Clinical Diagnosis

CLINICAL DIAGNOSIS
• Introduction
• Case history
• Extraoral examination
• Intraoral examination
• Etiologic factors
• Study models
• Laboratory investigations
• adiogra!hic examination
• Su!!lementary diagnostic aids
• Diagnosis of !eriodontal diseases
• Conclusion
Diagnosis is the determination of the nature of a case or a disease.
Periodontal diagnosis is determined after careful analysis of the case history and evaluation of
the clinical signs and symptoms, as well as the results of various tests.
A decision is then made regarding the disease category that is most closely associated with the
patient’s clinical status. The information routinely collected during a periodontal examination
includes demographic data (e.g., age, gender, etc.), medical history, history of previous and
current periodontal problems, periodontal probe measurements (i.e., probing depths, clinical
attachment loss, etc.), radiographic findings, and miscellaneous clinical features or observations
(e.g., gingival inflammation, plaquecalculus, mobility, occlusal problems). !n some situations,
supplemental qualitative or quantitative assessments of the gingival crevicular fluid ("#$) and
subgingival microflora are performed. !n addition, a genetic test for susceptibility to chronic
periodontitis has become commercially available %Armitage, &''().
*laque+induced periodontal diseases have traditionally been divided into two general categories
based on whether attachment loss has occurred, gingivitis and periodontitis. "ingivitis is the
presence of gingival inflammation without loss of connective tissue attachment. *eriodontitis can
be defined as the presence of gingival inflammation at sites where there has been a pathological
1
detachment of collagen fibers from cementum and the -unctional epithelium has migrated
apically.
.emonstration of the progression of periodontitis requires documentation of additional
attachment loss occurring between at least two time points. /ince this is not always possible,
especially when a patient is examined for the first time, most clinicians assign the diagnosis of
0periodontitis1 to inflamed sites that also have loss of attachment and bone. This is a prudent
practice since such sites may be either currently progressing or are at an increased ris2 for further
periodontal destruction. Therefore, demonstration of progressive attachment loss is not generally
considered to be a requirement for using 0periodontitis1 as a diagnostic label.
.espite our increased understanding of the etiology and pathogenesis of periodontal infections,
the diagnosis and classification of these diseases is still based almost entirely on traditional
clinical assessments.
To arrive at a periodontal diagnosis, the dentist must rely upon such factors as,
&) presence or absence of clinical signs of inflammation (e.g., bleeding upon probing)3
4) probing depths3
5) extent and pattern of loss of clinical attachment and bone3
6) patient’s medical and dental histories3 and
() presence or absence of miscellaneous signs and symptoms, including pain, ulceration, and
amount of observable plaque and calculus.
Instruments and materials for complete periodontal assessment:
&. 7outh mirror
4. *eriodontal probe
5. $urcation probe
6. Articulating ribbonpaper, occlusal indicator wax
(. .ental floss
A working diagnosis is the pencil diagnosis generated by the clinician that is based upon the
scientific significance of the signs and symptoms recorded during the comprehensive
examination. !t is the clinician’s best estimate of the pathologic process, and the morbid
outcomes of the process present at the time of the examination. !t is the basis of the patient’s
initial treatment plan.
A differential diagnosis is one that includes two or more possible processes that may be
consistent with the initial clinical assessments. 8ather than commit to one wor2ing diagnosis, the
clinician may choose to provide a differential diagnosis and either perform or request additional
diagnostic testing.

CASE "IS#O$
!t is a planned professional conversation between the operator and the patient followed by an
accurate recording of facts.
9b-ectives,
• To get the relevant information
2
• To become sufficiently familiar with each other
• To gain patient’s confidence
• To put him at ease
DE%OGA&"IC DA#A
&atient's Name(
• for development of good rapport with the patient
• for communication (in their own language)
• affects patient’s psychology (gives personal touch)
• helps in eliciting history properly
• for record purposes (identification)
• helps decide patient’s community (any disease common in a specific community or any
practices related to specific community)
Age(
• #ertain diseases are more common in a particular age
 :oung individuals+;A*, prepubertal periodontitis, acute herpetic
gingivostomatitis)
 9lder individuals+ #hronic periodontitis
• $or manipulation of drug doses
• AgeAge <&4 = Adult dose (:oung’s formula)
• "ives information about dentition
• 7ental and chronologic age
• !nformed consent purposes, validity of consent at time of surgery
• .etermining diagnosis
• .etermining prognosis
• .etermining treatment plan
Sex(
#ertain diseases are more common in males (hemophilia, oral cancers) while some in females
(breast cancer, thyroid disorders)
>ormonal+related changes (pubertypregnancy gingivitis3 pregnancy tumor3 post+menopausal
changes)
Address(
• $ew diseasesconditions have got geographical distribution (fluorosis in endemic
areas li2e 8a-asthan, parts of 7aharashtra, "u-arat)
• To determine socio+economic status (which in turn affects treatment options)
• $or future correspondence
Occu!ation(
#ertain diseases are occupation+associated.
• /and factories, lung cancer
3
• 7inesconfectionary factories, wearing of tooth
• ;ead factories, plumbism (lead poisoning)
• 8adiographic technicians, x+ray irradiation
Income(
• .etermine socio+economic status
• *lan treatment according to budget permitted
C"IE) CO%&LAIN# * "+O &ESEN#ING ILLNESS(
To be recorded in patient’s own words.
9ne can determine patient’s expectations.
!f many complaints are present, have to be presented in chronologic order.
?valuate each complaint regarding onset, progress, duration, aggravating and relieving factors.
Sign( Any bodily change perceptible to a trained observer.
Sym!tom( Any bodily change perceptible to the patient.
%EDICAL "IS#O$(
• 7ay provide important clues to the diagnosis.
• 7ay greatly modify treatment plan
• 7ay determine the prognosis of the disease
• An inadequate medical history may put the health of the patient, the dentist and
supporting staff at ris2 (e.g. infectious diseases li2e >epatitis+@, >!A)
• 7andatory for medico+legal purposes
>o >ospitaliBation, indicates serious problems in the pastanaesthic tolerancebleeding
problems drug reactions)
>o medications ta2en (underlying problemdiseasecondition3 drug allergy3 drugs prescribed for
dental purposes may interfere with pre+existing medications3 drug+induced gingival enlargement,
steroid+related immunosuppression)
>o blood donation (blood borne infections)
>o -aundice, hepatitis, liver problems (drug metabolism, bleeding problems, cross+infection)
>o cardiac problems (ris2 of angina with stress, ongoing medications li2e aspirin, drug+induced
gingival enlargement)
>o rheumatic fever (infective endocarditis)
>o respiratory problems (general anaesthetic ris23 drug prescription)
4
>o infectious diseases li2e T@, >epatitis+@. >!A (infection control)
>o diabetes (more susceptible to infection, multiple abscesses3 periodontal disease progression3
ris2 of hypoglycemiahyperglycemia3 wound healing)
>o epilepsy (ris2 of seiBure, drug induced gingival enlargement)
>o renal disorders (care while prescribing drugs)
>o puberty, pregnancy, menopause (hormonal disturbances)
>o endocrinal disorders (Thyroid, parathyroid, pituitary gland, pancreas, A#T>)
&AS# DEN#AL "IS#O$(
• 7otivation (internalexternal)
• ;i2ely future compliance
• 7ay hint at present problem
• Anxiety, health+problems, complications in the past
• 9ral hygiene maintenance, 2nowledge of prevention
• .rug allergies (eg. ;ocal anaesthesia)
)A%IL$ "IS#O$+"EEDI#A$ &O,LE%S(
$amilial predisposition
#onsanguineous marriages
>emophilia.iabetes?pilepsy#ardiac problems@reast cancerAggressive periodontitis
SOCIAL "IS#O$(
Diet,
• Adequateinadequate inta2e (weight lossanorexia)
• Appetite (reduced in >!A, T@)
• Type of diet (nutritional deficiencies, citrus products)
• Cature of diet (fibroussoft)
#obacco * #obacco !roducts+Smo-ing(
• /uppresses signs and symptoms of gingival and periodontal disease
• 8ecession
• Affects post+surgery healing
• ACD"
• ;eu2opla2ia, oral cancer
• Atherosclerosis
5
ALCO"OL(
;iver disorders, bleeding, drug+interaction+disulfiram li2e reactions, affects progression of
disease
S#ESS(
ACD", disease progression
"A,I#S(
.efinition( The tendency towards an act that has become a repeated performance, relatively
fixed, consistent and easy to perform by an individual.
#lassification,
&. Dseful (essential for normal function) E harmful habits (with deleterious effects)
4. ?mpty (no psychological bearing) and meaningful habits (with psychological problems)
5. *ressure (thumbsuc2ing), non+pressure (mouthbreathing) and biting habits
6. #ompulsive E non+compulsive habits
#humbsuc-ing
• The placement of thumb or one or more fingers in varying depths into the mouth.
• #linical features, labial tipping of maxillary anterior teeth3 increased over-et3 A9@3
narrow maxillary arch3 hypotonic upper lip and hyperactive mentalis
• 7anagement,
*sychological approach (.unlop’s hypothesis)
7echanical approach (habit+brea2ing appliances)
#hemical approach (bitter tasting preparations li2e pepper, quinine, asafetida
#ongue.thrusting
• !t is a condition in which the tongue ma2es contact with any teeth anterior to the molars
during swallowing.
• ?tiology, genetic3 habitual3 maturational3 mechanical restrictions3 neurological
• Types, /imple tongue thrust (anterior openbite)
#omplex tongue thrust (anterior E posterior open bite3 occlusion is poor)
• 7anagement, >abit interception3 treatment of malocclusion
%outh breathing
• #lassification, obstructive, habitual, anatomic
• #linical features, adenoid facies3 short and flaccid upper lip3 anterior marginal gingivitis3
dry mouth3 anterior open bite
• .iagnosis,
>istory
#linical examination, mirror test, water test, butterfly test
8hinomanometry (study of nasal air flow characteristics)
• Treatment, removal of obstruction3 interception of habit3 maxillary expansion
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,ruxism
• "rinding of teeth for non+functioning purposes.
/ome authors refer to nocturnal grinding as bruxism while day time grinding is referred to as
bruxomania.
• ?tiology, psychological E emotional stress3 occlusal interference3 pericoronitis,
periodontal pain is thought to trigger grinding in some.
• #linical features, occlusal wear facets3 fracture of teethrestorations3 mobility of teeth3
tenderness and hypertrophy of masticatory muscles3 T7F pain and discomfort.
• .iagnosis,
>istory
#linical examination
Articulating paper, occlusal discrepancy
?7"
• Treatment,
*sychological counseling
>ypnosis, relaxing exercises and massage
9cclusal ad-ustments
Cight guards or occlusal splints
E/#A.OAL E/A%INA#ION(
)ace( for facial symmetry, swellings, lesions, scars, face type, etc
Con0unctiva( any signs of icterus, ecchymosis, pallor in lower palpebra %-aundice, trauma,
anaemia)
Sclera( icterus
Li!s(
• competentincompetentpotentially competent
• any ulcerations, lesions, herpetic lesions, vesiculobullous lesions, angular chelitis
%nutritional deficiencies, trauma, s2in disorders)
• muscle tone %drooping of commissure or inability to purse lips in @ell’s palsy
• changes in colour or texture
Lym!h Nodes(
A normal lymph node cannot be felt.
7ost lymphnodes should be examined by extraoral, bimanual palpation. Dse the pulp of the
finger tips and try to roll the node against harder structures.
