Gingiva (Macroscopic features)

GINGIVA - (MACROSCOPIC FEATURES)
- N.PREM KUMAR 1st year PG (PERIODONTICS)

CONTENTS :
 Introduction.
 Definition.
 Development of gingival tissues.
 Clinical features of gingiva.
 Pristine gingiva.
 Parts of gingiva.
 Colour.
 Contour.
 Surface texture.
 Size and shape.
 Position.
 Bleeding on probing.
 Age changes in gingiva.
 Implications.
 Conclusion.

INTRODUCTION :
 The Periodontium (peri = around , odontos = tooth) comprises of,
 Gingiva
 Periodontal ligament
 Cementum
 Alveolar bone

 Function - To attach the teeth to the bone tissue of the jaws.
 Oral mucosa consists of following 3 zones :
 Masticatory mucosa (Gingiva and covering of hard palate)
 Specialized mucosa (Dorsum of tongue)
 Mucous membrane (Lining the remainder of the oral cavity)

DEFINITION :
 “The gingiva is the part of the oral mucosa that covers
the alveolar processes of the jaws and surrounds the
neck of the teeth”.
 “The gingiva is that part of the masticatory mucosa
which covers the alveolar processes and surrounds the
cervical portion of the teeth”.

DEVELOPMENT OF THE PERIODONTIUM
NEURAL CREST DEVELOPMENT:
 By about 8 days of embryonic development, two distinct types of
cells are produced, Ectoderm and Endoderm which forms a
Bilaminar disc.
 By the 3rd week Mesoderm forms between these two layers.
 The ectoderm thickens and forms a raised margin to form Neural
fold and ultimately to Neural tube by the next few weeks.
 From the neural crest, the neural crest cells develop.

 By the 28th and 40th days of gestation Stomatodeum (primitive
oral cavity) is formed.
 The epithelium of the stomatodeum contains the Superficial layer
of flattened cells and Basal layer of columnar cells.
 The Neural crest cells migrate into 1st branchial arch, where they
form a band of ectomesenchyme beneath the epithelium of the
stomatodeum.
 Now the epithelium releases certain factors which initiate epithelial
ectomesenchyme interactions.
 Now the ectomesenchyme takes the dominant role in the further
development.

 During 6th week of embryogenesis tooth development begins
with the thickening of oral epithelium lining Stomatodeum to
form Dental lamina.
 Once Dental lamina is formed, a series of process are
initiated.(Bud stage, Cap stage and Bell stage with root
development).
 During cap stage, condensation of ectomesenchyme cells in
relation to epithelium forms,
 Dental papilla - (which gives raise to dentin and pulp)
 Dental follicle - (periodontal supporting tissues)

DEVELOPMENT OF GINGIVAL TISSUES :
 The Gingival tissues are composed of a,
1. Superficial epithelium - (Ectodermal origin)
2. Connective tissue - (Mesodermal origin)

 The epithelium of gingival tissues consists of ;
1) Non-keratinised junctional epithelium - (From enamel organ)
2) Non – keratinised sulcular epithelium - (From oral mucosa)
3) Keratinised gingival epithelium - (From oral mucosa)

 The gingival connective tissue is largely a fibrous connective
tissue.
 Both epithelial and connective tissue attach to tooth via separate
mechanisms.
 Epithelial tissues – interface with tooth by attachment called
Junctional Epithelium which is located at (or) coronal to CEJ.
 Connective tissues attach to the root surface at or below the CEJ
via fibres insertion into the cementum of the root surface.

 The epithelial covering of the completely formed enamel has few
layers of cells.
 These cells are called Reduced enamel epithelium.
 They originate from ameloblasts and cells of stratum intermedium
of the enamel organ).
 It also includes remnants of stellate reticulum and outer enamel
epithelium.

• These cells will eventually give rise to Junctional epithelium.
• As the erupting tooth approaches the overlying epithelium, the cells
of the REE proliferate and causing the epithelial covering of the
enamel to thicken.
• Proliferation of the cells begins at the cusp tips of the tooth and
slowly progresses to the cervix of the tooth.

CLINICAL FEATURES OF THE GINGIVA :
 The healthy gingiva is coral pink (SALMON) and fully covers the
root surface and supporting alveolar bone.
 It is characterised by an outer layer of stratified squamous
epithelium and underlying connective tissue layer called lamina
propria.(LINDHE et al)
 The gingiva obtains its final shape and texture in conjunction with
eruption of the teeth.
 In the coronal direction it terminates in free gingival margin and
covers the tooth to a level just coronal to the cementoenamel
junction.

 On the palatal aspect, the mucogingival line is absent as the
gingiva here is continuous with the keratinised , non-mobile
palatal mucosa.
 It may be pigmented, which is based on the ethnic origin of the
people.

