ITS FOR THE DENTISTS WHO WANT TO SEE THE PERIODONTAL INFECTIONS FROM MORE OF RADIOLOGICAL ASPECT

1. PERIODONTAL
DISEASESPRESENTED BY : DR HIMANI TYAGI

2. CONTENTS
• Introduction
• Components
• Classification
• Etiology
• Clinical features
• Assesment of periodontal disease.
• Radiographic changes in PDL Disease
• Radiographic appearance of chronic periodontal disease.
I. Periodontal abcess
II. Generalized aggressive periodontitis
• Implants and periodontium
• Recent advances in the diagnostic aids

3. INTRODUCTION
Periodontal diseases are infections that are
caused by microorganisms that colonise the
tooth surface at or below the gingival margin

5. • PERIODONTIUM
Includes structures and tissues that surround and
support the teeth
– Alveolar Process
– Gingiva
– Periodontal Ligament/Membrane
– Cementum

6. Cementum
• Characteristics:
– Covers root of tooth – forms a thin layer around
the root
– 45-50% inorganic(slightly less than that of bone)
– Contains fibers that attach tooth to the alveolar
bone

7. • Clinical concerns:
– May be exposed with recession of gingiva
– Removal of some of cementum could expose
dentin
– Extreme sensitivity is experienced by patients with
exposed cementum and dentin
– Cemental spurs may form at C E J
• Calculus is easy to remove, spurs are not
– Hypercementosis – occurs at apex in response to
trauma

8. Alveolar bone
• Structure:
– Bones in the maxilla and mandible are formed by
osteoblasts
– Extended areas of bone that hold the teeth are
referred to as the alveolar process
• CORTICAL BONE(LAMINA DURA) – outside layer
of bone surrounding the periodontal ligament
• Cortical bone – compact or dense layer of bone

9. • Cancellous bone – inner or central part of
alveolar bone
• Cancellous bones is also referred to as trabecular
bone
• Spongy or porous in appearance
• Function:
– Supports the tooth
– Stabilizes the root

10. The normal alveolar crest lies 0.5 to 2.0 mm below
the adjacent cementoenamel junctions and forms
a sharp angle with the lamina dura of the adjacent
tooth.
Between the anterior teeth, the normal
alveolar crest is pointed and well
corticated, coming to within 0.5 to 2.0
mm of the adjacent cementoenamel
junctions.

11. • Clinical concerns:
– Periodontal disease can cause loss of bone
– Bone is stimulated from chewing and speech – if
teeth are removed this stimulation is lost and
bone resorbs

12. Periodontal ligament
• Surrounds the root of the tooth
• Composed of fibers, or ligaments, that
support and suspend the tooth in the socket
• Fibers are arranged in bundles
• Forms a ‘shock-absorber’ for the tooth in the
socket

13. • Contains fibers for attachment
• Contains nerves, blood vessels and lymph vessels
FUNCTIONS:
• Supportive – maintains tooth in socket
• Sensory – nerves supply ‘sense of touch
• Formative – fibroblasts, cementoblasts
• Protective- cushion-like action from shock
• Nutritive– blood vessels provide nutrients

14. Periodontal fibres group
• Alveolar crest fibers-extend from cervical area
of tooth to alveolar crest
• Horizontal group – run at right angles
• Oblique group – slants into alveolar bone
• Apical group – extend from apex
• Interradicular –only in multi-rooted teeth
• Transseptal – from one tooth to another

16. • Clinical considerations:
– Occlusal trauma does not cause periodontal
disease but can accelerate an existing condition
– Chronic periodontal disease causes the fiber
groups to become disorganized and lose
attachment due to resorption

17. Gingiva
• Only portion of periodontium visible in oral
cavity
• Made up of epithelial tissue covered with
mucosa
• Surrounds cervix of tooth
• Fills interproximal spaces

18. • Free Gingiva – movable – fits snugly around
the crown just above the cervix of tooth
• Attached Gingiva – non-movable – extends
from the base of the sulcus to the
mucogingival junction
– Attached directly to the cementum and alveolar
process