/ubmental ;Cs, tip the head forward
/ubmandibular ;Cs, tip the head to the side to be examined
;ymph nodes can be divided into two main groups,
I] Circular group
7
• 9uter circle, /ubmental
/ubmandibular
$acial (buccal)
*reauricular
*ostauricular
9ccipital
• !nner circle, 8etropharyngeal
*retarcheal
*aratracheal
II] Cervical group
• .eep cervical chain
• /uperficial cervical chain
• Fugulo+digastric
• Fugulo+omohyoid
!f a node is palpable, record site, siBe, texture, tenderness, fixation to surrounding tissues etc
;ocal infections, pericoronitis, periodontalpericoronalperiapical abscesslesions, ACD",
apthous ulcers, acute herpetic gingivostomatitis, malignancy
/ystemic infections, syphilis, T@, @acterialfungalparasitic infections, malignancy, >!A,
lymphomas, leau2aemias
#em!oromandibular 1oint(
!nvestigate,
• 8ange of movements %7aximum mouth opening, 7ales,6G+(Gmm3 females,5(+6(mm)
• ;ateral deviation %usually deviates to affectedpainful side3 maximum lateral excursion,H
mm)
• Tenderness %bimanual palpation by pressing over the lateral aspect of the -oint followed
by intra+auricular palpation by placing the little finger towards the external auditory
meatus and gently pressing forwards.
• /ounds %Clicks are caused by sudden movement of disc relative to the condyle3 they may
be early, late, reciprocal3 Crepitus is a prolonged, continuous, grating or crac2ling noise3
occurs with degenerative diseases or acute inflammation)
• ;oc2ingdislocation %due to malposition and distortion of the disc)
• 7uscle tenderness
IN#AOAL E/A%INA#ION(
&eriodontal ,ioty!e
a) Thin, scalloped periodontium
b) Thic2, flat periodontium
%9schenbein E 8oss, &'I'3 9lsson E ;indhe, &''6)
Thin, scalloped periodontium
8
• *ronounced periodontal architecture with delicate, friable soft tissue curtain
• ?xaggerated gingival scallop (6+Imm)
• Attached soft tissue is minimal
• 8eveals contours of prominent roots
• @ony dehiscence, fenestration characteriBe underlying osseous structure
• Triangular anatomic crowns3 small id contacts
• 8eacts to surgical/prosthetic interventions with soft tissue recession, apical migration of
attachment and loss of underlying alveolar bone
Thic2, flat periodontium
• 8elatively flat soft tissue and bony architecture
• /oft tissue curtain is dense and fibrotic and abundance of soft tissue
• "ingival scallop
• Dnderlying bone is thic2 E dense
• /quare anatomic crowns3 large contact areas
• /hort interdental papillae
• 8esist recession and reacts to surgicalrestorative insults with pocket formation
Oral mucosa2 tongue( by visual examination supplemented by palpation
&alate( %/hallowmoderate deep, gives an estimation while harvesting soft tissue autograft)
• ?pithelium of hard palate, G.5mm (max. G.Imm)
• ;amina propriaconnective tissue, &.4(+5.Gmm
• Pars corporis adiposa: contains adipose tissue and renders in the area of premolars.
• Pars corporis glandulosum: glandular tissue and extends posteriorly to the soft palate.
• The two are separated by the thin mucosa over the palatal root of &
st
molar.
• "reater and lesser palatine foramina are located apical to the 5
rd
molar at the -unction of
vertical and horiBontal component of the palate (midway etween the gingival margin of
!
nd
molar and mid palatine raphae". The vessels and nerve lie in a bony groove, at the
#unction of hori$ontal and vertical palate. The location of this neurovascular line varies
relative to the #?F.
• %hallow palatal vaults: Jmm from #?F
• &verage vaults: &4mm from the #?F
• 'igh vaults: &Jmm from #?F
)EN3%(
& memranous fold of skin or mucous memrane that supports or restricts the movement of a
part or organ.
& frenum is a mucous memrane fold containing muscle and connective tissue fires which
attaches the lip and cheek to the alveolar mucosa, gingiva and underlying periosteum.
 Types of freni,
.epending of site of frenum,
 ;abial frenum
 ;ingual frenum
9
 @uccal frenum
.epending on number,
 /ingle
 7ultiple
.epending on level of attachment of frenum,
Insertio mucosum: mucosal attachment of frenum
Insertio in mucosum fi(um: attached gingiva
Insertio in papillam: papillary
Papilla penetrating attachment
Types of frenum in primary dentition,
&. /imple
4. *ersistent tectolabial
5. /imple with appendix
6. /imple with nodule
(. .ouble
I. @ifid
J. Kith nichum
H. 4 or more variation at the same time
Evaluation of an aberrant frenum(
&. Aestibular depth
4. Kidth of attached gingiva
5. @lanching of frenum
6. 7arginal tissue recession
(. 7idline diastema (controversial)
E/A%INA#ION O) GINGI4A(
56 COLO3
Cormal colour, #oralpale pin2
Kithwithout melanin pigmentation
*roduced by its vascularity and modified by,
&. 9verlying epithelial layers
4. .egree and thic2ness of 2eratiniBed epithelium
5. *resence of pigment containing cells
)edder: !ncreased vascularityreduced 2eratiniBation
Pale: !ncreased 2eratiniBationreduced vascularity
*luish: #hronic inflammationvenous stasiscompression of epithelium by inflammatory tissue
reduced 2eratiniBation
/ite, 7arginal gingiva %gingivitis, ACD")
10
.iffuse gingiva %herpetic gingivostomatitis)
*atch+li2e %chemical irritation)
!nitially in acute inflammations, the colour may be red (inflammatory changes) to shiny gray to
dull gray (indicating necrotic changes)
+etallic pigmentation:
@ismuth, arsenic, mercury, blac2 line on gingiva
;ead, 0@urtonian line1 bluish reddeep blue
/ilver, violet marginal line
• #ause, absorbed metals are precipitated in perivascular areas as metallic sulfides into the
subepithelial connective tissue.
• *igmentation only occurs in areas of inflammation (since increased permeability of
irritated blood vessels permit seepage of metal into surrounding tissues)
• /ite, gingiva, inner surface of lips, at the level of occlusal line in chee2s, lateral border of
tongue
• Treatment, 8emoval of local irritating factors3 discontinuity of metal containing drugs3
topical application of concentrated peroxide to oxidiBe dar2 metallic sulfides.
,ndogenous pigmentation:
7elanin (Addison’s disease, *eutB+Fegher’s syndrome, Albright’s /yndrome, neurofibromatosis)
@ilirubin (Faundice)
>emoglobiniron
,(ogenous pigmentation:
#oal
7etal dust
#oloring agents
Tobacco
Amalgam
76 CON#O3 O) GINGI4A(
.epends on,
&. /hape of teeth
4. Alignment of teeth
5. ;ocation E siBe of proximal contact
6. .imensions of facial and lingual gingival embrasures
(. Dnderlying bone
Types,
• Cormally, scalloped and 2nife+edgedArcuate
• Accentuated (labially placed toothincreased mesio+distal convexity of tooth)
• $lathoriBontalthic2ened (lingual version)
• 8olled8ounded marginsblunt papillae (periodontal disease)
• ?xaggerated scalloping (recession)
11
Stillman’s Cleft:
!t was first proposed by /tillman, &'4&.
!t is an apostrophe+shaped indentation extending from and into the gingival margin for varying
distances.
8ecently, it is thought to be a type of gingival recession.
#ause,
• 9riginally, thought to be due to occlusal trauma
• !t was later described as pathologic poc2ets in which the ulcerative process had extended
to the facial surface of the gingiva (@ox, &'(G). These repair spontaneously or persist as
surface lesions of deep periodontal poc2ets.
Types,
• /imple, cleavage in one direction
• #ompound, cleavage in more than one direction
McCall’s Festoon:
!t is a life+preserver shaped enlargement of the marginal gingiva (Tishler, &'4J).
86 S3)ACE #E/#3E O) GINGI4A( Peau d’orange
/tippling is the form of adaptive specialiBation of gingiva or reinforcement for function.
7icroscopically, it is produced by alternate rounded protruberances and depressions in the
gingival surface.
/ite, it is present on the attached gingiva and center of papilla. !t is less prominent on lingual
than buccal surfaces.
Age variations,
• Absent in infancy
• !ncreases with age
• .ecreases in old age
*rominence of stippling is directly proportional with the degree of 2eratiniBation. !t is a feature
of healthy gingiva, and reduction or loss of stippling is a common sign of gingival disease.
!n chronic inflammation, the gingiva can be smooth and shiny (exudative changes) or firm and
nodular (fibrotic changes).
;eathery texture (hyper2eratosis)
*eels off (chronic desquamative gingivitis)
%mooth (senile atrophic gingivitis)
Peled (drug+induced gingival enlargement)
96 CONSIS#ENC$ O) GINGI4A(
12
"ingiva is normally firm and resilient. >istopathologically, gingival fibres, collagenous lamina
propria and contiguity with the mucoperiosteum of alveolar bone determine the consistency of
attached gingiva.
!n chronic inflammation, gingiva is soft E edematous when destructive changes are
predominant3 and fibrotic when reparative changes are predominant.
:6 &OSI#ION O) GINGI4A(
!t refers to the level at which the gingival margin is on the tooth. Cormally, it is &mm above the
#?F.
Recession is the exposure of the teeth by the apical migration of the gingiva.
8ecession is the displacement of the soft tissue margin apical to the C,-.
The more accurate term .marginal tissue recession/ was coined y +aynard 0 1ilson (2343".
#y!es (
• *athologic recession
• *seudorecession, !n labially positioned tooth, there may be less 2eratiniBed tissue on the
facial surface and gingival margin may be at the #?F, appearing as recession (7aynard
and 9chsenbien, &'J().
• Aisible recession, clinically visible
• >idden recession, covered by the gingiva
&ctual position of gingiva, !t is the level of the epithelial attachment on the tooth.
&pparent position of the gingiva, !t is the level of the crest of the gingival margin.
The severity of recession is determined by the actual position of the gingiva and not its apparent
position.
?tiology,
&. $aulty brushing
4. Tooth malposition
5. $riction (gingival ablation)
6. "ingival inflammation
(. Aberrant frenum
I. Airus
9ther contributing factors, T$9, orthodontic therapy, position of tooth in the arch, root+bone
angle, mesiodistal curvature of the tooth surface.
#linical significance,
/usceptibility to caries, abrasion, sensitivity, pulp hyperemia, accumulation of plaque E food
debris
#lassification of recession,
&. /ullivan E At2ins (&'IH),
• /hallow+narrow
• /hallow+wide
13
• .eep+narrow
• .eep+wide
4. 7iller’s #lassification (&'H(),
• #lass !, marginal tissue recession not extending upto 7"F3 no loss of bonesoft tissue in
interdental area.
• #lass !!, marginal tissue recession extending uptobeyond 7"F3 no loss of bonesoft
tissue in interdental area.
• #lass !!, marginal tissue recession extending uptobeyond 7"F3 loss of bonesoft tissue
in interdental area3 malposition of tooth.
• #lass !A, marginal tissue recession extending uptobeyond 7"F3 severe loss of bonesoft
tissue in interdental area3 severe tooth malposition.
,LEEDING ON &O,ING(
Appears earlier than a change in colour. !t is a more ob-ective sign that requires less sub-ective
estimation.