Pristine gingiva:
 A state of super health where normal gingiva is free from
accumulation of inflammatory cells.
 Without any bacteria (0% bacteria) . It is seen only in infants.
 Goal of treatment is to achieve pristine gingiva but impossible.

Experimental gingivitis :
Loe et al in 1965 demonstrated in students with clinically healthy
gingiva :
 Clinical symptoms of gingivitis is developed in 2- 3 weeks if dental
plaque was allowed to accumulate freely.
 But after adequate tooth cleaning, the gingival inflammation
subsided within a week.
 The thickness of gingival plaque gradually increased within 3 weeks
of time period.
 For first few days:
 Gram positive cocci
 Rods, representing the indegenous microflora of tooth surface.

After 4-5 days :
 Filamentous organisms.
 Gram negative cocci as well as rods.
 Non attaching spirochaetes were also developed in the sulcus.
 While the collection of micoorganisms in the biofilm increased
continously.

PARTS OF THE GINGIVA: (SCHLUGER..ET AL,1990)
 The gingival tissues are anatomically subdivided into,
1. Marginal gingiva or Free gingiva.
2. Interdental gingiva.
3. Attached gingiva

MARGINAL GINGIVA :
 The marginal or unattached gingiva is the terminal edge or the border
of the gingiva
 The free gingiva is coral pink, has a dull surface and firm
consistency. (Lang)
 In about 50% of the cases, it is demarcated from the adjacent gingiva
by a shallow linear depression called free gingival groove.

• The most apical point of the marginal gingiva scallop is called
the gingival zenith. Its apicocoronal and Mesiodistal dimensions
vary between (0.06 and 0.96mm).

 The marginal gingiva is usually 1- 1.5mm wide and the inner wall
forms the soft tissue wall of the gingival sulcus.
 It means when a probe is placed at the gingival margin in a healthy
mouth, it can be inserted upto 3mm into the sulcus formed between
the tooth and the mucosa, since soft tissue is movable.(kenhub)
 After complete tooth eruption, the free gingival margin is located on
the enamel surface approximately (1.5-2mm) coronal to CEJ.
(Lang)

GINGIVAL SULCUS :
 The gingival sulcus is the shallow crevice or space around the
tooth bounded by the surface of the tooth on one side and the
epithelium lining the free margin of the gingiva on the other side.
 It is V-shaped and barely permits the periodontal probe. Under
normal conditions, the depth of the gingival sulcus is 0mm.
 In clinically healthy gingiva, a sulcus of some depth(Histological
depth) can be found, it is around 1.8mm with variations from 0 to
6mm.(Also called Biologic depth) (Orban B et al, 1924)

 Probing depth is the clinical evaluation used to determine the
depth of the sulcus involves the introduction of metallic
instrument called (periodontal probe)
 The so called probing depth of clinically normal gingiva sulcus in
humans is 2-3mm.
 The probing depth usually depends upon 3 factors,
 Probe diameter.
 Probing force.
 Level of inflammation.
 It is not necessary that probing depth and biologic depth must be
equal.

 The sulcus has a depth of 3mm where food particles and bacteria can
enter. This results in bacterial overgrowth and periodontitis.(ICOI)
 When gingiva is healthy, the pH of gingival sulcus is (6.9)
 The ecosystem of gingival sulcus is more anaerobic and the site is
filled with Gingival crevicular fluid(GCF).
 GCF will be increased by 47% when gingivitis is present and to 30%
when periodontitis is present.
 This is because GCF provides for cellular defense and humoral
factors to combat against the microbial insult.(Marsh P)

 Deepening of the gingival sulcus leads to periodontal pocket
formation.
 Sulcus is the primary plaque forming domain and is the portal entry
for periodontic pathogenic bacteria (i.e) porphyromonas gingivalis,
aggregatibacter actinomycetumcomitans. (KvArun)
 Incase of periodontal pocket it is (7.4 – 7.8) (Van DykeTE,
Dommisch H..et al,2018)

PATHOLOGY:
 Sulcus depth is chronically in excess of 3mm :
The accumulated microbes will penetrate and ultimately destroy
the delicate soft tissue and periodontal attachment
fibers.(Chapple, Mealy BL..et al,2018)

 Also result in recession, destruction of periodontium, tooth
mobility and tooth loss.(Lang NP, Bartold PM..et al 2018)
 The depth of gingival sulcus is directly proportional to the severity of
periodontitis.

ATTACHED GINGIVA :
 Orban(1948) was the first to describe attached gingiva.
 The attached gingiva is continuous with the marginal gingiva.
• The dense connective tissue fibers of the attached gingiva ensure its
firm attachment to the bone and “toughness”.