19. CLASSIFICATION
AAP Classification of Periodontal Diseases and
Conditions (1999)
• Gingival Diseases
– Dental plaque-induced gingival diseases
– Non-plaque induced gingival lesions
• Chronic Periodontitis (Slight: 1-2mm CAL; moderate: 3-4mm
CAL; severe: >5mm CAL)
– Localized
– Generalized (>30% of sites are involved)
• Aggressive Periodontitis (Slight: 1-2mm CAL; moderate: 3-
4mm CAL; severe: >5mm CAL)
– Localized
– Generalized (>30% of sites are involved)

20. • Periodontitis as a Manifestation of Systemic Diseases
– Associated with hematological disorders
– Associated with genetic disorders
– Not otherwise specified
• Necrotizing Periodontal Diseases
– Necrotizing ulcerative gingivitis
– Necrotizing ulcerative periodontitis
• Abscesses of the Periodontium
– Gingival abscess
– Periodontal abscess
– Pericoronal abscess

21. • Periodontitis Associated with Endodontic Lesions
– Combined periodontic-endodontic lesions
• Developmental or Acquired Deformities and Conditions
– Localized tooth-related factors that modify or predispose
to plaque-induced gingival diseases periodontitis
– Mucogingical deformities and conditions around teeth
– Mucogingival deformities and conditions on edentulous
ridges
– Occlusal trauma
The Periodontal Disease Classification System of the American Academy of Periodontology - An Update, Journal
of Canadian Dental Association, 2002; 66:549-7
Crystal S. Baik

22. Microbial complexes

23. Etiology
1) Plaque : structured resilient yellowish greyish
substance that adhere tenaciously
2) Calculus : hard deposit that forms by
mineralization of dental plaque
3) Food impaction
BIOFILM?????
Plaque and its associated bacteria which populate the
periodontal pocket, release lipopolysaccharide and other
bacterial products into the sulcus, affecting both the
immune cells in the connective tissue as well as the
osteoblasts.

24. Open contacts

25. Faulty restorations

26. 4) Anatomic factors:
 Cervical enamel projections
Palatogingival grooves
Proximal root grooves
Malaligned teeth

27. TRAUMA FROM OCCLUSION
• WHO in 1978 defined trauma from
occlusion as “ damage in the
periodontium caused by stress on the
teeth produced directly or indirectly by
teeth of the opposing jaw.”

28. INFLUENCE OF OCCLUSIONON THE PERIODONTIUM
The following changes occur on changing the normal
occlusal forces: -
Increase in magnitude widening of the PDL
Constant pressure resorption of bone
Intermittent force formation of new bone

29. PERIODONTITIS AS MANIFESTATION
OF SYSTEMIC DISEASE
1) HEMATOLOGICAL DISORDERS :
• LEUKAEMIAS
• NEUTROPENIA
2) GENETIC DISORDERS
• DOWN SYNDROME
• CYCLIC NEUTOPENIA
• EHLERS DANLOS SYNDROME
• CHEIDIAK HIGASHI SYNDROME
• COHEN SYNDROME
• PAPILLON LEFEVRE SYNDROME

30. OTHER SYSTEMIC FACTORS
• DIABETES
• HIV
• CARDIAOVASCULAR DISORDERS

31. Radiographic technique
• Optimal projection in posterior teeth is bite
wing radiographs.
• In significant amount of bone loss;vertical
bitewing radiographs

32. • Both clinical and radiographic data is essential
for diagnosing the presence and extent of
periodontal disease

33. CLINICAL FEATURES
1) REDNESS AND SPONGINESS OF GINGIVAL
TISSUE
2) GINGIVAL ARCHITECTURE
3) BLEEDING
4) PRESENCE OF PERIODONTAL POCKETS
5) RECESSION
6)BONE LOSS
7) FURCATION INVOLVEMENT
The bacterial products induce local factor
production including IL-1α, IL-1β, IL-6, prostaglandin
E2 and TNF-α.
COLOUR
CONTOUR
CONSISTENCY
TEXTURE
POSITION

34. GINGIVAL BLEEDING
Two earliest signs of Inflammation are:
1) Increased GCF Production Rate
2) Bleeding On Gentle Probing
Note: Smoking decreases Bleeding (NHANES III )

