Notes about the clinic

 Please do not leave the clinic before disinfecting it and informing the
dispensary that you did (Students who do not will receive a penalty of
minus 2 marks the first time, penalty of zero for the whole clinic in the
second).

 Please document your work on the electronic system. The marks on the
electronic system is going to be used for calculating your grades for the
continuous clinical assessment.

 Please get your work documented and marked on the student evaluation
form. This is your evidence of work in case records are missing from the
electronic system.
Periodontal and Gingival health
and Biofilm Induced Gingivitis
By: Dr. Ammar Aldawoodyeh
BDS, MFD RSCI, MSc (Clin) Periodontology, MPerio RCSEd, Jo Board Perio
Periodontal and Gingival health
definition
 In its pristine form, periodontal health would be defined as “the absence
of histological evidence of periodontal inflammation and no evidence of
anatomical change to the periodontium”.

 However, it must be recognized that in most (if not all) adults this is unlikely.

 Therefore, the term clinically healthy should be adopted to cover the

absence of (or very significant reduction in) clinical periodontal
inflammation on either an anatomically intact periodontium or a reduced
periodontium.

 Clinical gingival health is generally associated with an inflammatory

infiltrate and a host response consistent with homeostasis.
Biofilm induced gingivitis
Definition

 Biofilm‐induced gingivitis is defined at the site level as

“a reversible inflammatory lesion resulting from interactions between the

dental plaque biofilm and the host's immune‐inflammatory response, which
remains contained within the gingiva and does not extend to the periodontal
attachment (cementum, periodontal ligament and alveolar bone). Such
inflammation remains confined to the gingiva and does not extend beyond
the mucogingival junction and is reversible by reducing levels of dental
plaque at and apical to the gingival margin”.

 Gingivitis can be considered a relatively nonspecific inflammatory response

to nonspecific (indigenous) subgingival microbiota.
 The initiation of gingivitis
 The initiation of gingivitis occurs
if dental plaque accumulates
over days or weeks without
disruption or removal, due to a
loss of symbiosis between the
biofilm and the host’s
immune‐inflammatory
response, and development of
an incipient dysbiosis.

 Plaque‐induced gingivitis
begins at the gingival margin
and may spread throughout
the remaining gingival unit.
Characteristic of biofilm induced gingivitis
 The clinical characteristics common to
dental plaque–induced inflammatory
gingival conditions include:

1) Clinical signs and symptoms of

inflammation that are confined to the
gingiva and do not extend beyond the
mucogingival junction.

2) Reversibility of the inflammation by

removing or disrupting the biofilm.

3) The presence of a high bacterial plaque

burden to initiate and/or exacerbate the
severity of the lesion (although this varies
among individuals)
Characteristic of biofilm induced gingivitis

4) Systemic modifying factors may be

present. Examples include hormones,
haematological conditions, diet and
drugs which can alter the severity of
the plaque‐induced inflammation and
the immune response.

5) Stable (i.e., non‐changing)

attachment levels on a periodontium
which may or may not have
experienced a loss of attachment or
alveolar bone.
Biofilm induced gingivitis, a prerequisite
for periodontitis
 Gingivitis is a major risk factor, and a necessary pre‐requisite, for
periodontitis. The management of gingivitis is thus a primary prevention
strategy for periodontitis.
The signs of biofilm induced gingivitis
 The clinical signs of any inflammation in the body are erythema,
edema, pain (soreness), heat, and loss of function.

 These are known as the cardinal signs of inflammation

 The signs of biofilm induced gingivitis
 These may manifest clinically in
gingivitis as:

a. Swelling, seen as loss of knife‐edged

gingival margin and blunting of
papillae
b. Bleeding on gentle probing.
c. Redness.
d. Discomfort on gentle probing.