The attached gingiva is thus firmly entrenched between two movable
structures,
1. The marginal gingiva – Coronally.
2. Alveolar mucosa – Apically.
It is demarcated from the alveolar mucosa by mucogingival junction

BOUNDARIES:
 Facial aspect - Extend to relatively loose and movable alveolar
mucosa.
 Lingual aspect – terminates at the junction of lingual alveolar
mucosa, which is continuous with mucous membrane lining the floor
of the mouth. (LOE H..et al,1996)
 Palatal aspect – blends imperceptibily with firm and resilient palatal
mucosa.

WIDTH OFATTACHED GINGIVA :
 It refers to the apico-coronal dimension.
 (i.e) the distance between the mucogingival junction and the projection
on the external surface of the bottom of the gingival sulcus.
 Average thickness of attached gingiva is 1.25mm.
 The width varies in different area of the mouth :
 Greater in the incisor region :
 3.5mm to 4.5mm in maxilla anterior.
 3.3mm to 3.9mm in mandibular anterior.
 Narrower in the posterior region :
 1.9mm in maxillary posterior.
 1.8mm in mandibular posterior.

 The width is often least in the premolar region due to the presence
of accessory frenae in those areas.
 With the progression from primary to permanent dentition the width
of attached gingiva is decreased.

 The width increases around 4 years of age and in Supraerupted
teeth due to passive eruption.(Ainamo J)
 The mucogingival line remains stationary throughout life that
separates not only the attached gingiva from the alveolar mucosa,
but also the alveolar process from the basal bone.(Talari A)

BIOLOGIC WIDTH : GARGIULO ET AL,1961
 The dimension of epithelial attachment , which is attached to the
portion of the tooth coronal to the crest of the alveolar bone.
 In 1977, Ingber et al. described "Biologic Width" and credited
D.Walter Cohen for first coining the term.
 A sulcus depth (0.69 mm) an epithelial attachment (0.97 mm)
and a Connective tissue attachment of (1.07 mm).
 So, Biologic width is commonly stated to be 2.04 mm, which
represents the sum of the epithelial and connective tissue
measurements.
 Essential for preservation of periodontal health and removal of
irritation that might damage the periodontium (prosthetic
restorations).

THE SIGNS OF BIOLOGIC WIDTH VIOLATION ARE:
 Chronic progressive gingival inflammation around the restoration.
 Bleeding on probing.
 Localized gingival hyperplasia with minimal bone loss.
 Gingival recession.
 Pocket formation.
 Clinical attachment loss and alveolar bone loss.
 Gingival hyperplasia is most frequently found in altered passive
eruption and subgingivally placed restoration margins.

MEASUREMENT OF WIDTH OF ATTACHED GINGIVA :
Methods to determine mucogingival junction :
 Visual method.
 Functional method.
 Visual methods after histochemical staining.
 Assessed as a borderline between movable and immovable tissue.
 Tissue mobility is assessed by running a horizontally positioned
probe from the vestibule towards the gingival margin using light
force.

Assessed visually after staining the mucogingival junction
with ( Schiller’s potassium iodide solution ):
 (KI) solution do not stain the keratinized epithelium;(i.e)
marginal gingiva, attached gingiva and interdental papilla.
 But stains the Alveolar mucosa because, it differs from
keratinized gingiva histochemically
1. Glycogen content
2. Acid phosphatase and nonspecific esterase content
3. Increased amount of elastic fiber content within the corium
resulting in an iodo-positive reaction.

 The attached gingiva, which is keratinized, has no glycogen in the
most superficial layer and gives an iodo-negative reaction.
 Thus the solution stains only the Alveolar mucosa and clearly
demarcates the mucogingival junction.
 The total width of gingiva is measured that is from gingival margin
to mucogingival line.
[ Stained total gingival width - pocket depth
gives = Width of attached gingiva ]

INADEQUATE WIDTH: (ERICSSON I , LINDHE J..ET AL)
 Inadequate width of gingiva may facilitate subgingival
plaque formation because of improper pocket closure
resulting from the movability of the marginal tissue.
PULL OF GINGIVAL MARGIN :
 Insufficient attached gingiva (causing recession and bone
loss)
 Abnormal frenal attachment.
 Deep pockets that reach the level of mucogingival junction.
 Vigorous brushing in people with naturally thin tissue.

 (Miyasato et al) concluded that there is no relationship between
inflammation and amount of attached gingiva whether or not plaque
is present.
 (De tray and Berimoulin) adequacy of attached gingiva cannot be
determined by measurement of its width alone.