35. Periodontal pocket
• Classification :
1) Gingival pocket
2) Periodontal pocket:
Infrabony : Subcrestal , intraalveolar
Suprabony : supracrestal , supraalveolar
 Clinical features:
Sign: Bluish red thickened marginal gingiva
Bleeding and suppuration
Mobility
Diastema
• Symptom
Pain : deep bony pain

36. Probes for measuring PP
1) WILLIAMS PROBE
2) UNC 15
TECHNIQUE: WALKING OF THE PROBE(vertical)
:0.75 N FORCE (25gms)
:oblique position of probe can
detect depth of crater
3) Probing around implants : periimplantitis
create pocket- plastic periodontal probe

37. Recession
• Millers classification : 1956

40. Millers class III

41. Millers class IV

42. • FENESTRATION
• Isolated areas in which the
root is denuded of bone and
the root surface is covered
only by periosteum and
overlying gingiva is termed
Fenestrations.
• DEHISCENCES
• When the denuded area
extends through the
marginal bone, the defect
is called Dehiscence.

43. 1. Contribution of radiographs
• Status of periodontium and permanent record of
condition of bone throughout disease.
• Extent of destruction of alveolar bone
• Condition of alveolar crest
• Bone loss in furcation areas
• Width of PDL space
• Local irritating factors that increase the risk:
calculus,poor ontoured restorations
• C:R ratio
• Interproximal contacts

44. • Anatomic considerations:position of maxillary
sinus irt periodontal deformity,missing
,supernumery, impacted.
• Pathologic considerations:caries, periapical
resorption, root resorption.

45. Limitations of radiographs
• Two dimesnsional,bony defects overlapped by
higher bony wall may be hidden.
• Radiographs typically show less severe bone
destruction than actually present.
• Do not demenstrate soft tissue to hard tissue
relationship, no pocket depth
• Bone level measured from CEJ however this
reference point not valid in situation like
supraeruption , severe atttrition

46. Radiographic features of PDL Disease
• Divided into two
1. Changes in morphology of alveolar bone
2. Changes in internal density and trabecular
pattern of bone.
Presence of inflammation in
soft tissue immediately
adjacent to bone, the later
may some decalcification
without actually being
involved in disease known as
hyperemic decalcification
Primarily radiolucent
reaction around this
maxillary lateral incisor.
Note that the trabeculae
toward the alveolar crest
on the mesial and
distal aspect of the tooth
are barely perceptible
and the marrow spaces are
enlarged.

47. A periapical film revealing a predominantly sclerotic bone reaction
resulting from the periodontal disease involving the mandibular
molars. Note that the trabeculae are thickened and the marrow spaces
are barely perceptible.

48. Morphology of alveolar bone
• Early bone changes
Appears as area of localized erosion of the
interproximal alveolar bone crest.
Anterior region shows- blunting of alveolar
crest
Posterior region shows-appear rounded off,
having an irregular and diffuse border.

49. Early radiographic changes in
periodontitis
• Glickman in 1972 listed following sequence of
changes:
1) Crestal irregularities
2) Triangulation (funneling)
3) Interseptal bone changes

50. Crestal irregularities
• Indistinctness and interruption in the
continuity of the lamina dura seen along the
mesial and distal aspect of the interdental
alveolar crest.

51. Triangulations
• Widening of PDL space by the resorption of
bone along either the mesial or distal aspect
of interdental bone.
• Sides of triangle formed by alveolar bone and
root surface, base towards the crown and
apex of triangle pointing towards root

52. Interseptal bone changes
• Finger like radiolucent projections extending
from the crestal bone into interdental alveolar
bone.result of deeper extension of
inflammation from connective tissue of the
gingiva.
• They represent widened blood vessel channels
within the alveolar bone that allows
inflammatory exudate and cells into bone.
• Reults mineralized tissue per area.

53. • When alveolar bone support is lost,tooth
seems to float in air on R/G known as terminal
stage of chronic destructive periodontitis.
• Reactive sclerosis can sometimes be seen at
the margins of the remaining bone of terminal
chronic destructive periodontitis.