The intensity of the clinical signs and

symptoms will vary among individuals as
well as among sites within a dentition.
 The symptoms of biofilm induced
gingivitis
 The symptoms a patient may report include
a. Bleeding gums
b. Pain (soreness)
c. Halitosis and metallic/altered taste
d. Difficulty eating
e. Appearance (swollen red gums)
f. Reduced oral health–related quality of life

 Radiographs cannot be used to diagnose

gingivitis.
 Physiological bone levels range from 1.0 to
3.0 mm apical to the cemento‐enamel
junction.
Bleeding on Probing (BoP)
 Monitoring health or inflammation of
the gingival tissues is best
documented by the parameter of
BoP.

 clinical and histological data suggest

that bleeding is an earlier sign of
gingivitis than are the visual signs of
inflammation (redness and swelling).

 a gingivitis case can be simply,

objectively and accurately defined
and graded using a bleeding on
probing score (BOP%), which is also
known as Full mouth bleeding score
(FMBS).
Bleeding on Probing (BoP)%,
Advantages
 1) It is an obvious, objective clinical sign
that may be easily assessed and recorded

 2) At a site level, it has been correlated

with the severity of the inflammatory
condition of the gingival tissues. Severely
inflamed sites will bleed immediately,
more easily and more profusely with
probing than mildly inflamed sites.

 3) With suitable training, it is possible for

general dental practitioners to achieve
and maintain high levels of inter‐examiner
consistency in assessing bleeding.

 4) Bleeding on probing usually appears

earlier than colour changes or any other
visual signs of inflammation.
 Bleeding on Probing (BoP)%,
Advantages

 5) It has prognostic relevance for periodontal

deterioration at the site level (sites that do bleed
frequently are more likely to lose clinical
attachment in the future).

 6) Bleeding score can be effectively used to

inform and motivate the patient as well as
monitor the efficacy of preventive and
treatment strategies aimed to control
periodontal diseases.

 7) BOP recording is user‐friendly, economic, and

requires minimal/no technology

 8) Gingival bleeding represents a clinical sign

often perceived by the patient
Bleeding on Probing (BoP)%
Drawbacks and limitations
 Factors that can affect the accuracy of BoP%
include:

1) Lack of standardized periodontal probes (e.g.

probe dimensions, taper)

2) Examiner variability (probe pressure, angle).

3) Patient related factors such as gingival biotype.

4) Certain medications, such as aspirin, may

increase the recorded bleeding (False positive).

5) Smoking reduces the bleeding (False Negative).

 Probing force

 clinicians often use a probing force > 25 g. This results in

increase in BOP prevalence (False positive).

 The ideal probing force (20-25 grams) is a very light

force which equivalent to the force required to blanch
a fingernail if the probe was applied on the nail.

 Higher probing forces will also lead to overestimated

probing depth and clinical attachment loss readings.

 Pain during probing is frequently a sign of too much

force.
Biofilm induced gingivitis, epidemiology
 Epidemiologic data have shown plaque‐induced gingivitis to be prevalent
at all ages in dentate populations.

 This disease is considered the most common form of periodontal diseases

Biofilm induced gingivitis
Modifying and predisposing factors
Predisposing factors are
defined as any agent or
Vs
condition that contributes to
the accumulation of dental
plaque (e.g., tooth anatomy,
tooth position, restorations).
Modifying factors are defined
as any agent or condition that
alters the way in which an
individual responds to
subgingival plaque
accumulation (e.g., smoking,
systemic conditions,
medications).
Biofilm induced gingivitis
Controllable vs non-controllable risk factors
 Both predisposing and modifying factors could be controllable or non-
controllable :

• Controllable: Examples: removal of overhangs, smoking cessation, good

diabetes control.

• Non- Controllable: Examples: genetic predisposition, immune status, use of

critical medications

Vs
Biofilm induced gingivitis
Modifying and predisposing factors
The factors that can influence the severity and the extent of biofilm indued
gingivitis are seen in the table below. These are not considered a separate
diagnosis to biofilm induced gingivitis.
 Biofilm induced gingivitis
Sex Steroid Hormones, Puberty
 The dramatic rise in steroid hormone levels during puberty has a transient effect
on the inflammatory status of the gingiva.
 The incidence and severity of gingivitis in adolescents are influenced by a
variety of factors, including dental plaque biofilm levels, dental caries, mouth
breathing, crowding of the teeth, and tooth eruption.
 A number of studies have demonstrated an increase in gingival inflammation of
circumpubertal age and in both genders, even when plaque levels remain the
same.
 Biofilm induced gingivitis
Sex Steroid Hormones, Menstrual Cycle
 During the menstrual cycle, inflammatory
changes in the gingiva have been documented.