INTERDENTAL GINGIVA :
 The interdental gingiva occupies the gingival embrasure which is
the interproximal space beneath the area of the tooth contact.
 It can be “pyramidal” or it can have a “col” shape.
 It presents a valley like depression that connects the facial and
lingual papilla.
 The shape of gingiva in a given interdental space depends upon the
presence or absence of contact point between adjacent teeth.

 The lateral borders and tips of interdental papillae are formed by the
marginal gingiva of the adjoining teeth.
 The interwining portion consists of attached gingiva.
 Incase of diastema, the gingiva is tightly bound to the underlying
interdental bone to form a smooth, rounded surface without
interdental papillae.

 Anterior – Pyramidal form.
 Molar – Flatter in buccolingual direction.
 Premolar – Since these teeth have approximal contact surfaces
rather than contact points so, col shape is established in these
regions.(Lang Lindhe)

INTERDENTAL RECESSION : (KIA REZAVANDI,..ET AL2016)
 In the esthetic zone, the loss of interdental papilla height can
be unsighty.
 The two most frequenty qouted factors influencing the
papilla height are the
1) Types of Gingival biotype.
2) Position of contact point.

GINGIVAL BIOTYPE : (OCHSENBEIN C, ROSS S, SEIBERT JL, LINDHE J,ET AL )
Oshsenbein and Ross in their pioneer study indicated that there
were two main types.
1) Scalloped and thin
2) Flat and thick.

 So the gingival biotype means, the thickness of the gingiva in the
facio-palatal dimension.
 Later the term “periodontal biotype” was introduced by Seibert
and Lindhe.
 But the “periodontal biotype” not only includes thickness of
gingiva but also contour, alveolar bone thickness, amount of
keratinised gingiva present and crown shape.
 Gingival biotype may differ from tooth to tooth in a person and
may also differ with age, gender and dental arch location.

 Based on consensus published on 06 November 2019 by (David
M. Kim , Seyed Hossein Bassir ,Thomas T. Nguyen)
 The 2017 World Workshop on the Classification of Periodontal and
Peri‐Implant Disease and Conditions has recommended adoption
of the term “periodontal phenotype” by the periodontal
community.

THIN AND SCALLOPED TYPE :
 Have delicate and thin periodontium.
 Highly scalloped gingival tissue.
 Small incisal contact areas.
 Triangular crowns.
 Thin and translucent appearance.
 Tissue is friable with minimal zone of attached gingiva.
 Soft tissue is highly accentuated.
 Thin or minimal bone over the labial roots.
 Surgical exposure cause highly incidence of fenestration and
dehiscence.
 Prevalance of thin biotype is 43 percent.

THICK AND FLAT TYPE :
 Thick and heavy periodontium.
 Wide zones of keratinized gingiva.
 Flat gingival contour, thick flat osseous gingival contour.
 Broad apical contact areas in teeth and square anatomic crown.
 Tissue is dense with wide zone of attached gingiva.
 The underlying bony architecture is thick.
 Surgical exposure demonstrate thick underlying osseous forms.
 Prevalence – 56 percent.

CLASSIFICATION
Authors Classification
1) Ochsenbein and Ross(1969) Scalloped and thin Flat and thick
2) Seibert and Lindhe(1989) (Thick) ≥ 2mm (Thin) < 1.5mm
3) Becker et al(1997) Flat: 2.1mm
Scalloped : 2.8 mm
Pronounced scalloped
: 4.1 mm
4) Kan et al(2010) Thick > 1mm Thin ≤ 1mm
5) Claffey and Shanley(1986) Thick ≥ 2mm Thin < 1.5mm
6) Egreja et al(2012) Thick >1mm Thin < 1mm

 Both type respond differently to clinical and surgical insults.
 In the event of inflammation or any insults , soft tissue in thick
biotype respond more of fibrotic changes and pocket formation.
 In thin, more inflammatory and recession of gingiva.
 Patients with thin type are more vulnerable to connective tissue
loss and epithelial damage.
 Thus they need special treatment and oral hygiene instructions.

METHODS OF MEASUREMENT :
1) Direct measurement :
 Accurate measurement however inavasive technique using topical
anaesthetic gel , endodontic reamer and caliper.
 It is measured from center of gingival margin and mucogingival
junction in perpendicular direction.

2) Visual examination - Very low accuracy and variation.
Clinically evaluated based upon the general appearances of gingiva :
 1) Thick – dense and fibrotic.
 2) Thin – delicate, friable almost translucent

OTHER METHODS INCLUDE:
Probe transparency Ultrasonic device CBCT.
TRAN

SIGNS OF HEALTHY INTERDENTAL PAPILLA :
1. Healthy pigmentation
2. Firm attachment.
3. Triangular shape.
4. Pain and blood free.
 A distance of upto 5mm between the contact point and the
interdental bone crest is considered as full interdental papilla
height.(Tarnow et al)

 In more recent study, the critical measurement for a
complete papilla is 6mm from the tooth bone crest and
8.5mm from the implant bone crest to contact point.
(Palmer et al)
 When distance is :
1. 5mm – 98 % papilla was present.
2. 6mm – 56 %. papilla was present.
3. 7mm – 27 %. papilla was present.