54. Evaluation of bone loss
• Radiograph is used indirectly to evaluate the
bone loss.
• Normal bone height is 1-1.5mm apical to CEJ.
• Bone loss –localized or generalized
• Direction of bone loss-horizontal or verical
• Localized juvenle periodontitiis-vertical bone
loss around molars and incisors

55. Activity of destructive process
• Can be evaluated using standard radiographs
taken over regular intervels.
• When interdental septal bone crest is rough
and irregular and the alveolar bone below the
crest is devoid of any bone opacity, resorptive
process is active.
• Nutrient canals indicate active and even rapid
bone resorption

56. Static destructive process
• Smooth surface of alveolar bone
• Condensation of remanining alveolar bone

57. Periodontal abscess
• May develop anywhere in membrane at the side
of a root, near the gingival margin or at the apex
of the tooth. In later site pulp is almost certain to
die.
• Radiographic picture is not very typical because
1)Stage of lesion: early stages no changes r/g
2) Location of abcess : abcess on facial and lingual
surface are obscured by radiopacity of root

58. • Localized thinning of adjacent lamina dura.
• Increased radiolucency in the adjacent bone
• At variable time bone structure may disapppear.
• Size vary - >cm
• Radiolucent area is irregular, poorly demarcated.
• Rarefying osteitis may arise at the side as a result
of infection of pulp;difficult to distinguish with
periapical abcess

59. Generalized aggressive periodontitis
• Rapid destruction of the periodontium which
lead to early tooth loss in the affected
individuals if not diagnosed early and treated
appropriately.
• “generalized interproximal attachment loss
affecting at least 3 permanent teeth other
than first molars and incisors”
N. Lang, P. M. Bartold, M. Cullinan, et al., “Consensus report: aggressive periodontitis,”
Annals of Peridontology, vol. 4, p. 53, 1999.

62. Necrotizing ulcerative periodontitis
• Clinically – 1) ulceration and necrosis of
coronal portion of interdental papillae.
2) Painfull bright red gingiva which bleeds easily.
3) Destructive progression of disease which
includes CAL & bone loss.
4) Deep interdental osseous craters – typical
feature
5) Periodontal pocket with deep probing depth
not found.

63. Skeletal disturbances manifested in
jaws
• 1) Osteitis Fibrosa Cystica-Recklinghausen’s
disease of bone
• Developed in advanced hyperparathyroidism
and causes osteoclastic resorption of bone
with fibrous replacement and heamorrahage
with haemosiderin deposition creating a mass
called brown tumour

64. Scleroderma
• PDL is uniformaly widened at the expense of
alveolar bone.

65. Malignancy
• Both primary and metastatic can affect the
alveolar ridge and often present as
periodontal disease.
• A uniform widening of PDL can be an early
sign of osteosarcoma.
• Irregular destruction of periodontal bone
without tooth displacement is frequently the
result of squamous cell carcinoma or
metastatic carcinoma.

66. BONE LOSS

67. Glickman (1964) :
1) Horizontal Bone Loss
2) Vertical or angular defects
3) Physiologic osseous defects
4) Osseous craters
5) Bulbous bone contours
6) Reverse architecture
7) Ledges
8) Furcation involvement

68. Classification of
Osseous Defects:
Goldman
& Cohen
(1958)
classified
angular
defects
as:-
Depending
on number
of walls
presentThr
ee osseous
walls
Proximal,
buccal and
lingual
walls
Buccal,
mesial and
distal wall
Lingual,
mesial and
distal walls

69. HORIZONTAL BONE LOSS
Horizontal bone loss is the
most common pattern of
bone loss in periodontal
disease.
The bone is reduced in
height, but the bone margin
remains approximately
perpendicular to the tooth
surface

70. MILD BONE
LOSS
• 1 mm of attachment loss
Moderate
• Greater than 1 mm upto midpoint of the
length of roots or to furcation level of molars
severe
• Loss beyond moderate and evidence of
furcation involvement of multirooted teeth
The interdental septa and facial and lingual plates
are affected, but not necessarily to an equal
degree around the same tooth

71. VERTICAL OR ANGULAR DEFECTS:
These defects occur in an oblique
direction, leaving a hollowed out
trough in the bone alongside the
root ; the bone of the defect is
located apical to the surrounding
bone.
In most instances, angular defects
have accompanying infrabony
pockets; such pockets always have
an underlying angular defect.
Bony lesions localized to one or
two teeth

72. Example of a developing vertical defect;
note the abnormal widening of the
periodontal ligament space (arrow).
Maxillary periapical film reveals two
examples of more severe vertical
defects affecting the mesial surface
of the first molar and the distal
surface of the canine.