 Most clinical studies have shown there are only

modest inflammatory changes that may be
observable during ovulation.

 Although there may be a very small cohort of

women who are extremely sensitive to hormonal
changes in the gingiva during the menstrual
cycle, most women with menstrual cycle–
associated gingival inflammation will present with
clinically non‐detectable signs of the condition
Biofilm induced gingivitis
Sex Steroid Hormones, Pregnancy
 During pregnancy, the prevalence
and severity of gingivitis has been
reported to be elevated. The gingival
probing depths are also deeper.

 The features of pregnancy‐

associated gingivitis are similar to
plaque‐induced gingivitis, except the
propensity to develop frank signs of
gingival inflammation in the presence
of a relatively small amount of plaque
during pregnancy.
 Biofilm induced gingivitis
Sex Steroid Hormones, oral contraceptives
 Oral contraceptive agents were once associated
with gingival inflammation and gingival
enlargements.

 In the early studies, the features of gingivitis

associated with oral contraceptives in
premenopausal women were similar to
plaque‐induced gingivitis, except the propensity to
develop frank signs of gingival inflammation in the
presence of relatively small amounts of plaque.

 Current oral contraceptive concentrations are much

lower than the original doses, and so they do not
induce the clinical changes in gingiva that were
reported with the old, high‐dose contraceptives.
Biofilm induced gingivitis
Hyperglycaemia

 Gingivitis is a consistent feature found in children

with poorly controlled type 1 diabetes mellitus, and
the level of glycaemic control may be more
important in determining the severity of gingival
inflammation than the quality of plaque control.

 Similarly, hyperglycermia in type II diabetes is also

associated with exaggerated inflammatory
response to plaque.
 Biofilm induced gingivitis
Hyperglycaemia

 Excess glucose is toxic and directly

induces mitochondrial stress and an
enhanced respiratory burst in
inflammatory cells that may activate
various proinflammatory mediator
cascades.

 Excess glucose causes the formation

of molecules known as advanced
glycation end‐products (AGEs)
which when bind to its receptor
(known as RAGE) activates
proinflammatory signalling
cascades and downstream
proinflammatory events.
Biofilm induced gingivitis
Leukaemia
 Oral manifestations have been
described primarily in acute leukaemia
and consist of cervical
lymphadenopathy, petechiae, and
mucosal ulcers as well as gingival
inflammation and enlargement.

 Gingival enlargement has also been

reported, initially beginning at the
interdental papilla followed by the
marginal and attached gingiva, and is
caused by infiltration of gingivae by
leukemic cells.

 Although local irritants can predispose to

exacerbate the gingival response in
leukaemia, they are not prerequisites for
lesions to form in the oral cavity.
Biofilm induced gingivitis
Leukaemia
 Signs of inflammation in the gingiva include swollen, glazed, and spongy tissues
which are red to purple or occasionally pale gingiva due to leukemic cell
infiltration. In addition, gingival bleeding that is inconsistent with levels of dental
plaque, due to thrombocytopenia and/or clotting‐factor deficiencies
Biofilm induced gingivitis
Smoking
 Smoking is one of the major environmental risk factor for periodontal disease.
 Both the local and systemic effects of cigarette smoke should be considered.
 Inhaled cigarette smoke is absorbed from the capillary vessels via the pulmonary
alveolar epithelium and enters the systemic circulation.
 Biofilm induced gingivitis
Smoking
 In addition, direct exposure of inhaled cigarette smoke to periodontal tissues causes
vasoconstriction of the periodontal microvasculature and gingival fibrosis, which is
often observed in smokers.

 Although plaque accumulation and disease progression are exacerbated in smokers,

smokers have fewer clinical signs and symptoms of gingival inflammation, and
therefore smoking can mask an underlying gingivitis.
Biofilm induced gingivitis
Nutritional deficiency
 The one nutritional deficiency that has well‐documented
effects on the periodontium Is the depletion of plasma
ascorbic acid (i.e., vitamin C deficiency).

