PERIODONTAL DISEASES

PRESENTED BY : DR HIMANI TYAGI

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

INTRODUCTION

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

• PERIODONTIUMIncludes structures and tissues that surround and

support the teeth– Alveolar Process– Gingiva– Periodontal Ligament/Membrane– Cementum

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

• 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

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

• 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

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.

• 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

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

• Contains fibers for attachment• Contains nerves, blood vessels and lymph vesselsFUNCTIONS:• 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

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

• 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

Gingiva

• Only portion of periodontium visible in oral cavity

• Made up of epithelial tissue covered with mucosa

• Surrounds cervix of tooth• Fills interproximal spaces

• 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

CLASSIFICATIONAAP 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)

• 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

• 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

Microbial complexes

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.

Open contacts

Faulty restorations

4) Anatomic factors: Cervical enamel projectionsPalatogingival groovesProximal root groovesMalaligned teeth

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.”

INFLUENCE OF OCCLUSION ON 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

PERIODONTITIS AS MANIFESTATION OF SYSTEMIC DISEASE

1) HEMATOLOGICAL DISORDERS :• LEUKAEMIAS• NEUTROPENIA2) GENETIC DISORDERS• DOWN SYNDROME• CYCLIC NEUTOPENIA• EHLERS DANLOS SYNDROME• CHEIDIAK HIGASHI SYNDROME• COHEN SYNDROME• PAPILLON LEFEVRE SYNDROME

OTHER SYSTEMIC FACTORS

• DIABETES• HIV• CARDIAOVASCULAR DISORDERS

Radiographic technique

• Optimal projection in posterior teeth is bite wing radiographs.

• In significant amount of bone loss;vertical bitewing radiographs

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

CLINICAL FEATURES

1) REDNESS AND SPONGINESS OF GINGIVAL TISSUE

2) GINGIVAL ARCHITECTURE3) BLEEDING4) PRESENCE OF PERIODONTAL POCKETS5) RECESSION6)BONE LOSS7) FURCATION INVOLVEMENT

The bacterial products induce local factor production including IL-1α, IL-1β, IL-6,

prostaglandin E2 and TNF-α. COLOUR

CONTOURCONSISTENCY

TEXTUREPOSITION

GINGIVAL BLEEDING

Two earliest signs of Inflammation are:1) Increased GCF Production Rate2) Bleeding On Gentle ProbingNote: Smoking decreases Bleeding (NHANES III )

Periodontal pocket• Classification :1) Gingival pocket2) Periodontal pocket: Infrabony : Subcrestal , intraalveolar Suprabony : supracrestal , supraalveolar Clinical features:Sign: Bluish red thickened marginal gingivaBleeding and suppurationMobilityDiastema • Symptom Pain : deep bony pain

Probes for measuring PP

1) WILLIAMS PROBE2) UNC 15TECHNIQUE: WALKING OF THE PROBE(vertical) :0.75 N FORCE (25gms) :oblique position of probe can

detect depth of crater3) Probing around implants : periimplantitis

create pocket- plastic periodontal probe

Recession

• Millers classification : 1956

Millers class III

Millers class IV

• 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.

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

• Anatomic considerations:position of maxillary sinus irt periodontal deformity,missing ,supernumery, impacted.

• Pathologic considerations:caries, periapical resorption, root resorption.

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

Radiographic features of PDL Disease

• Divided into two1. Changes in morphology of alveolar bone2. 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 trabeculaetoward the alveolar crest on the mesial anddistal aspect of the tooth are barely perceptibleand the marrow spaces are enlarged.

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.

Morphology of alveolar bone

• Early bone changesAppears as area of localized erosion of the

interproximal alveolar bone crest.Anterior region shows- blunting of alveolar

crestPosterior region shows-appear rounded off,

having an irregular and diffuse border.

Early radiographic changes in periodontitis

• Glickman in 1972 listed following sequence of changes:

1) Crestal irregularities2) Triangulation (funneling)3) Interseptal bone changes

Crestal irregularities

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

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

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.

• 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.