73. Gutta-percha may be used to visualize the depth of infrabony defects
.
Radiograph fails to show the
osseous defect without the use of
the gutta-percha points.
B, Radiograph reveals an
osseous defect extending to the
region of the apex.

74. CRATER
These are concavities in the crest of the
interdental bone confined within the facial and
lingual walls.
These are most common bony lesions in
periodontal disease.

75. CRATERS HAVE BEEN FOUND TO MAKE UP ABOUT ONE THIRD OF ALL
OSSEOUS DEFECTS AND TWO THIRDS OF ALL MANDIBULAR DEFECTS

77. According to Goldman HM & Cohen DW in 1958,
angular defects are classified on the basis of
number of osseous walls into one, two or three
walls.

78. Frequently, intrabony defects present a complex
anatomy consisting of a three-wall component in
the most apical portion of the defect, and two-
and / or one-wall components in the more
superficial portions. Such defects are frequently
referred to as combination defects.

79. A, Loss of the lingual alveolar crest adjacent to this mandibular fi rst bicuspid without
associated interproximal bone loss.
B, Loss of the buccal cortical bone adjacent to the maxillary central and lateral incisors. The
black arrow indicates the level of the buccal alveolar crest, which demonstrates more
profound loss relative to the lingual alveolar crest (white arrow)

80. Hemiseptal defects
Ramping defects
vertical defects in the presence of
adjacent roots and where half of a
septum remains on one tooth.

82. BULBOUS BONY CONTOUR
Bony enlargement caused
by exostosis, adaptation
to function, or buttressing
bone formation.
Found more frequently in
the maxilla than in
mandible .

83. LEDGES
Plateau like bone margins caused by
resorption of thickened bony plates.
The width of the alveolar housing
around a tooth is often greater in a
more apical location.
As the bone resorbs because of
periodontitis, the osseous margin in
the new apical position may be
considerably thicker than in the
normal periodontium, giving the
appearance of a bony ledge.

84. REVERSED ARCHITECTURE
Produced by loss of interdental bone,
including the facial plates, lingual
plates, or both, without concomitant
loss of radicular bone, such defects are
more common in maxilla.
Also called as inconsistent bony
margins , results when the
interproximal crest is more apical than
the buccal or palatal/ lingual radicular
bone height , producing a reverse
pattern in comparison to the normal
scalloped alveolar process.

85. Osseous deformities in the furcation
• Progressive periodontal disease And its
associated bone loss extends to furcation
• Widening of PDL space at the apex of
interradicular bony crest of the furcation is
strong evidence that periodontal ds involves
furcation.

86. FURCATION
It refers to the invasion of
the bifurcation and
trifurcation of multirooted
teeth by periodontal
disease
Mandibular first molar are
the most common site
and maxillary premolar
are the least common site.

87. Classification of furcation
• Naber’s probe

88. A periapical fi lm revealing very early
furcation involvement of a mandibular
molar characterized by slight widening of
the periodontal ligament space in the
furcation region
A periapical film revealing a profound
radiolucent lesion within the furcation
region (arrow) resulting from loss of
bone in the furcation region and the
buccal and lingual cortical plates.

89. The angulation of this periapical view of
a maxillary fi rst molar projected the
palatal root away from the trifurcation
region revealing early widening of the
furcation periodontal ligament space
Example of an inverted “ J ” shadow
(arrow) resulting from bone
destruction extending into the
trifurcation region of a three-rooted
maxillary fi rst bicuspid