#auses,
&. #hronic inflammation
4. 7echanical trauma (brushing, toothpic2s, food impaction)
5. /olidhard foods
6. Acute gingival inflammations
(. Ait #L deficiency
I. @lood dyscrasia (hemophilia, purpura, leu2aemia, multiple myeloma)
J. .rugs (Aspirin, anticoaugulants)
7ethod, *robe is carefully inserted into the bottom of poc2etsulcus E gently moved laterally
along the poc2et wall. 8e+chec2 after 5G seconds.
According to Amritage et al (&''I), bleeding is an important ris2 predictor for loss of
attachment.
S3&&3A#ION+E/3DA#ION(
The presence of an abundant number of neutrophils in the gingival fluid transforms it into a
purulent exudate (Amritage et al, &''I). !t is not a good indicator of progression of periodontitis
since it is present in a very low percentage of sites with disease (5+(M).
.etection, *lacement of the ball of the index finger along the lateral aspect of the marginal
gingiva and applying pressure in a rolling motion toward the crown.
A,SCESS(
&scess is a localiBed accumulation of pus.
A periodontal ascess is a localiBed accumulation of pus within the gingival wall of a
periodontal poc2et. !ts diagnosis requires correlation of history, clinical and radiographic
14
findings. The suspected area should be probed carefully and continuity of the lesion with the
gingival margin is clinical evidence that the abscess is periodontal.
The principal differences between a periodontal and gingival ascess are location and history.
The gingival abscess is confined to the marginal gingiva, and often occurs in previously disease+
free areas. !t is usually an acute inflammatory response to forcing of foreign material into the
gingiva.
To distinguish between periodontal and periapical abscess, evaluate vitality of tooth. !f tooth is
non+vital, it may be periapical abscess. >owever, at times, a periodontal abscess may occur in a
previously non+vital tooth. #ontinuity of lesion with gingival margin may be by a periodontal
abscess. *resence of extensive caries may lead to periapical abscess. 8adiographic evaluation
may, at times, aid in evaluating the origin of abscess.
A##AC"ED GINGI4A(
.efinition, !t is the distance between 7"F and the pro-ection on the external surface of the
bottom of the gingival sulcus or the periodontal poc2et.
1idth of keratini$ed gingiva5 &ttached gingiva 6 +arginal gingiva
1idth of attached gingiva57otal width of 8ingiva from the margin to the +8- 9 Pocket depth
+ethods of determination:
2. Tension test (when stretching of lip or chee2 induces movement of the free gingival
margin, gingiva is considered inadequate).
!. *ushing ad-acent mucosa coronally with a dull instrument.
:. *ainting mucosa with /chiller’s *otassium !odine solution.
;. ;ocal anaesthesia
!n maxillary anteriors, 5.( + 6.( mm
mandibular anteriors, 5.5 N 5.' mm
!n premolars (maxillary), &.' mm
!n premolars (mandibular), &.H mm
#ension test
• Application of tension at the 7"Fn by retracting chee2, lip E tongue (upwards, outwards
E downwards) to tighten alveolar mucosa and test for the presence of attached gingiva.
• Area of missing attached gingiva is revealed when alveolar mucosa and frenum are
connected directly to free gingiva.
*D8*9/?,
&. To detect adequacy of A"
4. To locate frenal attachment and their proximity to free gingiva
5. To identify 7"Fn
15
*89#?.D8?,
<acial, 8etract chee2s and lips laterally away . Katch 7"Fn. 7ove the lips up, down and across,
creating tension at 7"Fn.
=ingual, >old mouth mirror to tense mucosa of floor of mouth, gently retract side of tongue so
7"Fn is clearly visible.
9@/?8AAT!9C/,
• @lanching at 7"Fn
• $renal attachment
• 8ecession
• 7ovement of free gingival margin3 A"

&OC;E#(
The pathologic deepening of gingival sulcus is a poc2et.
Considerations:
&. ;ocation of poc2et on tooth surface
4. *oc2et depth
5. ;evel of attachment on root
6. Type of poc2et
(. *oc2et configuration
%igns 0 symptoms:
&. #olour changes
4. 8olled edge
5. @leeding, suppuration
6. /ometimes painless3 at times dull+gnawing pain or sensation of pressure or itching
(. $oul taste
I. /entisitvity to hot and cold
Proing depths:
2. *iologic/histologic depth:
!t is the distance between the gingival margin and the base of the poc2et (the coronal end
of the F?).
!. Clinical proing depth:
!t is the distance to which an ad+hoc instrument (probe) penetrates into the poc2et.
7ypes of pockets:
• 7rue pocket (due to periodontal disease)
• Pseudopocket (due to inflammation of gingiva)
• %upraony pockets, !t is a true poc2et with base of poc2et coronal to underlying alveolar
bone crest. #linically, after probe is inserted into the gingival sulcus and when lateral
pressure is applied, if soft tissue resistance is felt, then it is diagnosed as suprabony
poc2et.
16
• Infraony pocket: it is a true poc2et with base of poc2et apical to the level of ad-acent
alveolar bone. #linically probe is inserted into the gingival sulcus and when lateral
pressure is applied, hard tissue resistance is felt.
• Active
• !nactive
• $ibrous
• ?dematous
&robing techni<ue(
*robe is to be placed parallel to vertical axis of tooth and 0wal2ed1 circumferentially around
each surface.
"utta percha points or calibrated silver points with radiographs can also be used.
!n clinical practice, conventional periodontal probes are widely used to obtain two important
measurements, probing depth (*.) and clinical attachment loss (#A;).
• *. is defined as the distance from the gingival margin to the base of the probeable
crevice.
*robing depth measurements are clinically important since they provide a useful overall
assessment of the depth of periodontal poc2ets which are the principal habitats of periodontal
pathogens. !n addition, *. measurements can be rapidly recorded and give a good assessment of
the distribution of periodontal problems within a given patient. They are an essential component
of a complete periodontal examination.
• >ertical proing attachment loss (P&="/Clinical attachment loss (C&=":
#A; is the distance from the cementoenamel -unction to the base of the probeable crevice.
8ingival margin is located on anatomic crown:
*A;O *. N (gingival margin to #?F)
8ingival margin coincides with C,-:
*A;O*.
8ingival margin is located apical to C,-, i.e. recession:
*A;O *. < (gingival margin to #?F)
!n single+rooted teeth, ;9A occurs only vertically. !n multirooted teeth, loss of attachment can
also occur horiBontally, indicating furcation involvement.
17
#hanges in *A; can be due only to gain or loss of attachment E afford a greaterbetter indication
of the degree of periodontal destruction. /hallow poc2ets attached at the apical third of root are
more destructive than deep poc2ets attached at the middle third of root.
#A; assessments are more difficult to accurately measure, but they give a better overall estimate
of the amount of damage to the periodontium than do *. measurements. !n prospective studies,
#A; measurements are the most valid method of assessing treatment outcomes.
*robing depth as well as loss of attachment (;9A) can be measured by manual probing or by
more sophisticated, automated, computer+lin2ed, pressure+sensitive periodontal probes.
%anual &robing(
Aertical *A; can be measured manually with a millimeter+graded probe. The probe is held with a
light pencil grasp so it can be moved and directed with minimal force. The end of the probe is
then placed against the enamel surface coronal to the margin of the gingiva, so that the angle
formed by the wor2ing end of the probe to the long axis of the tooth crown is approximately 6(
degrees. Kith slightly decreased probe+crown angle, the distance between the free gingival
margin and the #?F is measured.
Automated !robing(
@ecause probing force is one of the ma-or variables affecting the extent of probe penetration,
several automated or controlled+force probes have been introduced. The >unter+*robe is a
disposable device calibrated to insert the probe tip with a force of 4Gg. The $oster+7iller probe is
a controlled force device capable of automatically recording the position of the #?F. 9f the
controlled+force probes, the $lorida *robe is the most widely used. #omparative reproducibility
data do not show ma-or differences between conventional and controlled+force probes. 8eddy et
al (&''J) showed that both manual and controlled+force probes can provide measurement to
within less than & mm of error.
7ultiple studies indicate that, in the hands of experienced practitioners, #A; measurements
ta2en with conventional periodontal probes at different visits are repeatable to within & mm
more than 'GM of the time %"reenstein, &''J3 Armitage, &''I). Dnder clinical conditions,
comparable repeatability values have been obtained with computer+lin2ed, controlled+force
electronic periodontal probes.
?lectronic probes have the advantage of controlling insertion forces and automatically recording
clinical information into a computer %"reenstein, &''J3 Armitage, &''I). !n addition to
controlled insertion force, electronic probes have a better resolution than standard manual
probes. This feature is important since it ma2es it theoretically feasible to detect smaller changes
in clinical attachment levels than are possible with manual probes. $or example, in one study,
untreated chronic periodontitis patients were examined over a I+month period using a prototype
of an automated probe which has an accuracy of G.4 mm. !t was found that if a threshold of G.6
mm was used to indicate that a change in attachment level had occurred, the prevalence of sites
that had progressed was 4'M over the I+month period. !f a large threshold (i.e., 4.6 mm),
comparable to that achievable with a manual probe was used, only 4M of the sites were
18
determined to have experienced additional attachment loss %Feffcoat, 8eddy3 &''&). 7anual
(conventional) periodontal probes are highly satisfactory for the performance of routine
periodontal examinations. #omparable results are obtained when either manual or electronic
probes are used. /ome practitioners prefer electronic over conventional periodontal probes,
especially because of the automatic data entry feature afforded by these devices.
The main drawbac2 of electronic probes is their tendency to underestimate *. and #A;
measurements in untreated patients %"reenstein, &''J). !n such patients, the presence of
subgingival calculus can interfere with probe insertion. To minimiBe this problem,
reproducibility of clinical measurements ta2en with controlled+force probes can be improved by
using a 0double+pass1 method (i.e., measuring each site twice) %"reenstein, &''J3 Armitage,
&''I3 9sborn et al, &''G). !n treated patients, this reproducibility problem is not as great.
!ndeed, in treated patients, lower standard deviations of replicate single+pass clinical
measurements have been obtained with controlled+force compared to conventional probes.
.epth of penetration of probe depends on
• /iBe of probe
• $orce of introduction
• .irection of penetration
• 8esistance of tissues3 inflammatory cell infiltrate
• #onvexity of crown, anatomic factors
Dimensions of the !eriodontal !robe(
.ifferent shapes and siBes of periodontal probes yield different penetration depths into
periodontal tissues. *eriodontal probes with a point diameter of G.6+G.( mm have been used
successfully. 7ost probes are circular in cross+section. The probe should be thin enough to reach
the 0true1 attachment level under healthy conditions, with F? and 0resistant1 connective tissue,
but will penetrate the less resistant, inflamed connective tissue in diseased poc2ets and over+
estimate loss by G.(+&.G mm. A thic2er periodontal probe will not reach the true attachment level.
A thin blade+shaped probe will give the most accurate result, but to access all the sites, it has to
be able to be rotated 5IGP (Axelsson, &'H4).
&robing forces(
The probe is inserted along the long axis of the tooth into the poc2et with gentle (approximately
4( g) force until resistance is met. 4(+g of force is necessary to indent the pad of the thumb about
&+4 mm. !n clinical application, what would be considered 0gentle1 insertion force, do not
penetrate apical termination of F?. According to some authors, forces of G.J( C have been well
tolerated E accurate %Aan der Aelden, &'J'). The tip of the probe has been assumed to identify
the level of the most apical cells of the dentogingival epithelium. This, however, is not the case
always (/aglie et al, &'J(3 *olson, &'HG).