LOSS OF INTERDENTAL PAPILLA : (RES J, 2013)
 Plaque associated lesions.
 Traumatic oral hygiene procedures.
 Abnormal tooth shape.
 Improper contours of restoration.
 Spacing
 Loss of teeth.

Classification of loss: (Norland and Tarnow,et al 1998)
Class 1 : Tip lies between the interdental contact point and the coronal
extent of CEJ.
Class 2 : Tip lies at or the apical to CEJ, but coronal to the apical
extent of facial CEJ.
Class 3 : the tip lies at the level with or apical to the facial CEJ.

RECONSTRUCTION OF LOST PAPILLA :
Non surgical techniques
Treatment :
 Traumatic procedures must be initially discontinued and
successively modified.
 Re-epithelialization of the traumatic lesion can restore
papilla.

Restorative :
 Abnormal tooth shape cause missing papilla.
 So appropriate restorative technique is indicated.
 By restoration, the contact point may be lengthened and
located more apically; embrasure is reduced.
Orthodontic :
 The aim is to reduce the diastema and create contact point.
 Coronal movement of tooth through orthodontic appliance cause
alterations, changes in bone level, soft tissue contour, creating
new papillae.(Ingber)

Surgical techniques :
1. Papilla – recontouring.
2. Papilla – preservation.
3. Papilla – reconstruction.
 Han and Takei ‘Semilunar Coronally Advanced Flap’.
 Azzi et al Envelope flap technique.
 Takei et al. in 1985 introduced conventional papilla preservation
technique.
 Cortellini et al. (1995) introduced a new modification of conventional
papilla preservation flap.
 Bianchi and Basseti in 2009 introduced a technique known as Whale’s
tail technique.

CORRELATION OF CLINICAL AND MICROSCOPIC FEATURES.
Colour :
 Normal gingiva is coral pink in color.
 There are four factors that determine the colour of the gingiva,
they are,
1. Vascular supply.
2. Thickness of the epithelium.
3. Degree of keratinization.
4. Physiologic pigmentation.

 Vascularity determines the basic colour of the gingiva which
undergoes modification depending on,
1. Degree of keratinization.
2. Presence of pigments.
 Physiologic pigmentation (Melanin) :
 Melanin is a non hemoglobin – derived brown pigment with
following characters ;
1. Responsible for the pigmentation of the skin, the gingiva and
remaining oral mucous membrane.
2. Absent or severely diminished in albinos.
3. Pigmentation is higher in oral cavity of black individuals.
4. Ascorbic acid down regulates the pigmentation in gingival tissues.

 The distribution of pigmentation in black individuals is,
1. Gingiva- 60 %.
2. Hard palate- 61%
3. Mucous membrane – 22%
4. Tongue – 15%

Appearance :
 Occurs as a diffuse, deep purplish discoloration or as irregularly
shaped brown and light brown patches.
 It may appear in the gingiva as early as 3hours after birth.
Oral repigmentation :
 Clinical reappearance of melanin pigment after a period of clinical
de-pigmentation of the oral mucosa.
 Result of chemical, thermal, surgical, pharmacologic or idiopathic
factors.

Colour in diseased conditions :
1. Chronic inflammation – appears reddish pink/ bluish in colour.
2. Acute inflammation – appears bright red in colour.
o These changes are due to increased blood flow, increased
permeability of capillaries and increased collection of defense cells
and tissue fluid.

DISEASE COLOUR CHANGES
Chronic gingivitis Reddish pink / bluish
Acute gingivitis Bright red
ANUG/ HIV Shiny slate gray
Herpetic gingivostomatitis Dull whitish gray
Smoking / trauma White
Mild inflammation Pale red

Smoking / trauma
Herpetic
gingivostomatitis
ANUG/ HIV

ORAL PIGMENTATION INDEX – DUMMET ET AL
(1964)
SCORE CLINCIAL ASPECT
0 Pink gingiva (No clinical
pigmentation)
1 Mild light brown colour (Mild
clinical pigmentation)
2 Medium brown or mixed pink
and brown colour (Moderate
clinical pigmentation)
3 Deep brown or bluish black
colour (Heavy clinical
pigmentation)

CONDITIONS :
Diseases that increase melanin pigmentation include the following :
1) Addison disease : (Adrenal dysfuntion)
- produces isolated patches of discoloration that vary from bluish
black to brown colour.
2) Peutz – jeghers syndrome :
- produces intestinal polyposis and melanin pigmentation in oral
mucosa and lips.
3) Albright syndrome or Polyostotic fibrous dysplasia
4)Neurofibromatosis or Von reck – linghausen disease
They both produce oral pigmentation.