90. Bone Destruction Caused By Extension Of Gingival
Inflammation
advanced stages of disease
number of motile organisms and
spirochetes increases
number of coccoid rods and straight rods
decreases .
Substances produced by the subgingival bacterial flora and the tissue
differentiation & stimulation of osteoclasts inhibiting bone formation by osteoblasts.
extension of inflammation from the marginal gingiva into the supporting
periodontal tissues.
inflammatory invasion of the bone
surface
initial bone loss mark the conversion of
gingivitis into periodontitis
Once the inflammation reaches bone, spreads into the marrow
spaces
replaces the marrow with a leukocytic and fluid exudate.
Multinuclear osteoclasts and mononuclear phagocytes increase in
number and the bone surfaces appear, lined with Howship lacunae
In the marrow spaces, thinning of the surrounding bony trabeculae
and enlargement of the marrow spaces.
Reduction in bone height
Bone destruction in periodontal disease not a process of bone
necrosis. It involves the activity of living cells along viable bone

91. Evaluation of periodontal therapy
• Radiographs may show signs of successful
treatment of periodontal disease.
• In some cases there may be reformation of
the interproximal cortex and the sharp line
angle between the cortex and lamina dura.
• The relatively radiolucent margins of bone
that were undergoing active resorption before
treatment may become more sclerotic
(radiopaque) after successful therapy.
An example of a case where the
interproximal cortex of the alveolar
crest has reformed after successful
periodontal therapy.

92. • Sequential radiographs made with different beam
angulations may give the false impression that
bone has grown into the periodontal defects.
• Therefore in a longitudinal study effort should be
given to duplicate the image geometry as well as
using ideal exposure and processing variables
• Underexposed or underdeveloped fi lms may give
the false impression of bone growth.

93. DIFFERENTIAL DIAGNOSIS
• The majority of cases of bone loss around
teeth are caused by periodontal diseases.
• This fact can make the clinician less sensitive
to other diseases with similar manifestations
that should always be considered in the
differential diagnosis.

94. Loss of lamina dura -generalized
• Commonly seen in Pagets disease,leukemia
• Uncommonly seen in:
• Metastatic malignancy
• Hyperparathyroidism
• Multiple myeloma
• Osteomalacia
• Cushing syndrome
• Scleroderma

95. Increased width of PDL space
• Commonly seen in : traumatic occlusion,
periapical inflammation, normal finding
around neck of teeth, fractured root.
• Uncommonly seen in : intentional
reimplantation, osteomyelitis, diabetes,
malignant tumours.

96. Crestal radiolucency leading in
decreased alveolar bone
• Commonly seen in : hyperemic decalcification,
juvenile periodontitis, ANUG
• Uncommonly seen in : leukemia, malignancy,
radiotherapy,cyclic neutropenia, papillon
lefevre syndrome, acrodynia, peripheral giant
cell tumour

97. IMPLANTS AND PERIODONTIUM
• PRE-IMPLANT
• IMPLANT PLANNING
• POST-IMPLANT

98. These various radiographic investigations
are used to show:
• The position and size of relevant normal
anatomical structures, including the:
— inferior dental canals
— mental foramina
— incisive or nasopalatine foramen and
canal
— nasal floor
• The shape and size of the antra, including the
position of the antral floor and its relationship to
adjacent teeth

99. • The presence of any underlying disease
• The presence of any retained roots or buried
teeth
• The quantity of alveolar crest/basal bone,
allowing direct measurements of the height,
width and shape
• The quality (density) of the bone, noting:
— the amount of cortical bone present
— density of the cancellous bone
— size of the trabecular spaces.

100. PRINCIPLES OF IMAGING FOR
DENTAL-IMPLANT ASSESSMENT
• Images should have appropriate diagnostic quality and
not contain artifacts that compromise anatomic-
structure assessments.
• Images should extend beyond the immediate area of
interest to include areas that could be affected by
implant placements.
• thorough review of normal maxillofacial anatomy,
common anatomic variants, and imaging signs of
diseases and abnormalities.
• The goal of radiographic selection criteria is to identify
appropriate imaging modalities that complement the
goals at each stage of implant therapy.

102. BONE IS STUDIED UNDER
• HEIGHT OF BONE
• WIDTH OF BONE
• LENGTH OF BONE
• BONE CONTOUR
• CROWN IMPLANT
RATIO

105. • CBCT should be considered as the imaging
modality of choice for preoperative
crosssectional imaging of potential implant
sites.
• Do not use CBCT imaging for periodic review
of clinically asymptomatic implants.