*robe penetration depends on tissue inflammation. !n health, probe tip penetrates most coronal
intact fibres of connective tissue attachment (G.5 mm) into F? %;istgarten et al, &'JI). There may
be over9estimation (probe may penetrate beyond apical termination of dentogingival epithelium
due to inflammation) or under9estimation (reduction in inflammation after successful therapy
19
with concomitant deposition of new collagen prevents complete penetration of probe) of the true
poc2et.
&ositioning of the !robe(
7anual probing is sub-ect to measurement error because of variations in the angulation and site
of insertion of the probe and because of the difficulty in obtaining a fixed landmar2 as a
reference point. The probe should be 2ept as parallel as possible to the long axis of the root. The
tip should continuously follow the root surface, to prevent penetration of the poc2et epithelium
and connective tissue, resulting in underestimation of attachment loss. ?ach tooth is examined at
I locations, 7@, @, .@, .;, ;, and 7;. The probe may be angled approx. &GP in interproximal
areas.
,ONE SO3NDING+#ANSGINI4AL &O,ING(
!n order to arrive at a correct diagnosis with respect to the alveolar bone level, presence of
angular bony defects and interdental osseous craters, etc, 0sounding1 may be done.
*rocedure,
&. ;ocal anaesthesia
4. Tip of probe is inserted into the poc2et and forced through supraalveolar connective
tissue to ma2e contact with the bone and the distance from #?F to bone level is assessed.
)3CA#ION IN4OL4E%EN#(
.efinition, !nvasion of bifurcationtrifurcation of multirooted teeth by periodontal disease.
The difficulty, and sometimes the impossibility, of controlling plaque in furcations are
responsible for the presence of extensive lesions in this area.
#ontributing etiological factors,
*eriodontal disease
T$9
.ental caries
Anatomical factors, root trun2 length, root morphology, cervical enamel pro-ections, enamel
pearls, accessory pulpal canals
"lic2man’s classification,
"rade &,
• incipient or early bone loss3
• suprabony poc2et with primarily soft tissue involvement3
• no radiographic evidence3
• clinically a 0catch1 is felt with the probe.
"rade 4,
• partial bone loss3 furcation lesion is 0cul+de+sac1 , can affect more than one furcation of
the same tooth3
• definite horiBontal component, with or without vertical component3
20
• partial penetration of probe.
"rade 5,
• total bone loss with through+and through opening of the furcation3
• furcation entrance is not visible clinically3
• complete penetration of probe.

"rade 6,
• total bone loss with through+and through opening of the furcation3
• furcation entrance is visible clinically3
• complete penetration of probe.
9ther furcation systems may measure the horiBontal ("oldman E #ohen, &'IH3 $edi, Aernino E
"ray, 4GGG3 /taffelino, &'I'3 ;indhe, &'H'3 >amp, Cyman E ;indhe, &'J(3 "lic2man, &'(5) or
vertical (Tarnow and $letcher, H63 8icchetti, &'H4) components of furcation involvement.
$or accurate diagnosis, a slim, curved instrument is necessary, eg., the double+ended curette,
"oldman+$ox Co. 5 or a furcation probe li2e Cabers 4C probe.
=)urcation arro>? (>arde2opf et al, &'HJ)
!t is a small triangular radiographic shadow seen across mesial or distal roots of maxillary
molars. !t is empirically associated with proximal furcation involvement. !t is generally
associated with grade !! and !!! furcations. According to .avid .eas (4GGI), furcation arrow is
not clinically reliable. Khen furcation arrow is present, only JGM of times invasion is present3
and when furcation is involved, furcation arrow is seen only in 6GM of cases.
@AS#ING DISEASES(
Any gradual loss of tooth substance characteriBed by the formation of smooth, polished surfaces,
without regard to the possible mechanism of this loss.
&ttrition, is the physiologic wearing of tooth substance resulting from functional contacts with
opposing teeth. !t typically affects the incisal and occlusal surfaces. These are highly polished
surfaces that appear on marginal, transverse and oblique ridges, and on cusps and restored
surfaces.
&rasion, refers to the pathologic loss of tooth substance induced by mechanical wear other than
that of mastication. !t results in saucer shaped or wedge+shaped indentations with smooth, shiny
surface. Abrasion starts on exposed cementum rather than on the enamel. /harp 0ditching1 is
seen around #?F.
#auses,
• 9verBealous tooth brushing with abrasive dentifrice
• Action of clasps
• >olding ob-ects
21
,rosion, is a chemically induced loss of tooth substance that occurs primarily through acid
dissolution. !t is a sharply defined wedge+shaped depression in the cervical area of the facial
tooth surface. The long axis of eroded area is perpendicular to vertical axis of tooth. !t generally
starts on enamel.
#auses, decalcification by acid beverages or citrus fruits, friction, acid regurgitation.
&fraction, *athological loss of hard tooth substance by biomechanical loading forces. Angular
or wedge+shaped defects that occur at the #?F of affected teeth as a result of flexure and eventual
fatigue of enamel and dentine. The prismatic structure of enamel is strong under compression,
but vulnerable in areas of tension. The occlusal loads which generate cervical flexure may
disrupt >A crystal bonds, and result in microfracture and eventual loss of associated enamel.
?entoalveolar alation, forceful friction between soft and hard tissues %/ognnaes).
&O/I%AL CON#AC#S(
Tight
9pen, $ood lodgement+ gingival inflammation+ disease
$aulty Abnormal, .ifficulty in brushing, accumulation of plaquecalculusN gingival
inflammation + disease
E%,AS3ES(
Type !, "ingival marginpapillae fill the embrasure completely %dental floss)
Type !!, ;ittle soft tissue loss
Type !!!, #omplete papilla loss %uni+tufted toothbrush)
!n 5AAB2 #arno> and Nordland proposed a classification system for loss of papillary height
utiliBing the following identifiable anatomic landmar2s,
&. !nterdental contact point.
4. The facial apical extent of the #?F.
5. The interproximal coronal extent of the #?F.
6. $our categories were identified,
NO%AL ( !nterdental papilla fills embrasure space to the apical extent of the interdental
contact pointarea.
CLASS I ( The tip of the interdental papilla lies between the interdental contact point and the
most coronal extent of the #?F. (/pace present but #?F not visible).
CLASS II ( The tip of the interdental papilla lies ator the apical to the interproximal #?F but
coronal to the apical extent of facial #?F. (!nterproximal #?F visible)
CLASS III ( The tip of the interdental papilla lies level with or apical to the facial #?F.
#A3%A )O% OCCL3SION(
.efinition, Khen occlusal forces exceed the adaptive capacity of the tissues, tissue in-ury results.
The resultant in-ury is termed T$9.
Types, *rimary and /econdary
22
#linical features,
&. ?xcessive tooth mobility3 pain
4. !nfrabony poc2ets
5. *athologic migration
6. "ingival recession
(. /tillman’s cleft7c#all’s festoon
I. $ood impaction
J. Kearing of teeth E appearance of facets
H. >ypersensitivity of teeth
'. Tenderness of T7F E muscles of mastication
&G. /mudging of articulating paper
&&. .ull percussion note
&4. Aibrations from fremitus
8adiographic features,
&. Kidening of *.; space
4. ;amina dura thic2ened
5. Aertical angular bony destruction
6. 8adioluscence E condensation of alveolar bone
(. @uttressing bone
I. 8oot resorption
7ethods of determination,
2. <remitus test:
!t is the measurement of the vibratory pattern of the teeth when the teeth are placed in the
contacting positions and movements are made.
To measure fremitus, dampened ungloved index finger is placed along the buccal and
labial surfaces of maxillary teeth (or the tooth in question) E the patient is as2ed to tap the teeth
together in maximum intercuspation (#9) E grind systematically in the lateral excursive
movements (lateral fremitus). Aibrations are perceived. !t is easier to detect fremitus in the
maxillary teeth than the mandibular teeth.
#lass ! fremitus, 7ild vibrations or movements detected
#lass !! fremitus, ?asily palpable vibrations but no movements detected
#lass !!! fremitus, 7ovements visible with na2ed eye
4. 9cclusal registration stripsarticulating paper
5. Auditory test, !n centric relation, there is a distinct ringing sound during tooth contact.
@ut in T$9, with deflection present, sound is dull and imperceptible.

&A#"OLOGIC #OO#" %IGA#ION(
.efinition, refers to the tooth displacement that results when the balance among the factors that
maintain physiologic tooth position is disturbed by periodontal disease.
23
$actors affecting tooth position,
&. Tooth morphology
4. #uspal inclination
5. *hysiologic tendency toward mesial migration
6. Cature E location of contact points
(. *roximal, incisal E occlusal attrition
I. Axial inclination of teeth
#auses,
• Kea2ened periodontal support
• Dnreplaced missing teeth
• T$9
• *ressure from tongue
• *ressure from granulation tissue of *.; poc2ets (the teeth may return to their original
position after poc2ets are eliminated, but if more destruction has occurred on one side of
tooth, healing tissues tend to pull in the direction of lesser destruction+ >irschfeld, &'55).
)OOD I%&AC#ION(
!s the forceful wedging of food into the periodontium by occlusal forces.
/equelae of food impaction,
• $eeling of pressure E urge to dig
• Aague pain that radiated deep in the -aws
• "ingival inflammation
• @leeding
• $oul taste
• "ingival recession
• Abscess formation
• /ensitivity to percussion
• .estruction of alveolar bone
• 8oot caries
#ontour of occlusal surface (due to marginal ridges E grooves), .eflects food away from
interproximal space +as teeth wear down+ flat surface+ wedging effect of opposing cusp.
;ateral food impaction, lateral pressure from lips, chee2s and tongue, forces food
interproximally
*lunger cusp, #usp that tend to forcibly wedge into interproximal embrasures.
!nterdental bone defects, *ressure E irritation from food impaction contribute to inverted bone
architecture.
#OO#" %O,ILI#$(
24
The movement of a tooth in its soc2et as a result of an externally applied force. Tooth mobility is
seen as one of the measures useful in evaluating the health of the periodontal tissues (*richard,
&'J'). The most common clinical method used to examine tooth mobility is to press the tooth in
a horiBontal or vertical direction with a finger, or with the handle of the blunt ends of two metal
instruments (*richard, &'J'). This method is imprecise and its value depends on the observers’s
s2ill and experience.
#auses,
• ;ocal $actors,
&. @one lossloss of tooth support (periodontitis, T$9, endodontic problems)
4. >ypofuction
5. *eriapical pathology
6. After periodontal therapy %Cyman E ;indhe (&'JI), *ersson (&'H&))
(. 9rthodontic forces3 heavy fuctional loads (from prosthetic appliances)
I. *arafunctional habits (bruxism, clenching)
J. *athologies (tumours, cysts, osteomyelitis)
H. Traumatic in-uries to dentoalveolar unit
'. Tooth morphology
• /ystemic causes,
&. Age, progressively increases
4. /ex E 8ace, femalesQmales3 Cegroes more
5. 7enstrual cycle, $riedman (&'J4) observed increased horiBontal tooth mobility
during 6
th
wee2 of menstrual cycle.
6. 9ral contraceptives (.orothy, &'H&)
(. /tress
I. Cutritional deficiency
J. *regnancy (7obility increases from 4
nd
to H
th
month progressively)
H. #ircadian rhythm (more during early morning E progressively decreases)
Tooth mobility measuring devices,
&. *eriodentometer (7uhleman, &'(&)
4. *ersson E /venson’s devices (&'HG)
5. *eriotest (/chultB, &'HJ) %!t helps in ob-ective assessment of tooth mobility. The tooth is
rapidly percussed &I times (four times per second) and then the rebound attenuation
patterns emanating from the tooth are electronically recorded).