Addison disease
Albright syndrome
Peutz – jeghers syndrome
Neurofibromatosis

Kaposi’s sarcoma Cushing syndrome
Malignant melanoma Blue nevus

 Endocrinopathic pigmentation:
1) Addison disease.
2) Cushings syndrome.
 Vascular lesion :
1) Kaposi’s sarcoma :
-Oral mucosa is red , blue, and purple .
-Hard palate is most favourable sight.
 Brown melanotic lesions:
1) Nevo cellular lesion.
2) Blue nevus.
3) Malignant melanoma.

CONTOUR :
 Normal gingiva has an arcuate contour with a scalloped outline
and a knife edge margin.
 The contour or shape of the gingiva varies considerably and
depends on the ,
 shape of the teeth.
 Their alignment in the arch.
 The location and the dimensions of the facial and lingual
embrasures.

1. It follows a scalloped outline on the facial and lingual surfaces.
2. It forms a straight line along teeth with relatively flat surfaces.
In canine and labial teeth :
 They have pronounced mesiodistal convexity.
 In these teeth, the normal arcuate contour is located farther apically.

In lingual teeth :
 The gingiva is horizontal and thickened.
 In addition, the gingiva biotype varies significantly.

 In health :
1. Marginal gingiva – Scalloped and knife edged.
2. Interdental papilla – (Anterior) : Pyramidal shape.
(Posterior) : Col shaped

In Diseased conditions :
:Chronic gingivitis :
- Marginal gingiva becomes Rounded and Bulbous.
- Interdental papilla becomes Flat and Blunt.
ANUG :
Punched out crater like depression at the end crest of interdental
papilla extending to marginal gingiva
Stillman’s cleft :
Exaggerated scalloping apostrophe shaped intendations
extending from and into the gingival margin for varying distance
on the facial surface.
McCall’s festoon ;
Life saver like enlargement of marginal gingiva.
Chronic Desquamative gingivitis :
Irregular denuded appearance.

ANUG
Chronic Desquamative gingivitis
Chronic gingivitis

SURFACE TEXTURE
 The gingiva presents a textured surface similar to that of an orange
peel appearance and is referred to as Stippled.
 It varies among different individual and different areas of
mouth.(LOE H..et al,1996).
 Stippling is viewed by drying the gingiva. This occurs as a result of
the epithelial retepegs in growth in connective tissue.

 The papillary layers of connective tissue extends into the epithelium
and this feature is known as stippled appearance.
1. Marginal gingiva is not stippled.
2. Attached gingiva is stippled.
3. Central portion of Interdental papillae is stippled, but margins
are smooth.

Differences :
i. Stippling is less prominent on lingual surfaces.
ii. Stippling varies with age. It is absent during infancy, appears
in some children at about 5 years of age.
iii. Increases in adulthood and disappears in old age.
Microscopic feature :
 Microscopically, stippling is produced by alternated rounded
protuberances and depressions in the gingival surface.
 The elevated and depressed layers are covered by stratified
squamous epithelium.

Functions :
 It is a form of adaptive specialization or reinforcement for
function to withstand mechanical stresses.
 On a study , gingival stippling was found to be a normal
characteristic in 56 percent of 3 to 10 year old children, without
significant difference in arch , gender or age.( J Clin Pediatr
Dent, 2003)

Loss of stippling :
 It is common sign of gingival disease.
 It is reversible in nature.
 It has been observed in a study where , thick gingiva has coarse and
diffuse stippling, whereas thin gingiva has fine and scanty stippling.

STUDY
 AUTHORS : Thushara Mohanan, Vanadana KL,..et al 2020
 The study was about evaluation of gingiva, where 180 sites were
examined in 15 patients aged 17-25 years.
 Result :
Out of 50,
 (27.7 percent) sites had coarse dense stippling
 13.3 percent sites had thin gingiva(1mm)
 14.44 had thick gingiva (1mm)

SIZE
 Size of the gingiva corresponds with the sum total of the bulk of
cellular and intercellular elements and their vascular supply.
 The size of gingiva is increased in some conditions that are called
Gingival enlargement.
Size :
 0-2mm for Marginal gingiva.
 0-9mm for Attached gingiva.
Disease :
 Inflammatory – increased in cells and decrease in fibers.
 Non inflammatory – decrease in cells and increase in fibers.

Normal Gingiva
Inflammed Gingiva

SHAPE
 Shape of gingiva depends upon,
1. Contour of proximal tooth surface.
2. Location and shape of gingival embrasures.
Hence in ,
 Anterior region – Pyramidal shape.
 Posterior region – More flat in buccolingual direction.