 Scurvy is the most severe form of Vit. C deficiency. Not all

patients with Vit. C deficiency develop Scurvy.
 Scurvy
 Severe Vitamin C deficiency, or scurvy, results
in compromised antioxidant micronutrient
defences to oxidative stress and also
negatively impacts collagen synthesis
(defects in collagen cross‐linkage), resulting
in weakened capillary blood vessel walls and
a consequent propensity to enhanced
gingival bleeding.

 Gingival enlargement with scurvy is marginal.

The gingiva is bluish red, soft, and friable, and
it has a smooth, shiny surface. Haemorrhage
that occurs spontaneously or on slight
provocation and surface necrosis with
pseudomembrane formations are common
features.
 Biofilm induced gingivitis
Vitamin C deficiency

 Scurvy is rare nowadays.

 In the absence of frank scurvy,

the effect of declining ascorbic
acid levels on the gingiva can be
difficult to detect. When it is
detected, it usually has
characteristics that are similar to
regular plaque induced gingivitis.
Biofilm induced gingivitis
Prominent subgingival restorations margins
 Restoration margins placed apical to the gingival margin are detrimental to
gingival health. Prominent subgingival restoration margins promote gingivitis by
increasing the local accumulation of bacterial plaque.

 Thus, subgingival restoration margins need to be carefully designed in order to

minimize plaque retention.
 Biofilm induced gingivitis
Hyposalivation
 It is known that some health
conditions/diseases such as Sjögren's
syndrome, anxiety, and poorly
controlled diabetes may cause
xerostomia due to hyposalivation.

 It is also frequently observed as a side

effect of medications such as
antihistamines, decongestants,
antidepressants, antihypertensive and
anti-parasympathetic medications.

 Hyposalivation may cause progressive

dental caries, taste disorders, halitosis,
and inflammation of the oral mucosa,
tongue, and gingiva.
Biofilm induced gingivitis
Hyposalivation and mouth dryness
 Dryness in the mouth may make
plaque control difficult, and gingival
inflammation may be worsened, most
likely because of the lack of cleansing
and antimicrobial effects of saliva.

 Mouth breathing in people who may

have enhanced gingival display
and/or an incompetent lip seal also
causes the mouth to be dried of saliva,
thus causing similar effects to
hyposalivation.
Diagnosing Biofilm induced gingivitis
How to Diagnose biofilm induced gingivitis and periodontitis

 The first step in diagnosis is to determine if the case is periodontitis case or not:
The case is a periodontitis case if: Interdental CAL is detectable at ≥2 non‐adjacent teeth,
or Buccal or lingual CAL ≥3 mm with pocketing >3 mm is detectable at ≥2 teeth.

 When there is no clinical attachment loss, the case will be either be a case of biofilm
induced gingivitis or a case of gingival health. To determine this, the full mouth bleeding
score (FMBS) is used:
1. If the FMBS is less than 10%, then the case would be diagnosed as a case of gingival
health.
2. If the FMBS is 10-30%, then the case would be diagnosed a localized biofilm induced
gingivitis.
3. If the FMBS is more than 30%, then the case would be diagnosed as generalized
biofilm induced gingivitis.
How to calculate BoP% or FMBS
 BoP% is assessed as the proportion of
bleeding sites (dichotomous yes/no Example:
evaluation) when stimulated by probing to
the apical end of the sulcus at six sites on all After recording the bleeding
teeth present.
on probing, you found 75
sites that bleed on probing.
 The Full Mouth Bleeding Score (FMBS) is then The patient has 26 teeth,
calculated using the following formula: calculate the FMBS.
FMBS = Number of sites that bleed / Total number of
sites X 100% Answer:

 Because bleeding on probing is recorded for 6 sites FMBS = 75 / (26 * 6) * 100%

for each tooth: = 75 / 156 * 100%
Total number of sites = number of teeth present X 6 = 48%
Additional descriptors for biofilm
induced gingivitis
 Several descriptors can be used to describe gingivitis:

1) Course and duration:

A) Acute gingivitis. B) Chronic gingivitis. C) Recurrent gingivitis.