Aalues are calculated as,
+H to <', #linically firm teeth
&G to &', *alpable mobility
4G to 4', Aisible mobility
5G to (G, mobility in response to lip and tongue pressure
6. *eriodontal pulse
The three+dimensional physiological tooth movement synchroniBed with the heartbeat is called
periodontal pulsation (.iemer, &'I5, &'II3 LRrber, &'J&a,b3 !garashi et al., &'H&). !t is produced
by changes in the calibre of periodontal vessels due to cardiac pulsation. !t has been suggested
that the degree of periodontal pulsation reflects the condition of the microcirculation and the
25
pathophysiological properties of the periodontal tissues (>ofmann and .iemer, &'II3 LRrber,
&'J&a). The measuring device consisted of a small magnet attached to the tooth and an
amorphous sensor that was used to detect displacement of the tooth without actually contacting
it.
Tooth mobility indices,
&. 7iller’s index (&'5H)
!, first distinguishable sign of movement
!!, movt. of tooth which allows crown to deviate within &mm of its normal position
!!!, easily noticeable E allows tooth to move more than & mm in any direction or to be
rotated or depressed in the soc2et
4. 7odified 7iller’s index
/cores, G, S, &, &S, 4S, 5 are utiliBed
5. *richard’s index (&'J4)
&, /light mobility
4, 7oderate mobility
5, ?xtensive mobility in a lateral or 7+. direction combined with vertical displacement
in alveolus
6, /igns can be used for added refinement
6. Kasserman’s index (&'J5)
&, Cormal
4, /light mobility less than &mm of buccolingual movement
5, 7oderate upto 4 mm of buccolingual movement
6, /evere mobility more than 4 mm movement
(. "lic2man’s index (&'J4)
Cormal mobility
*athologic mobility
"rade !, /lightly more than normal
"rade !!, moderately more than normal
"rade !!!, severe mobility with vertical displacement
The clinical importance of increased tooth mobility is frequently overestimated. !t has clearly
been shown in animal experiments that, if plaque+induced inflammation is controlled, increased
tooth mobility has no effect on the level of the connective tissue attachment (?ricson and ;indhe,
&'JJ). >ypermobility of tooth does not necessarily mean that it has a poor prognosis, and the
mobility frequently persists after successful periodontal treatment (;indhe and Cyman, &'J(,
&'H6). Cevertheless, increasing tooth mobility over time should alert the clinician to a possible
deterioration of periodontal support, and such teeth require careful evaluation for loss of clinical
attachment.
ESID3AL IDGE
26
Seibert’s Classification:
• #lass !, loss of faciolingual width, with normal apicocoronal height
• #lass !!, loss of ridge height with normal width
• #lass !!!, loss of both height E width
DEN#AL ES#OA#IONS
• 9verhanging restorations and subgingival margin placement play an important role in
providing an ecological niche for periodontal pathogens.
• ;eads to increased plaque accumulation, inflammation, impinge interdental papilla,
encroach biologic width and attachment loss
"$&ESENSI#I4I#$
• ?entine hypersensitivity is characteri$ed y short, sharp pains arising typically when
thermal, evaporative, mechanical or osmotic stimuli are applied to the e(posed dentin
that cannot e e(plained y any other form of dental defect or pathology.
Etiology and !redis!osing factors(
&. "ingival recession.
4. ;oss of enamel
5. .enudation of the root surface by loss of the overlying cementum and periodontal tissue
6. #hronic trauma from faulty tooth brushing
(. Acute chronic inflammatory gingival E periodontal diseases
I. $ollowing surgical periodontal treatment
#heories Of Dental "y!ersensitivity
&. .irect innervation of dentin
4. 9dontoblast as receptor
5. Ceural theory
6. The odontoblastic transduction theory
(. >ydrodynamic theory
Stimuli 3sed #o Assess Dentine "y!ersensitivity
7echanical (tactile) stimuli
• ?xplorer probe
• #onstant pressure probe (:eaple)
• 7echanical pressure stimulators
• /caling procedures
ChemicalCosmoticD Stimuli
• >ypertonic solutions (Ca#l)
• "lucose, /ucrose E #alcium chloride.
Electrical stimulation
• ?lectrical pulp tester
• .ental pulp stethoscope
Eva!orative stimuli
• #old air blast
• :eh air thermal system
• Air -et stimulator
27
• Temptronic device(micropressor temperature controlled air delivery system)
#hermal stimuli
• ?lectronic threshold measurement device
• #old water device
• >eat
• Thermoelectric devices(@iomet thermal probe)
• ?thyl chloride
• !ce stic2.
S#AINS
?epending on its origin:
• ?ndogenous
• ?xogenous
• !ntrinsic
• ?xtrinsic
!ntrinsic stains,
&. Convital tooth (brownish red, bluish blac2)
4. .entine exposure (yellowish brown)
5. $luorosis (whitish opaque to brownish)
6. Tetracycline7inocycline stains (fluorescent yellowish to grayish brown)
?xtrinsic stains
• Tobacco3 coffee3 tea (brown)
• #hlorhexidine3 stannous fluoride (brown)
• "ram+positive rods eg @ melaninogenicus (blac2 line )
• #hromogenic bacteria (flavobacter etc) (greenoramge stain)
E#IOLOGIC )AC#OS(
• ;ocal factors,
&. *rimary, plaque
2. /econdary, (plaque retentive factors)
• #alculus
• #aries
• #ontacts
• T$9
• Aberrant frenum
• 8educed width of attached gingiva
• Tension test
• $aulty restoration (overhangs, defective margins, unpolished
restorations)
• $aulty toothbrushing
• Tobacco, smo2ing
• *oor oral hygiene
28
• >abits

• /ystemic factors, /ystemic diseases and conditions
CLINICAL &EIODON#AL SCEENING E/A%INA#ION(
The *eriodontal /creening and 8ecording (*/8) ?xamination was developed in order to
streamline the data gathering and record2eeping for screening periodontal examination. The */8
?xam is patterned after the #*!TC of the K>9. This exam is completed with a periodontal
probe that has a ball+end tip and a blac2 coloured band from 5.(+(.( mm. I sites are examined
per tooth and a score for each sextant is determined and recorded.
*/8 #odes,
#ode G, *robing is less than 5.(mm (colour band is completely visible)3 no bleeding, calculus, or
defective restorations3 only preventive care required.
#ode &, colour band is completely visible3 no calculus or defective restorations3 bleeding is
present at gingival margin3 proper oral hygiene.
#ode 4, colour band is completely visible3 detectable calculus andor defective restorative
margin3 removal of plaque, calculus3 correction of plaque retentive factors3 oral hygiene
instructions.
#ode 5, colour band is partially submerged in the poc2et3 indicates comprehensive periodontal
examination and charting for the sextant in question3 4 or more sextants with a score of 5
indicates a full mouth examination and charting.
#ode 6, colour band on the probe is completely submerged at one site3 indicates a comprehensive
full mouth periodontal examination and charting.
#ode =, an asteris2 is added to the numerical sextant score when furcation involvement, mobility,
mucogingival problem, or recession is present.
DISCLOSING AGEN#S
A disclosing agent is a preparation in liquid, tablet or loBenge which contains a dye or other
coloring agent. !t is used for identification of bacterial plaque.
*urpose,
*ersonaliBed patient instruction E motivational aid
/elf+evaluation by patient
To evaluate effectiveness of oral hygiene maintenance
$or plaque indices
!n research studies with regard to effectiveness of plaque control devices li2e toothbrushes and
dentifrices, etc.
29
Agents used for disclosing plaque,
a) !odine preparations
b) 7ercurochrome preparations
c) @ismar2 @rown (?aslic2’s disclosing solution)
d) 7erbromin
e) ?rythrosine, $.E# Co. 5Co. 4H
f) $ast green, $.E# Co.5
g) $luorescin, $.E# yellow no. H (used with special DA light to ma2e the agent visible)
h) Two+tone solutions, $.E# green Co. 5, $.E# red no. 5 (it mainly stains thic2er (older)
plaque blue E thinner (newer) plaque red.
i) @asic $uschin
S#3D$ %ODELS
To study occlusion, relation of teeth, edentulous sites (for implants), for splinting, preparation of
acrylic plates, for treatment planning, communication, for record purposes.
LA,OA#O$ IN4ES#IGA#IONS
"aemoglobin
7ales, &6+&Hgmdl3 $emales, &4+&Igmdl
/ignificance, if reduced, hampers healing3 ris2 of syncope
,C count(
7ales, 6.I+I.4 millionscumm
$emales, 6.4+(.6 millionscumm
Decreased: anemia, dietary def., pregnancy, one marrow failure, hodgkin@s disease, multiple
myeloma, hemogloinopathies, renal dis., collagen vascular dis.
Increased: CAP?, C'?, polycythemia vera
@,C count(
IGGG+&&GGG cumm
.ecreased in, reduced defence
!ncreased in, infections, leu2aemia
&latelet Count(
&,(G,GGG+6,GG,GGGcumm
!f less than & la2hcumm, surgery cannot be done
,leeding time(
.u2e’s method, T ( mins
*rolonged, thrombocytopenia, leu2aemia, liver disease, drugs(C/A!.s,warfarin, strepto2inase,
anticoagulants), .!#, collagen vascular dis., connective tissue dis.

Clotting time(
#apillary tube method, &+J min
Lruse and 7oses method, 4.(+( mins
30
;ee and Khite method, (+&G mins
*rolonged, >emophilia, fibrinogen deficiency
&rothrombin time C&#D(
Uuic2 7ethod, &G+4G s
.eficiency of factor !!, A, AA, V
*rolonged, ;iver disease, fibrinogen deficiency, vit Ldef., .!#, massive transfusion
Activated !artial thrombo!lastin time CA&##D(
5G+6G s
.eficiency of factor !!, A, A!!!, !V, V, V!, V!!
*rolonged, cirrhosis, .!#, coumarin, heparin, vit L def., clotting factor deficiency
International Normalised atio CIND(
!t is used only to assess the control of oral anticoagulant treatment. !t is the ratio of patient’s *T
to a normal control based on an international reference thromboplastin which ensures
standardiBation of anticoagulation between different centers. !C8 should generally be less than
4.G. $or simple surgical procedures, !C8 less than 4.( is generally safe.
Glucose levels
$asting levels, IG+&GG mgdl
*ost prandial, T&6G mgdl
!ncreased in .iabetes
/ignificance, nutrient for bacterial growth, reduced healing
lycated !emoglobin "#b$%c&
6+IM, Cormal
TJM, good diabetic control
J+HM, moderate diabetic control
QHM, poor diabetic control (poor response to surgery)
,IO&S$
It is the removal of tissue from the living organism for the purposes of microscopic e(amination
0 diagnosis.
T:*?/,
• ?xcisional biopsy(total excision of lesion)
• !ncisional biopsy (removal of small section of lesion)
• Ceedle aspiration (fine%$CA#)thic2 bore)
• ?xfoliative cytology(desquamative gingivitis, pemphigus, mucous membrane
pemphigoid, lichen planus)
&3NC" ,IO&S$
• (mm disposable punches
• #utting core of 5+6mm in depth
INCISIONAL ,IO&S$
• Co. &( blade
,3S" ,IO&S$
31
• /pecial bristled instrument to retrieve cells from the spinous layer of epithelium when
firmly rotated over the mucosal lesion.