Anterior Tooth Posterior Tooth
Proximal surface of
crowns are flat
faciolingually.
Proximal surface flare
away from area of contact
Interdental bone is thin
mesiodistally.
Mesiodistal diameter of
the interdental gingiva is
broad.
Interdental gingiva is
narrow mesiodistally.
The height of the
interdental gingiva varies
with the location of the
proximal contact.

CONSISTENCY :
 The gingiva is firm and resilient and with the exception of the
movable free margin, tightly bound to the underlying bone.
 The collagenous property of lamina propria and its contiguity with
the mucoperiosteum of the alveolar bone determine the firmness of
the attached gingiva.
 The gingival fibers contribute to the firmness of the gingival
margin and also cellular and fluid content of the tissue.

In Diseased condition:
 Gingiva is soft and spongy increased fluid (edema) red, smooth,
shiny bleeds easily.
 Flabby due to connective tissue loss.
Chronic gingivitis : (Inflitration by fluids and cells)- Soggy puffiness.
Acute gingivitis : Vesicle formation.
Fibrotic condition : - Firm leathery.
 Diffuse puffiness.
 Sloughing.
Exudative :Marked softness and friability.

POSITION :
 The position of the gingiva is the level at which the gingival
margin is attached to the tooth.
 The position of the gingiva is usually 1.5- 2mm above the
cementoenamel junction.
Factors responsible for position :
 Position of tooth in the arch.
 Root bone angle.
 Mesiodistal curvature of tooth surface.
Formation of position :
 When the tooth erupts into the oral cavity the margin and the sulcus
are at the tip of the crown.

 As the eruption progresses, they are seen closer to the root. During this
eruption process, the juntional epithelium, undergo extensive
alterations and remodeling.
 Thus maintaining the shallow physiologic depth of the sulcus.
 Without this remodeling, an abnormal anatomic relationship between
the gingiva and tooth would result.
 In disease :
Gingival recession :
 Due to tooth brush trauma caused by abnormal or faulty methods.
Pseudopockets :
 Due to gingival inflammation, high frenum attachment, tooth
malposition and friction from soft tissue.

Tooth brush trauma
Gingival inflammation
High frenal
attachment

BLEEDING ON PROBING :
 During probing for examination of sulcular depth, bleeding occurs,
this is due to intact sulcular epithelium and normal capillaries.
 Whereas in chronic gingivitis, bleeding on probing is present due to
dilation and engorgement of capillaries and thinning.
 Similarly in ANUG and systemic diseases, chronic recurrent
bleeding in seen and spontaneous or slight bleeding is seen.
 Ulceration of sulcular epithelium may also cause bleeding on
probing.

AGE CHANGES IN GINGIVA
 The gradual changes taking place in the dental tissues after the teeth
are fully formed is known as age changes.
 Comfort (1956) defined aging as a biological process that causes
increased susceptibility to disease.
 Gottlieb & Orban – Believed that with age, gingival recession and
alveolar bone resorption occur and termed it as Senile Atrophy.

 People aged 65-74 are young elderly.
 People aged 75-84 are old or mid old.
 People above 85 years are oldest-old.
Gingival epithelium changes :
 Thinning and decrease in keratinization of the gingival epithelium
have been reported with age.
 This results increase in epithelial permeability to bacterial antigens,
a decreased resistance to functional trauma or both.
 If so, such changes may influence long term periodontal outcomes.
 Flattening of rete pegs and altered cell density.

Junctional epithelium :
 Migration of junctional epithelium from to more apical position on
the root surface with accompanying gingival recession.
 The width of attached gingiva increases with age.
 The migration of junctional epithelium to the root surface could be
caused by (passive eruption) as a result of tooth surface loss from
attrition.

TOOTH PERIODONTIUM RELATIONSHIP:
 The reduction in bone height that occurs with aging.
 Bone loss results in an increase in crown to root ratio.
 Wear of teeth also occurs on the proximal surfaces accompanied by
mesial migration of teeth.
 Proximal wear reduces the Anteroposterior length of dental arch by
0.5cm in age of 40.

 Progressive alteration - Maxillary-Mandibular overjet in the molar
area.
 Proximal wear – Edge to edge bite Anteriorly.
 Increased role for Porphyromonas gingivalis and decreased role for
Aggregatibacter actinomycetemcomitans.

EFFECTS OF AGING ON THE PROGRESSION OF
PERIODONDAL DISEASES
 In a classic experimental gingivitis study, subjects were rendered
plaque and inflammation free through frequent professional
cleaning.
 Later the subjects are stopped from oral hygiene measures for periods
of 3 weeks to allow gingivitis to develop.
 A comparison of gingivitis between young and older individuals
demonstrated a greater inflammatory response in older age.
 Findings included a greater size of infiltrated connective tissue,
increased gingival crevicular fluid flow and increased gingival
index.