2) Extent: A) Localized. B) Generalized. (Explained in the previous slides)

3) Distribution: A) Papillary. B) Marginal. C) Diffuse.

4) Severity: mild, moderate or severe.

The new periodontal classification (2017) only recognizes the extent of gingivitis. And
this is what you will apply in the undergraduate clinics. However, it is still important to
know and understand the other descriptors listed here.
Gingivitis
Course and duration description
 Acute Gingivitis: can develop with sudden onset and have a short
duration, and it can be painful. In such case, it is possible that cause of
the gingivitis is not biofilm related, and it is important to investigate the
underlying cause.

 Chronic gingivitis develops slowly and has a long duration. It is

painless, unless it is complicated by acute or subacute exacerbations, and
it is the type that is most often encountered, and in the vast majority of
the cases, it is biofilm induced gingivitis.

 Recurrent gingivitis: reappears after having been eliminated by

treatment or after disappearing spontaneously.
 Gingivitis Distribution

Papillary gingivitis is confined to Marginal gingivitis is confined to one

one or more interdental spaces. or more areas of the marginal
gingiva. The interdental papillae are
also usually affected

Diffuse gingivitis extends from the gingival margin to the mucobuccal fold.
 Gingivitis Distribution

Generalized diffuse gingivitis involves the entire gingiva. Because the alveolar
mucosa and attached gingiva are affected, the mucogingival junction is sometimes
obliterated . Systemic conditions can be involved in the case of generalized diffuse
gingivitis and should be evaluated if they are suspected as an etiologic cofactor.
 Gingivitis severity
 The most commonly used index to determine the disease severity is known as
the gingival index, which was invented by two periodontists, Leo and Silness.
This index is shown in the table below.
Gingivitis severity, calculation

 To evaluate the severity of gingivitis at the

patient‐level, a the gingival index (GI) score has
to be calculated for six teeth. These teeth are
the maxillary right first molar and lateral incisor;
maxillary left first premolar; mandibular left first
molar and lateral incisor mandibular right first
premolar , these are known as Ramfjord ‫راﻣﻔﻮرد‬
teeth, shown in the figure to the side.

 Each of these teeth is divided into four surfaces;

buccal, lingual, mesial and distal, just like what
we do with the plaque score. The score of each
of these surfaces is then evaluated by probing
and visual inspection, and the score is recorded.
Ramfjord teeth
Gingivitis severity, calculation
 The GI score is then calculated for the patient using the following formula:
 GI = The sum of GI scores in all sites / Number of sites.
 The score is then interpreted as seen in this table:
 Gingivitis severity calculation, example
 After examining the patient, you recorded the following gingival index scores for the
patient:
UR6: 1 buccal, 1 mesial, 2 distal, 2 palatal. LL6: 3 buccal, 2 mesial, 2 distal, 2 lingual.
UR2: 1 buccal, 1 mesial, 1 distal, 2 palatal. LL2: 1 buccal, 2 mesial, 2 distal, 2 lingual.
UL4: 2 buccal, 0 mesial, 0 distal, 2 palatal. LR4: 0 buccal, 2 mesial, 1 distal, 1 lingual.

Calculate the GI index and determine the severity of gingivitis in this patient.

Answer:
GI = The sum of GI scores in all sites / Number of sites.
= 35 / (6 * 4)
= 1.5
1.5 is between 1.1 and 2.0, so the patient has moderate gingivitis.
Gingivitis severity
Drawbacks of the gingival index to define
gingivitis cases?
 1)The GI was originally proposed to describe gingivitis in
pregnant women rather than the general population. For
example, a score of 3 represents a tendency for spontaneous
bleeding, which is a rare occurrence in the general gingivitis
population in contrast to women with pregnancy gingivitis

 2) Since it is based on both visual inspection and mechanical

stimulation of the gingival margin, the assessment of GI will
result in a time‐consuming procedure when incorporated in a
comprehensive, whole‐mouth examination (i.e., 4–6 sites per
each tooth present) to obtain data representative of the
inflammatory burden of the entire dentition.