#echni<ue
• Tissue should be perpendicularly incised with a scalpel
• 8emoved tissue should be handled carefully
• ;esion less than & cm+excisional biopsy
• ;arger than & cm, suspicious+incisional biopsy
• !n clinically most suspected area
• *art of lesion and part of clinically healthy mucosa should be included in the biopsy
• !n gingival biopsies, marginal and attached gingiva (effect of local irritants less li2ely to
be present) should be included
ingi'al biopsy and leukemia
• The existence of leu2emia is sometimes revealed by a gingival biopsy to clarify the
nature of a troublesome gingival condition and may indicate the extent of leu2emic
infiltration. >owever, they are not sufficient to warrant routine gingival biopsy in such
patients.
ADIOGA&"IC E/A%INA#ION(
The use of radiographic imaging as an aid in diagnosis and treatment of periodontal disease is
widely accepted.
The information supplied by radiographs includes,
&. 8oot length, root form, root proximity
4. ?stimates of remaining alveolar bone
5. 9sseous defects
6. *.; space
(. ;amina dura
I. *eriapical area
J. 8estorations, calculus
H. Type and density of alveolar bone
'. Anatomical landmar2s
Types of imaging,
!) #onventional,
A) !ntra+oral radiographs
&. *eriapical
4. @itewing
5. 9cclusal
Technique, @isecting angle *aralleleing cone
@) ?xtra+oral radiographs
9rthopantomogram and other extraoral views
!!) .igital,
.etectors,
32
&. /olid+state detectors (#harged+coupled device (##.) E #omplimentary metal oxide
semiconductor technology (#79/)
2. *hoto+stimulable phosphor (*/*) detector
• !ntra+oral radiographs
• ?xtra+oral, digital 9*" and other extraoral views
• /pecialiBed techniques,
&. .igital subtraction radiography (./8)
Khen two images of same ob-ect are registered and the image intensities of
corresponding pixels are subtracted, a uniform difference image will be obtained.
!f a change of follow+up image has occurred, it will show up as a righter area
when the change represents the gain and as a darker area when the change
represents loss. /ubtraction images allow detection of mineral changes of as little
as ( M.
4. Tuned aperture computed tomography (TA#T)
TA#T is built on basic principles of tomosynthesis by shifting and combining a
set of basis pro-ections, arbitrary slices through the ob-ect can be brought into
focus. ?ach radiograph is ta2en from different angle relative to the ob-ect and the
receptor. !t is shown to improve the ability of observers to detect osseous defects
around implants.
5. #omputed Tomography (#T)
#T provides exquisite 5+. views, however, its ability to show very small details
remains limited. The application of #T imaging for periodontal diagnosis appears
to have an unfavorable cost+benefit ratio.
6. #omputer+assisted densitometric image analysis (#A.!A)
Aideo camera measures the light transmitted through a radiograph, and the signals
from the camera are converted into gray+scale images. The camera is interfaced
with an image processor and a computer that allows storage and mathematical
manipulation of the images.
!n the past decade, many advances have been made in radiographic imaging methods for
periodontal structures. Advanced direct digital (filmless) radiographic and computed
tomographic techniques have been developed to the stage where they are already being used on a
day+to+day basis by practitioners. !ntraoral radiographs, such as periapical films and vertical or
horiBontal bitewings, provide a considerable amount of information about the periodontium that
cannot be obtained by any other non+invasive means. >owever, there are limitations of
radiography li2e two+dimensional representation of three+dimensional ob-ect3 uncertainty
regarding the validity, accuracy and precision of quantitative measurements. Although valid
periodontal diagnoses cannot be made from radiographs alone, they are an essential component
of a complete periodontal examination.
The standard recommendation for the initial examination of a periodontitis patient was for many
years a full+mouth periodontal probing complemented by a full+mouth set of intraoral
radiographs. To decrease the radiation dose, 7olander et al (&''() proposed the use of an
orthopantomogram after the initial clinical examination, supplemented by a limited number of
33
periapical radiographs, depending on the severity and distribution of increased probing poc2et
depths, furcation involvements or various nonperiodontal findings.
#onventionally read periapical radiographs as well as orthopantomograms routinely
underestimate or overestimate the amount of bone loss (A2esson et al, &''4). The alveolar bone
level may be obscured, especially in vertical defects. >owever, if the available diagnostic
methods only detect &M (orthopantomogram) or 6M (periapical) of initial vertical lesions, no
radiographic method can really be preferred over the other one, despite the existence of a
statistically significant difference between the methods. !n deeper vertical lesions N confirmed by
later flap reflection N orthopantomogram readings were less accurate compared to periapical
radiographs. !nterexaminer variation is, however, reported to be considerable by both
radiographic methods.
!n addition, sequentially ta2en radiographs, when examined by eye, are able to reveal changes in
bone only after 5G to (GM of the bone mineral has been resorbed. /ubtraction radiography, on the
other hand, allows detection of changes in bone density as low as (M. Although subtraction
radiography detects changes after they have occurred, it is possible with this technique to detect
very small changes in alveolar bone that would go unnoticed with conventionally read films.
7any of the logistical problems initially associated with subtraction radiography are being
overcome. /oftware programs have been developed to correct for subtle differences in contrast,
pro-ection geometry, and other repeatability errors. /tandardiBation of film positioning and
angulation can be achieved by using a cephalostat or custom+made positioning devices. $uture
development of subtraction radiography techniques promises to have a profound impact on the
diagnosis of periodontal diseases. !t is of interest that there is approximately an HGM
concordance or agreement between probing and radiographic methods in identifying sites that
have lost attachment.
The discussion about the best radiographic technique for periodontal diagnosis is also driven by a
concern to offer diagnostic information with the least amount of radiation dose exposure.
According to Liefer et al (4GG6), the dose of a digital orthopantomogram corresponds to that of
&6 intraoral direct digital radiographs. >owever, the radiation dose of an orthopantomogram was
considerably lower than that of a film+based system. 9ther factors, such as comfort for patient,
ease of image handling, costs, diagnostic information of nonperiodontal findings, may favor
digital orthopantomogram. Kith further improvement of digital panoramic radiography and
digital sensors for periapical images, issues related to the radiation dose will become increasingly
less critical. >owever, the reality in a daily practice environment will ultimately determine the
use of improved radiographic techniques, due to better patient comfort, more detailed diagnosis,
less radiation dose, and W or reduced cost.
@y increasing the focusNs2in distance, using a fast film, and a collimation down to the shape of
the film or sensor, the radiation dose to the patient can be considerably reduced. The use of film
holders can improve the reproducibility and accuracy of dental radiographs. The paralleling
technique has a better performance compared to the bisecting technique (7cLinney, &'J4).
>owever, a survey of the radiographic equipment and techniques used in dental practices in
?ngland and Kales revealed that only &HM of the responding dentists, always or often, used a
34
low+dosage technique combining ?+speed film and rectangular collimation (Tugnait, 4GG5). A
similar low number had been reported for /wedish dentists, 5JM of the general practitioners
routinely applied periapical film holders. The use of .+film and round collimation rather than ?+
film and rectangular collimation has been listed as one example of negligent customary practice
that violates the standard of care. These rather strict recommendations for ta2ing radiographs are
contrasted by the fact that only an estimated &M of the /wiss population’s total annual V+ray
dose stems from dental diagnostic procedures.
!n conclusion, performing conventional radiography with a low radiation exposure is possible by
using reliable low dose procedures3 these radiographic techniques, however, have not yet been
fully adopted by dental professionals. .igital imaging per se is not superior to film+based
radiographs in its ability to detect detailed periodontal structures.
S3&&LE%EN#AL DIAGNOS#IC #ES#S
/upplemental diagnostic tests can be used to perform two basic tas2s. The first is screening, i.e.,
to separate diseased from non+diseased patients. The second is to detect sites or patients
undergoing the progression of periodontitis. The second tas2 is more demanding than the first. !t
is also of greater importance since the clinician can easily separate healthy from periodontitis
patients based on customary clinical criteria.
DIAGNOSIS O) DISEASED &EIODON#AL &OC;E#S AND AC#I4E LESIONS(
&. *resence of subgingival biofilms and high levels of specific periopathogens subgingivally
4. 8ecent increase in *. and #A;
5. ;oss of compact bone from the alveolar crest
6. @9*
(. !ncrease in periodontal poc2et temperature
I. !ncrease in volume of "#$
J. *resence of purulent exudate
H. !ncrease in levels of mar2ers of periodontal disease activity, *"?4, 77*s, !;+&X in "#$
&resence of subgingival biofilms and high levels of s!ecific !erio!athogens subgingivally(
The sole etiologic factor for periodontal disease is the microbial challenge, and a prerequisite for
development of the diseased poc2et and an active lesion is the presence of subgingival
periopathogens. 7ost of the subgingival microflora is attached to the root surface as plaque
(biofilm), but the depths of the poc2et also harbor many non+attaching, motile species,
particularly various siBes and forms of spirochetes.
!n the biofilms, the microorganisms live in a well+organiBed symbiosis, supplied with nutrients
via microchannels through the plaque matrix and inaccessible to phagocytoBing leu2ocytes,
chemical plaque control agents, and antibiotics.
At &''I Korld Kor2shop in *eriodontics, it was concluded that human periodontitis is caused
mainly by &ctinoacillus actinomycetemcomitans, Porphyromonas gingivalis (exogenous,
transmissible pathogens) and *acteroides forsythus (endogenous, opportunistic pathogen).
8ecently, %achtei et al C5AAED showed that, in deep periodontal poc2ets, high levels of *
forsythus increase the ris2 for further loss of periodontal attachment seven.fold. 9ther species of
35
opportunistic endogenous periopathogens are *revotella intermedia and Treponema denticola.
The presence and levels of subgingival periopathogens can be evaluated by subgingival
sampling, with a sterile curette or paper point, and .CA probe analyses, conventional anaerobic
culture techniques, or chairside tests.
56 ,acterial culturing
!t has been frequently used as the reference method when determining the performance of
a new detection method. !t is the only current method capable of determining the invitro
antimicrobial susceptibility of periodontal pathogens. !t can also provide a quantitative
measurement of all ma-or viable microorganisms in the specimen. !t identifies only live
microorganisms, therefore strict sampling and transport conditions are essential. /ome of
the putative pathogens are fastidious and difficult to culture. The sensitivity of culture
methods is rather low. !t requires sophisticated equipment, experienced personnel and is
relatively time+consuming and expensive.
76 Direct microsco!y
Dar-field or &hase.contrast microsco!y has been suggested as an alternative to culture
methods on the basis of its ability to directly and rapidly assess the morphology and
motility of bacteria in the sample. >owever, most of the putative periodontal pathogens
(Aa, *g, @f, ?c) are nonmotile and therefore cannot be identified.
86 Immunodiagnostic methods
!mmunodiagnostic methods employ antibodies that recogniBe specific bacterial antigens
to detect target microorganism.
Advantages,
• .o not require viable bacteria
• ;ess susceptible to variation in sample processing
• ;ess time consuming
• ?asier to perform (than culture)
.isdvantages,
• Accuracy of immunodiagnostic tests depends greatly on the quality of the
reagents used
• "enerally show poorer detection limits than .CA probe and *#8
• ?xpensive
a& Indirect immunofluorescent assay "IF$&:
!t employs a secondary fluorescein+con-ugated antibody that reacts with the primary
antigen+antibody complex.
b& Direct immunofluorescent assay "DIF$&:
!t employs monoclonal and polyclonal antibodies con-ugated to fluorescien mar2er
that binds with bacterial antigen to form a fluorescent immunocomplex detectable
under a microscope.

