticalização de Molar
8 pages
Furcation Involvement Classification - A Literature Review
No ratings yet
Furcation Involvement Classification - A Literature Review
6 pages
Furcation Involvement Classification - A Literature Review: Iva Yordanova, Irena Georgieva
No ratings yet
Furcation Involvement Classification - A Literature Review: Iva Yordanova, Irena Georgieva
5 pages
Hemisection of A Severely Decayed Mandibular Molar: A Case Report
No ratings yet
Hemisection of A Severely Decayed Mandibular Molar: A Case Report
4 pages

Periodontology 2000 - 2023 - Salvi

Uploaded by

Periodontology 2000 - 2023 - Salvi

Uploaded by

Received: 23 December 2022 | Revised: 16 February 2023 | Accepted: 14 March 2023

Clinical periodontal diagnosis

Giovanni E. Salvi1 | Andrea Roccuzzo1 | Jean-­Claude Imber1 | Alexandra Stähli1 |

1 | I NTRO D U C TI O N disease are lacking. Rather, periodontal diagnosis is based on clini-

Periodontology 2000. 2023;00:1–19. ﻿ wileyonlinelibrary.com/journal/prd | 1

2 | G E N E R A L A N D D E NTA L H I S TO RY • Protection of the patient against systemic effects of routine

The assessment of complaints and symptoms of disease represent a

3.5 | Assessment of BoP

BoP has been shown to represent a diagnostic clinical test to docu-

amount of alveolar bone destruction (Figure 2A,B).49 Furthermore, 4 | S I N G LE TO OTH D I AG N OS I S

F I G U R E 3 A–­C , Clinical and

F I G U R E 5 Clinical signs of gingivitis.

4.2 | Gingivitis - tooth level mild–­moderate periodontitis, horizontal as well as angular/vertical

F I G U R E 6 Clinical A and radiographic

F I G U R E 7 Clinical A and radiographic

F I G U R E 8 Clinical A and radiographic

TA B L E 1 Overview of gingival and periodontal conditions as

Gingival and periodontal conditions

Periodontal health, gingival Periodontal health & gingival

F I G U R E 9 Clinical evidence of necrotizing periodontitis in the Periodontitis

TA B L E 2 Classification of non-­plaque-­induced gingival diseases and conditions according to Ref. [56].

Genetic/ developmental disorders Reactive processes

5.1.2 | Inflammatory and immune Pemphigoid

5.1.3 | Autoimmune diseases Lichen planus

F I G U R E 1 0 Clinical frontal view of a young female patient with

F I G U R E 1 4 Clinical and radiographic

You might also like

Giovanni E. Salvi1 | Andrea Roccuzzo1 | Jean-Claude Imber1 | Alexandra Stähli1 |

Periodontology 2000. 2023;00:1–19. wileyonlinelibrary.com/journal/prd | 1

F I G U R E 3 A–C , Clinical and

4.2 | Gingivitis - tooth level mild–moderate periodontitis, horizontal as well as angular/vertical

TA B L E 2 Classification of non-plaque-induced gingival diseases and conditions according to Ref. [56].