106. 3. Postoperative imaging
• The purpose of postoperative imaging after dental
implant placement is to confirm the location of the
fixture at implant insertion.
• From 3 to 5 years and beyond, imaging is used to
assess the bone-implant interface and marginal peri-
implant bone height.
• Titanium implant fixtures inherently produce
artifacts such as beam-hardening and streak artifacts
obscuring subtle changes in marginal and peri-
implant bone.
• In addition, the resolution of CBCT images for the
detection of these findings is inferior to intraoral
radiography.

107. BONE QUALITY
• BONE DENSITY: An accurate method to
quantify bone density with medical CT is
through the Hounsfield scale, and relative
density with CBCT and visualizing the various
views these 3-D scans offer

108. Misch Bone Density Classification
Scheme

109. A= TYPE 1 mental ridge , B= TYPE II, 36 EJS, C= TYPE III Upper 2 molar , D= TYPE IV, EJS 17

110. Radiographic evaluation
• Radiographs are used to assess:
• The position of the fixture in the bone and its
relation to nearby anatomical structures
• Healing and integration of the fixture in the bone
• The peri-implant bone level and any subsequent
vertical bone loss — threaded fixtures allow
easy measurement if radiographs are
geometrically accurate

111. • Bone Implant interface
• Development of any associated disease,
e.g. perimplantitis
• The fit of the abutment to the fixture
• The fit of the abutment to the
crown/prosthesis
• Possible fracture of the implant/prosthesis.

112. Marginal bone loss
around the cervical
region of a root-form
dental implant
Periapical radiograph of
moderate bone loss
("saucerization" type) around
the cervical region of a root-
form dental implant

118. Newer modalities for diagnosing
• Advances in clinical diagnosis
1)gingival temperature
Periotemp:0.1 celcius
2) Periodontal probing
Pressure sensitive probes: controlled insertion
pressure
Florida probe system
Periprobe : automated probe
Foster miller probe: Measure probing depth with
detection of CEJ

119. Perio- Temp Probe
• Temperature sensitive probe
• Detects early inflammatory changes in gingival
tissue by measuring the temperature variation
in tissue.
• Red emitting diode: higher temperature
• Green emitting diode: lower temperature

120. Periodontal probing
• Pocket probing is a crucial and mandatory procedur
in diagnosing periodontitis and evaluating
periodontal therapy.
• Reading of clinical probing depth obtained with
periodontal probe do notnomally co-incide with
histologic pocket depth because probe generally
penetrates the coronal level of junctional epithelium

121. Automated probe system

122. Advantages
• Constant probing force with presice electronic
measurements.
• Eliminates potential erorrs associated with
visual reading and need of assistant to record
the measurements.

123. Disadvantages
• Lack tactile sensitivity due to independent
movement by operator
• Fixed- force setting in mouth regardless of site
leading to patient discomfort.
• Underestimation of deep probing depths.

124. Other commercially available probing
system
• Inter probe
• Periprobe

125. Peri probe

126. ADVANCES IN RADIOGRAPHY
• 1) DIGITAL RADIOGRAPHY:STORED,
MANIPULATED AND CORRECTED.
• SUBTRACTION RADIOGRAPHY
• CADIAS: COMPUTER ASSISTED
DENSITOMETRIC IMAGE ANALYSIS SYSTEM

127. Subtraction radiography

128. Computer assisted densitometric
image analysis system
• Alveolar bone density changes quantitatively
over time.
• Higher sensitivity and high degree of
reproducibility and accuracy.
Digital intraoral periapical radiograph with computer-assisted densitometric image analysis

129. ADVANCE IN MICROBILOGICAL
ANALYSIS
• BACTERIAL CULTURING
• DIRECT MICROSCOPY: DARK FIELD
MICROSCOPY
• IMMUNODIAGNOSTIC METHODS
DIRECT AND INDIRECT IMMUNOFLUROSCENCE
FLOW CYTOMETRY
ELISA
LATEX AGGLUTINATION
The microbiological tests have the potential to
support the diagnosis of various forms of
periodontal disease, to serve as indicators of
disease initiation and progression and to
determine which periodontal sites are at higher
risk for active destruction.