c& Membrane immunoassay"('alusite&:
36
!t is a commercially developed, antibody+based sandwich enByme+lin2ed
immunosorbent assay fro detection of Aa, *g, * intermedia. !t involves lin2age
between the antigen and membrane+bound antibody to form an immunocomplex that
is later revealed through a colorimetric reaction. The sample wells are first coated
with antibodies against antigens specific for the target bacterial species. Antibody+
antigen reactions are then detected by adding enByme+lin2ed antigen+specific
antibodies to the sample wells, followed by the addition of enByme substrate.
d& Flow cytometry)Cytofluorograp!y:
!t is for rapid identification of oral bacteria and involves labeling bacterial cells from
a patient plaque sample with both species+specific antibody and a second fluorecscein
con-ugated antibody. The suspension is then introduced into the flow cytometer,
which separates the bacterial cells into an almost single+cell suspension by means of a
laminar flow through a narrow tube. The sophistication and cost involved in this
procedure precludes its wide usage.
e& ELISA(
!t is similar to other radioimmunoassay in principle, but an enBymatically derived
color reaction is substituted as the label in place of radioisotope. The intensity of
colour depends on the concentration of the antigen and is usually read
photometrically for optimal quantification. !t has been used to detect
periodontopathogens.
f& Latex agglutination(
!t is a very simple immunological assay based on the binding of protein to latex.
;atex beads are coated with species+specific antibody, and when these beads come in
contact with the microbial cell surface antigens or antigen extracts, cross+lin2ing
occurs3 its agglutination or clumping is visible usually in 4+( mins. @ecause of their
simplicity and rapidity, these assay have great potential for chairside detection or
periodontopathogens.

96 EnFymatic methods
,ANA test
@ forsythus, *g, Treponema denticola and capnocytophaga species share a common
enBymatic profile, since all have in common trypsin+li2e enByme. The activity of this
enBtme can be measured with the hydrolysis of the colour substrate C+beBoyl+dl+arginine+
4+naphthylamide (@ACA). Khen the hydrolysis ta2es place, it releases the chromophore,
X+naphthylamide, which turns orange red when a drop of fast granet is added to the
solution.
.iagnostic 2its have been developed using this reaction (e.g. *erioscan).
@ACA test can serve as a mar2er of disease activity. ;oesche et al showed that shallow
poc2ets exhibited only &GM positive @ACA reactions, while deep poc2ets (QJmm)
exhibited HG+'GM positive @ACA tests. @ec2 et al used @ACA as a ris2 indicator for
periodontal attachment loss.
>owever, it detects a very limited number of pathogens.

:6 DNA !robes(
37
.CA probes entail segments of single+stranded nucleic acid, labeled with an enByme or
radioisotope that can locate and bind to their complementary nucleic acid sequences with
low cross+reactivity to target organisms. The assay can rapidly test for multiple bacteria,
including Aa, *g, @ intermedius, # rectus, ? corrodens, $ nucleatum, and T denticola.
G6 estriction endonuclease analysis
8estriction endonucleases recogniBe and cleave double+stranded .CA at specific base
pair sequences. The .CA fragments are separated by electrophoresis, stained with
ethidium bromide and visualiBed with DA light. These .CA fragment patterns constitute
a specific 0fingerprint1 to characteriBe each strain.
E6 &olymerase chain reaction C&CD
*#8 involves a reiterate (repeated) amplification of a region of .CA flan2ed by a
selected primer pair specific for target species. The presence of specific amplification
product indicates the presence of the target microorganism.
Advantages,
• @est detection limits among nucleic acid based assays
• Co cross+reactivity under amplification conditions
• ?asy to perform
.isadvantages,
• 7ost *#8 assays use relatively small quantity of sample for the amplification
process. !f this quantity does not contain the targeted microorganisms, the assay
will not detect it.
• /ubgingival plaque mat contain enBymes which may alter the amplification
process.
*#8 has the potential for being an ideal detection method of periodontal pathogens.

ecent increase in &D and CAL
8ecent increases in *. and #A; are highly indicative of diseased poc2ets, active lesions, and
further attachment loss. *eriodontal disease is characteriBed by periods of quiescence and
exacerbation. This was demonstrated by "oodson et al (&'H4)3 in untreated sub-ects with existing
periodontal poc2ets, *A; was measured every month for & year. .uring this period, H5M of sites
did not change significantly, IM exhibited significant further ;9A, and &&M exhibited loss of
attachment.
!n individuals who are more susceptible to periodontal disease (smo2ers, those with genetic !;+&
polymorphism, and type & diabetes) more attachment loss may be seen.
Loss of com!act bone from the alveolar crest
;oss of compact bone from alveolar crest and diffused lamina dura indicates active bone
resorption. !t can be evaluated by periodic radiographs.
,O&
The absence of @9* is a reliable parameter of periodontal stability, provided that the assessment
procedure is standardiBed (;ang et al, &''G). Cumerous studies have shown that a 5GM
38
probability for future attachment loss may be predicted for sites that repeatedly exhibit @9*
(#laffey et al, &''G3 ;ang et al, &'HI).
;ang et al (&''&) showed an almost linear relationship between probing force and the percentage
of bleeding sites. At probing forces of greater than G.4(C (G.4(g), bleeding is the result of tissue
trauma, rather than a sign of inflammation.
@ecause the absence of @9* at G.4(C indicates periodontal stability, with a negative predictive
value of 'H+''M (;ang et al, &''G), this is the most reliable clinical variable for monitoring
patients’ progress in daily practice.
Increase in !eriodontal !oc-et tem!erature
9ne of the cardinal signs of inflammation includes calor (increase in temperature) which is
related to vascular changes. 8egeneration of most human periopathogens is retarded at increased
temperature. $ever is one of the nonspecific host response to local and general infections.
@ecause body temperature has long been used to evaluate the occurrence and severity of
infectious diseases, it seems logical to include measurement of the subgingival temperature in the
evaluation of periodontal poc2ets. This was the rationale underlying the innovation of a digital
0microthermometer,1 combined with a flat, thin periodontal probe, to identify diseased
periodontal poc2ets (Axelsson, &'H4). #ommercial devices have been introduced in recent years
(e.g. *erioTemp /ystem).
The *erioTemp /ystem has been described by Lung et al (&''G). The device is about the siBe
and shape of a periodontal probe and uses a small thermistor bead to determine temperature. The
probe tip housed in a casing with low thermal conductivity so that the probe itself does not alter
the ambient temperature. The probe is sensitive to G.&P# and assesses the temperature rapidly so
that the entire mouth (I sites per tooth, &IH sites for 4H teeth) can be evaluated quic2ly. The
device is lin2ed to a computer. Advanced disease is associated with a mean increase of G.I(P# at
a site.
The reference temperature used is the sublingual temperature which is generally higher than the
subgingival temperature. The temperature increases in deeper poc2ets (56.I P# in 6 mm poc2ets
to 5(.H P# in I mm poc2ets). !n a study by $edi and Lilloy (&''4), the temperature of the poc2ets
more than ( mm deep with @9* was &+&.H P# higher than that of poc2ets less than 5 mm without
bleeding. Cormal temperature is indicated by emission of a green light, slightly elevated
temperature by a yellow light, and mar2ed elevation of temperature by a red light. Khen the
device was used to predict ris2 of future *A; (>affa-ee et al, &''4), the most obvious difference
was observed for shallow sites (less than 6 mm). !t was found that H.'M of sites with @9* and
mar2edly elevated temperature lost 4.G mm of *A;, compared to only &.6M of sites that did not
bleed and were in the normal temperature range.
A study of the relationship of temperature to subgingival microflora revealed that elevated
subgingival temperature was associated with the presence of some putative pathogens li2e
Prevotella intermedia and Peptostreptococcus micros (>affa-ee et al, &''4).
Increase in volume of GC)
39
There is strong statistical association between the volume of "#$ and the extent of gingival
inflammation which has led to the widespread use of measurements of "#$ as an ob-ective
assessment of gingival inflammation in clinical research studies.
&resence of !urulent exudate
#onceptually, purulent exudate can be regarded as a *7C;+rich variant of "#$. #linically,
suppuration is an important sign of ongoing infection. A strong association with the ris2 of
disease progression was reported by Armitage et al (&''6). !n sub-ects with untreated
periodontitis, the sites with suppuration at baseline (4(M of total sites) were at three+fold higher
ris2 of further bone loss during the following I months.
Increase in levels of ma-ers of !eriodontal disease activity( &GE72 %%&s2 IL.5H in GC)
#urtis (&''&) clearly differentiated disease mar2ers as
&. !ndicators of current disease
4. *redictors of future disease progression, and
5. *redictors of future disease at currently healthy sites.
"#$ has the potential to reflect both host systemic responses and local modulation of those
responses arising from interaction with the bacterial burden. The "#$ is regarded as a serum
transudate because most serum proteins are present in concentrations similar to those in serum
itself (#imasoni, &'H5)3 it thus broably reflects the systemic immunoglobulin and complement
status of the host. >owever, "#$ is modified by the local environment associated with the
periodontal crevice or poc2et.
As the "#$ migrates from the host microcirculation, through inflamed tissues, and into
periodontal poc2et, it acquires mediators involved in the destructive host response and by+
products of local tissue metabolism as well as *7C;s, microorganisms, and their products from
the periodontal poc2et. The following four mediators in "#$ have been investigated extensively
for their potential application in diagnosis of active periodontal disease and prediction of further
loss of periodontal support,
• *rostaglandin ?4 (*"?4)
• X+glucouronidase (X")
• Ceutrophil elastase (C?)
• Aspartate aminotransferase (A/T)
• &rostaglandin E7 C&GE7D
!t is a proinflammatory metabolite of arachidonic acid.
Y8eleased from, macrophages, *7C;s, fibroblasts
?ffects,
&. Aasodilationincreased vascular permeability
4. ?nhanced responsiveness of receptors to painful stimuli
5. 8elease of collagenase by inflammatory cells
6. Activation of osteoclasts
(. 8ecruitment of inflammatory cells
/tudies,
40
!n a study by 9ffenbacher et al (&'HI), crevicualr fluid levels of *"?4 were three times more in
sub-ects with aggressive periodontitis (who experience rapid disease progression) than those with
chronic periodontitis.
!n another study by 9ffenbacher et al (&'HI), "#$ from sites with active periodontal disease
contained a mean *"?4 concentration of 5G(.IZgml, while inactive sites contained about
I(.JZgml of *"?4.
• H.glucouronidase CHGD * neutro!hil elastase
X+glucouronidase (X") and neutrophil elastase (serine endopeptidase) two enBymes released
from the lysosomes of phagocytoBing *7C;s.
Actions of X" and C?,
&. "eneration of reactive oxygen metabolites (#ell damage, inactivation of protease
inhibitors)
4. .egradation of the connective tissue ground substance (#ollagenase, elastase)
X" has been correlated with the number of *7C;s in the crevice (which increase in no. during
periodontal disease).
>arper et al (&'H') observed that the total X" activity in "#$ was significantly correlated with
the occurrence of subgingival periodontal pathogens associated with the occurrence of
subgingival periodontal pathogens, associated with more severe periodontal disease.
;amster et al (&'HH) found that the total amounts of X" level in "#$ were related to the #A;
over time. !n another study it was found that the in previously treated patients, persistently
elevated levels of X" in "#$ were associated with an increase of I+&6 times in the ris2 *A;
during the monitoring period %;amster et al (&''()).