 3) Intra‐ and inter‐examiner reliability and reproducibility of the

GI, particularly the component associated with visual
inspection, while reported as very good in some studies,
appears problematic even after calibration and training
sessions in other reports.
 The plaque index

 Another index that was invented by

Silness and Leo is the plaque index,
which shown in the figure to the side.

 It is usually calculated on Ramjord

teeth in the exact same way the
gingival index is calculated.

 This index is used to rate the patient

plaque control as good, fair or poor,
as seen in the table to the side.
Biofilm induced gingivitis in patients with
reduced periodontium and previously
treated periodontitis patients
 Not all gingivitis patient will have
intact periodontium, some patient
will have a reduced periodontium
(periodontium that suffered clinical
attachment loss or bone loss).

 Such patient may have lost part of

periodontium because of gingival
recession not related to periodontitis,
or because of surgical procedures
such as crown lengthening or lesions
excision: if gingivitis develops in such
patients, it is diagnosed as gingivitis
on a reduced periodontium.
Biofilm induced gingivitis in patients with
reduced periodontium and previously treated
periodontitis patients
 Other patients may have history
of periodontitis that was
successfully treated, however,
the gingiva became inflamed
again due to plaque
accumulation. In this case, the
diagnosis becomes: gingivitis in a
patient with history of
periodontitis.

 The table in the following slide

shows the diagnostic criteria for
gingivitis in each of these cases
The stages of Pathogenesis of biofilm
induced gingivitis and periodontitis
The stages of Pathogenesis of biofilm
induced gingivitis and periodontitis
 The stages of Pathogenesis of biofilm
induced gingivitis and periodontitis

Please do not confuse these stages with the stages that describe the
severity of periodontitis clinically, which are a totally different thing.
Please do not confuse these stages with the stages that describe the
severity of periodontitis clinically, which are a totally different thing.
The stages of Pathogenesis of biofilm
induced gingivitis and periodontitis

Pristine gingiva versus clinically healthy

gingiva:

Pristine gingivae, free from any histological

inflammation are extremely difficult to achieve without
extreme measures of fastidious plaque control.

‘Clinically healthy gingiva’ is a term used to describe

the level of gingival health attained by patients
practising a meticulous standard of oral hygiene.
Nevertheless, an initial inflammatory lesion can form at
a histological level following plaque biofilm formation
even in such motivated patients
The stages of Pathogenesis of biofilm induced gingivitis
and periodontitis

 Initial lesion (Stage 1)

 Inflammation begins
within 24 hours of plaque
accumulation,

 The cellular response

develops in 2–4 days.

 Gingiva appear
clinically healthy.
The stages of Pathogenesis of biofilm induced gingivitis and periodontitis

Early lesion (stage 2)

After about 4-7 days of plaque accumulation, the early
lesion develops:

 Mild redness of the gingiva and clinical signs of

inflammation.
 An increase in lymphocytes and neutrophils occurs.
Lymphocytes predominate.
 Early signs of cell and collagen damage.
 Rete pegs proliferation in junctional epithelium in
attempt to maintain the epithelial barrier function.

The early lesion can persist without shifting to established

gingivitis.
The stages of Pathogenesis of biofilm induced gingivitis and periodontitis

Established lesion (stage III)

It is difficult to predict when this stage of the lesion will

develop, but usually it does between 2-3 weeks. it involves
the following:

 Plasma cells & B lymphocytes predominate

 The junctional epithelium is no longer attached
closely to the tooth and has transformed into a pocket
epithelium (gingival ‘false’ pocket). This allows the
subgingival plaque to extend more apically.
 Clinical features of gingivitis become obvious.

Established lesion may remain stable or may become active

and progress to periodontitis.
The stages of Pathogenesis of biofilm induced gingivitis and periodontitis

Advanced lesion (Stage 4)

 Plasma cells dominate and constitute >50% of
the cell types.

 Loss of periodontal connective tissue

attachment.

 Apical migration of the junctional epithelium

and the formation of a true periodontal
pocket.

 Alveolar bone loss.