132. PHASE CONTRAST MICROSCOPY

133. Direct IFA
• Employ both monoclonal and polyclonal
antibodies conjugated to a fluorescien marker
that binds with the bacterial antigen to form
fluorescent immune complex detectable
under microscope.

134. Cytoflurography
• Suspension is introduced into flow cytometer
which seperates bacterial cells into an almost
single cell suspension by meanse of laminar
flow through a narrow tube.

135. ELISA
• It is similar in principle to radio immuno asays
but instead of radio isotope an enzymatically
derived color reaction is substituted.
• Intensity of color depends on concentration of
the antigen and is read photometrically for
optimal quantification

136. LATEX AGGLUTINATION
• Based on binding of protein to latex
• Latex beads are coated with species specific
antibody and when these beads come in
contact with microbial cell surface antigen,
cross linking occurs and agglutination and
clumping is visible.

137. ENZYMATIC METHODS
• 1) PERIOSCAN
• 2) PERIOCHECK:GCF: ELASTASE
• 3)PERIOGARD: GCF: AST

138. Perio scan
• Perioscan requires a plaque sample to detect
the presence of enzymes capable of degrading
N-benzoyl-DL-arginine-2-naphthylamide
(BANA) from relatively few anaerobic
periodontal pathogens.
• Disadvantages :1) False positive results
2) Limited organism detected
3)Cannot detect disease activity.
Subgingival plaque is collected and placed on a BANA-
containing strip, which is then folded to contact a
second strip containing the “Fast-Black” dye reagent.
The folded card is placed inside an oven for 15 min at
55°C and any blue-black color that appears is scored
positive for the above species.

139. Periocheck
• Chair side test kit
• Detect neutral protease in GCF
• The GCF sample strip is placed on a gel
containing insoluble dye-labelled collagen
fibrils (remazobrilliant blue-collagen substrate
powder) and incubated.

140. Periogard
• PerioGard is based on the detection of an enzyme
called aspartate aminotransferase (AST).
• AST is a soluble intracellular cytoplasmic enzyme
that is released from within the cell upon its
death.
• Since cell death is an important part of
periodontal pathogenesis, AST levels in GCF have
great potential as markers of early periodontal
tissue destruction.

141. POCKET WATCH
• Simple method of analyzing AST at the
chairside.
• Provides not only an index of cell death but of
the extent of the destructive pockets.

142. Periotron
• GCF analysis
• Saliva is removed from tooth surface before
placement of periopaper strip into pocket to
collect GCF
• Moist paper strip is removed and placed
between the jaws for assesment of fluid
content.

143. MOLECULAR BIOLOGIC TECHNIQUES
• NUCLEIC ACID PROBES
• PCR
• CHECKERBOARD DNA-DNA HYBRIDIZATION
TECHNOLOGY

144. DNA PROBE SYSTEM

146. 146
References
• Oral radiology and principles of intrepetation;White and
pharoah: 6th edition,
• Gary C. Armitage , Classifying periodontal diseases – a long-
standing dilemma ; Periodontology 2000, Vol. 30, 2002, 9–23 .
• Gary C. Armitage , Periodontal diagnosis and classification of
periodontal disease. Periodontology 2000, Vol .34 , 2004 , 9-
21 .
• Clinical Periodontology ; Newmann and Carranza , 10th and 8
th edition
• Grant and Listgarten : Periodontics.
• Annals of Periodontology, Volume 4, Number 1, December
1999.
• Consensus Report: Periodontic -endodontic lesions. Annals of
Periodontology 1999 Dec; 4(1):90.

147. 147
• Armitage G. Development of a classification system for
periodontal diseases and conditions. Annals of
Periodontology 1999 Dec; 4(1):1-5.
• Consensus Report: Chronic periodontitis. Annals of
Periodontology 1999 Dec; 4(1):38.
• The Periodontal Disease Classification System of the American
Academy of Periodontology — An Update : Colin B. Wiebe,
Edward E. Putnins. J Can Dent Assoc 2000; 66:594-7.
• Purpose and problems of periodontal disease classification,
Ubele Van Der Velden ; Periodontology 2000, Vol. 39, 2005,
13–21