IMPLICATIONS
DEFENSIVE FUNCTIONS OF ATTACHED GINGIVA
 It prevents deflection of marginal gingiva thus aids in
plaque maintenance.
 By preventing this deflection, it also helps avoid food
entrapment between tooth and gingival sulcus.
 The dense collagenous structure of the attached gingiva
also aids in slowing down the inflammatory spread from
the marginal gingiva.

Attached gingiva aids in :
 Increase resistance to external injury and
contribute in stabilization of gingival margin.
 Acts against frictional forces.
 Dissipating physiological forces.

CLINICAL SIGNIFICANCE OF ATTACHED GINGIVA AROUND
IMPLANTS : (METTEST RM, LANGER B..ET AL)
I. Prevent spread of inflammation.
II. Prevent recession of marginal tissue.
III. Provides tight collar around implants.
IV. Enable patients to maintain good oral hygiene.

ROLE OF CONTOUR IN GINGIVAL HEALTH (SYDNEY S .WAGMAN)
 Total clinical crown contour is related to gingival health.
 The subgingival convexity of a tooth or a restoration should
extend facially or lingually no more than one half of the
thickness of the gingiva.
 This protects the gingival crevice and promotes a knifelike free
margin, important plaque control.

REFERENCES :
 Newman and Carranza’s clinical periodontology(13th edition).
 Clinical periodontology and implant dentistry by Jan Lindhe, Niklaus
P.Lang(6th edition).
 Molecular biology of periodontium (KV Arun).
 Biology of periodontal connective tissues (P.Mark Bartold.PhD and
A.Sampath Narayanan. PhD)
 Shirmohammadi A, Faramarzie M, Lafzi A. A clinical evaluation of anatomic
features of gingiva in dental students in Tabriz, Iran. Journal of dental
research, dental clinics, dental prospects. 2008;2(3):90.
 Singh S, Vandana KL. Assessment of width of attached gingiva in primary,
mixed, and permanent dentition: Part-2. SRM Journal of Research in Dental
Sciences. 2017 Oct 1;8(4):157.

 Shah R, Sowmya NK, Thomas R, Mehta DS. Periodontal biotype: Basics and
clinical considerations. Journal of Interdisciplinary Dentistry. 2016 Jan
1;6(1):44.
 Vandana KL, Shivani S, Savitha B, Vivek HP. Assessment of gingival sulcus
depth, width of attached gingiva, and gingival thickness in primary, mixed, and
permanent dentition. Journal of Dental Research and Review. 2017 Apr
1;4(2):42.
 Shah R, Sowmya NK, Thomas R, Mehta DS. Periodontal biotype: Basics and
clinical considerations. Journal of Interdisciplinary Dentistry. 2016 Jan
1;6(1):44.
 Ughabharathy R, Balu P, Muthu J, Saravanakumar R, Vineela K, Karthikeyan I.
Clinical evaluation of increase in the width of attached gingiva using modified
apically repositioned flap: A 9-month follow-up study. Contemporary clinical
dentistry. 2018 Apr;9(2):200.
 Nadkarni MA, Chhour KL, Browne GV, Byun R, Nguyen KA, Chapple CC,
Jacques NA, Hunter N. Age-dependent changes in Porphyromonas gingivalis
and Prevotella species/phylotypes in healthy gingiva and inflamed/diseased sub-
gingival sites. Clinical oral investigations. 2015 May 1;19(4):911-9.

 Sharma A, Singal V. Connective tissue: A gold standard for reconstruction
of black triangle. Journal of Current Research in Scientific Medicine. 2017
Jul 1;3(2):111.
 Bimstein E, Peretz B, Holan G. Prevalence of gingival stippling in
children. Journal of Clinical Pediatric Dentistry. 2004 Jan 1;27(2):163-5.
 KS P. Prevalence of Gingival Stippling among 4-8 Years Old Children.
 Kan JY, Morimoto T, Rungcharassaeng K, Roe P, Smith DH. Gingival
biotype assessment in the esthetic zone: visual versus direct measurement.
International Journal of Periodontics & Restorative Dentistry. 2010 May
1;30(3).
 Jamwal D, Kanade K, Tanwar VS, Waghmare P, Landge N. Treatment of
Interdental Papilla: A Review.
 Shirmohammadi A, Faramarzie M, Lafzi A. A clinical evaluation of
anatomic features of gingiva in dental students in Tabriz, Iran. Journal of
dental research, dental clinics, dental prospects. 2008;2(3):90.

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