C? activity is higher in patients with periodontitis than those with gingivitis3 C? increases with
development of experimental gingivitis (;istgarten and ;evin, &'H&)3 and periodontal therapy
tends to reduce C? activity in the fluid (;istgarten, &''4).
• As!artate aminotransferase CAS#D
!t is a cytoplasmic enByme present in many body tissues. !ts extracellular release is associated
with cellular damage and cellular death.
#revicular A/T levels are correlated with disease severity. !n a 4+year study by *ersson et al
(&''G), sites with loss of #A; by 4mm or more exhibited significantly elevated levels of A/T in
"#$.
• IL.5
"amonal et al (4GGG) showed that the amount of crevicular !;+&X, !;+H and !;+&G was associated
with periodontal status. ?ngebretson et al (&''') showed that the amount of !;+& was 4.( times
higher in "#$ and 5.( times higher in gingival tissues before periodontal treatment in patients
with genetic !;+&X polymorphism compared to patients without genetic polymorphism.
DIAGNOSIS O) 4AIO3S &EIODON#AL CONDI#IONS
41
Clinically healthy gingiva
• *ale pin2
• /tippled
• Thin margins
• $irm and resilient
At the 5AAA IN#ENA#IONAL @O;S"O& )O CLASSI)ICA#ION O)
&EIODON#AL DISEASES AND CONDI#IONS, a reclassification of the different forms of
plaque+induced periodontal diseases was developed %Armitage, &'''). This revised classification
includes seven general types of plaque induced periodontal diseases,
&) gingivitis,
4) chronic periodontitis,
5) aggressive periodontitis,
6) periodontitis as a manifestation of systemic diseases,
() necrotiBing periodontal diseases,
I) abscesses of the periodontium, and
J) periodontitis associated with endodontic lesions.
The ma-or departures from the previous classification system are, &) the term 0chronic
periodontitis1 has replaced 0adult periodontitis1 and 4) the term 0aggressive periodontitis1 has
replaced 0early+onset periodontitis.1 !n the new classification system, depending on a variety of
circumstances, all forms of periodontitis can progress rapidly or slowly and can be non+
responsive to therapy. !t was also ac2nowledged that gingivitis can develop on a reduced but
stable periodontium.
DIAGNOSIS O) GINGI4I#IS(
"ingivitis represents the inflammatory response in the gingiva to accumulation of bacterial
plaque. #linical signs of gingivitis include,
• 8edness
• /welling (due to increased vascular permeability3 ;indhe E 8ylander, &'J()
• @leeding on probing (ob-ective sign)
• ?xudate
@esides the clinical signs and symptoms, the severity of gingivitis may also be classified by
using different indices, eg. ;Re E /ilness "ingival index (&'I5). The probe is inserted -ust apical
to the gingival margin and the tissues are gently stro2ed laterally with the edge of a periodontal
probe. There are variables which influence the bleeding, e.g. angulation of probe insertion,
insertion force ([G.4( C3 ;ang et al, &''&), time, amount of bleeding, etc.
Gingival Index
G, Co inflammation
&, 7ild inflammation, Co @9*
4, 7oderate inflammation, @9*
5, /evere inflammation
/#98?, /um of all scorestotal no. of teeth
G.&+&.G, 7ild gingivitis
42
&.&+4.G, 7oderate gingivitis
4.&+5.G, /evere gingivitis
There is a strong correlation between the volume of "#$ and the severity of gingival
inflammation, and the composition of "#$ is different in gingivitis and periodontitis sites.
GINGI4I#IS
#;!C!#A; *8?/?CTAT!9C
• 7ost common form of periodontal disease
• *., &+5 mm
• #linical signs of inflammation
• *laque usually present3 calculus often seen
• *recedes periodontitis but does not always lead to periodontitis
• 8eversible
8A.!9"8A*>!# *8?/?CTAT!9C
• Co bone loss seen
A6 &la<ue induced
a) Associated with dental plaque only
b) 7odified by systemic factors
c) 7odified by medications
d) 7odified by malnutrition
,6 Non.!la<ue induced
a) @acterial origin
b) Airal origin
c) $ungal origin
d) "enetic origin
e) 7anifestations of systemic conditions
f) Traumatic lesions
g) $oreign body reactions
h) Cot otherwise specified
DIAGNOSIS O) &EIODON#I#IS
• ;ocal factors
• Age of onset
• $amily history
• #linical attachment loss
• 8ate.uration of destructionsymptoms
• 8adiographic evidence of destruction
• Cature and composition of microbial flora
• Alteration in host immune response
C"ONIC &EIODON#I#IS
• #;!C!#A; *8?/?CTAT!9C,
• *oc2et depth Q5mm
• @9*, suppuration, other signs of active disease
43
• $remitustooth mobility
• $urcation invasion
• 8A.!9"8A*>!# *8?/?CTAT!9C,
• >oriBontal to angular bone loss
LOCALIIED AGGESSI4E &EIODON#I#IS
J&E&3,E#AL &EIODON#I#ISK
#;!C!#A; *8?/?CTAT!9C,
• ;ittle or no inflammation of gingiva
• Dsually amenable to standard periodontal therapy with appropriate antibiotics
• /een after eruption of primary teeth
8A.!9"8A*>!# *8?/?CTAT!9C,
• @one loss localiBed to the distal of the deciduous first molar
GENEALIIED AGGESSI4E &EIODON#I#IS
J&E&3,E#AL &EIODON#I#ISK
#;!C!#A; *8?/?CTAT!9C,
• ?xtreme gingival inflammation
• 8apid bony destruction
• 9ften accompanied by sever functional defects of neutrophils and monocytes
• 9titis media and D8T! also found
• !n some cases more sever lesions are refractory to antibiotics
8A.!9"8A*>!# *8?/?CTAT!9C,
• "eneraliBed bone loss
LOCALIIED AGGESSI4E &EIODON#I#IS
CLOCALIIED 134ENILE &EIODON#I#ISD
• #;!C!#A; *8?/?CTAT!9C,
• 9ccurs around puberty
• Dsually localiBed to molars and incisors
• 7inimal inflammation and plaque
• 9ften associated to systemic host defense defect
• 8A.!9"8A*>!# *8?/?CTAT!9C,
• @one loss localiBed to distal of maxillary central incisors
GENEALIIED AGGESSI4E &EIODON#I#IS AS A %ANI)ES#A#ION O)
S$S#E%IC DISEASE CG1&D
#;!C!#A; *8?/?CTAT!9C,
• 9ccurs around puberty to young adulthood
• 8apid bone destruction
• Dsually accompanied by minimal inflammation and minimal visible plaque
• 9ften associated with a systemic host defense defect
• ;esions often refractory to antibiotics or other therapy
8A.!9"8A*>!# *8?/?CTAT!9C,
44
• /evere bone destruction around premolars and molars
GENEALIIED AGGESSI4E &EIODON#I#IS
CA&IDL$ &OGESSING &EIODON#I#ISD
#;!C!#A; *8?/?CTAT!9C,
• /een in young adults and some older patients
• #haracteriBed by periods of severe gingival inflammation, edema and rapid bone loss,
increasing *.s
• 7alaise, depression and lowered immune competency have been reported
8A.!9"8A*>!# *8?/?CTAT!9C,
• /evere bone loss
• /evere bony deterioration with time
DIAGNOSIS O) AC3#E &EIODON#AL LESIONS
&cute signifies
• 8ising to its crisis sharply
• >aving a short and relatively dramatic course
• "enerally respond dramatically to 0emergency1 periodontal therapy
CecrotiBing periodontal diseases
&. CecrotiBing Dlcerative "ingivitis (CD")
4. CecrotiBing Dlcerative *eriodontitis (CD*)
It is an infection characteri$ed y necrosis of gingival tissues, periodontal ligament and alveolar
one.
NecrotiFing 3lcerative &eriodontitis CN3&D
#;!C!#A; *8?/?CTAT!9C,
• Dsually observed in individuals with >!A3 immunosuppression3 or severe malnutrition
• "eneraliBed or localiBed rapid soft and hard tissue destruction
• @one sequestration, denudation
• Teeth may become mobile
• /pontaneous, usually nocturnal, gingival bleeding
• $etid breath
• !ntense, deep+seated pain
• 7ay be preceded by necrotiBing ulcerative gingivitis
A,SCESSES O) #"E &EIODON#I3%
• &scess is a localiBed accumulation of pus.
&. "ingival abscess
4. *eriodontal abscess
5. *ericoronal abscess
GINGI4AL A,SCESS
• !s a localiBed purulent infection that involves marginal gingiva or interdental papilla.
• #onfined to marginal tissues
• *reviously non+diseased site
45
• !mpaction of foreign material
• /hort history of onset
&EICOONAL A,SCESS
• ;ocaliBed purulent infection within the tissues surrounding a partially erupted tooth.
&EIODON#AL A,SCESS
A periodontal ascess is a localiBed accumulation of pus within the gingival wall of a
periodontal poc2et.
&. >istory of onset, progression, previous periodontal therapy
4. #ontinuity with gingival margin
5. Aitality of tooth
6. *resence absence of caries
(. 8adiographic examination

&eriodontitis associated >ith endodontic lesions
• A. &rimary endodontic lesion
• ,. &rimary endodontic lesion >ith secondary !eriodontal lesion
• C. &rimary !eriodontal lesion
• D. &rimary !eriodontal lesion >ith secondary endodontic lesion
• E. #rue combined lesions
. Simon J N Glick DH Frank AL
CONCL3SION,
At the present time, the diagnosis and classification of periodontal diseases are almost entirely
based on traditional clinical assessments. /upplemental quantitative and qualitative assessments
of the gingival crevicular fluid and subgingival microflora can potentially provide useful
information about the patient’s periodontal disease. !n certain situations, these supplemental ris2+
assessment tests may be particularly valuable in establishing the endpoint of therapy prior to
placing patients on a periodontal maintenance program.
Although the clinical utility of none of these tests has been validated, their further development
is warranted. *robing depth and clinical attachment loss measurements obtained with periodontal
probes are practical and valid methods for assessing periodontal status. #omputer+lin2ed,
controlled+force electronic periodontal probes are commercially available and are currently in
use by some practitioners. 7any of the logistical problems associated with subtraction
radiography are being overcome and this powerful diagnostic tool may soon come into
widespread use. $uture developments in this and other imaging techniques are li2ely to have a
profound effect on our approach to the diagnosis of periodontal diseases.
E)EENCES3
&. Cewman et al. #linical *eriodontology. H
th
, '
th
, &G
th
ed.
4. ;indhe. *eriodontology and !mpalnt .entistry.
5. .iagnosis of *eriodontal .iseases. - Periodontol !BB:C4;:2!:492!;4.
6. Axelsson. .iagnosis and 8is2 *rediction of *eriodontal .iseases.
46
(. 7ol, A. !maging methods in periodontology. *erio 4GGG, 4GG63 56,56+6H.
I. @ragger, D. 8adiographic parameters, biologic significance and clinical use. *erio 4GGG,
4GG(3 5',J5+'G.
J. "rant3 /tern E ;istgarten. *eriodontics.
H. Perio !BBB, 4GG63 56,56+6H.
'. Perio !BBB, 4GG(3 5',J5+'G.
&G. /erio, >awley. 7anual of #linical *eriodontics.
22. - Periodontol !BB:C4;:2!:492!;4.
2!. - Periodontol, !BBDC 44:E3393B!.
47