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

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

Static destructive process

• Smooth surface of alveolar bone• Condensation of remanining alveolar bone

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 because1)Stage of lesion: early stages no changes r/g2) Location of abcess : abcess on facial and lingual

surface are obscured by radiopacity of root

• 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

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.

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

feature5) Periodontal pocket with deep probing depth

not found.

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

Scleroderma

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

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.

BONE LOSS

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

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

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

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

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

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.

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 anosseous defect extending to the region of the apex.

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.

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

Reasons for high frequency of Interdental craters:

• The interdental area collects plaque and is difficult to clean

• The normal flat or concave faciolingual shape of the interdental septum may favor crater formation

• Vascular patterns from the gingiva to the centre of the crest may provide a pathway for inflammtion.

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.

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.

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)

Hemiseptal defects

Ramping defects vertical defects in the presence of adjacent roots and where half of a

septum remains on one tooth.

A defect that extends to the tooth and surrounds the tooth continuously to

two or more roots is called circumferential defect.

BULBOUS BONY CONTOUR

Bony enlargement caused by exostosis, adaptation to function, or

buttressing bone formation.

Found more frequently in the maxilla than in mandible .

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.

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.

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.

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.

Classification of furcation

• Naber’s probe

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.

The angulation of this periapical view of a maxillary fi rst molar projected the palatal root away from the trifurcationregion 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

Bone Destruction Caused By Extension Of Gingival Inflammation

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

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.

• 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.

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.

Loss of lamina dura -generalized

• Commonly seen in Pagets disease,leukemia• Uncommonly seen in:• Metastatic malignancy• Hyperparathyroidism• Multiple myeloma• Osteomalacia• Cushing syndrome• Scleroderma

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.

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

IMPLANTS AND PERIODONTIUM

• PRE-IMPLANT• IMPLANT PLANNING• POST-IMPLANT

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

• 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.

PRINCIPLES OF IMAGING FORDENTAL-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.

BONE IS STUDIED UNDER

• HEIGHT OF BONE • WIDTH OF BONE• LENGTH OF BONE• BONE CONTOUR• CROWN IMPLANT RATIO

• 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.

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.

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

Misch Bone Density Classification Scheme

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

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

• 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.

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

Newer modalities for diagnosing

• Advances in clinical diagnosis1)gingival temperature Periotemp:0.1 celcius2) Periodontal probing Pressure sensitive probes: controlled insertion pressureFlorida probe systemPeriprobe : automated probeFoster miller probe: Measure probing depth with

detection of CEJ

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

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

Automated probe system

Advantages

• Constant probing force with presice electronic measurements.

• Eliminates potential erorrs associated with visual reading and need of assistant to record the measurements.

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.

Other commercially available probing system

• Inter probe• Periprobe

Peri probe

ADVANCES IN RADIOGRAPHY

• 1) DIGITAL RADIOGRAPHY:STORED, MANIPULATED AND CORRECTED.

• SUBTRACTION RADIOGRAPHY• CADIAS: COMPUTER ASSISTED

DENSITOMETRIC IMAGE ANALYSIS SYSTEM

Subtraction radiography

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

ADVANCE IN MICROBILOGICAL ANALYSIS

• BACTERIAL CULTURING• DIRECT MICROSCOPY: DARK FIELD

MICROSCOPY• IMMUNODIAGNOSTIC METHODSDIRECT AND INDIRECT IMMUNOFLUROSCENCEFLOW CYTOMETRYELISALATEX 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.

PHASE CONTRAST MICROSCOPY

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.

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.

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

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.

ENZYMATIC METHODS

• 1) PERIOSCAN• 2) PERIOCHECK:GCF: ELASTASE• 3)PERIOGARD: GCF: AST

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 results2) Limited organism detected3)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.

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.

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.

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.

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.

MOLECULAR BIOLOGIC TECHNIQUES

• NUCLEIC ACID PROBES• PCR• CHECKERBOARD DNA-DNA HYBRIDIZATION

TECHNOLOGY

DNA PROBE SYSTEM

146

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• 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.

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• Armitage G. Development of a classification system for periodontal diseases and conditions. Annals of Periodontology 1999 Dec; 4(1):1-5.

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