Submitted by
Nithin Maerkose Reji
Introduction
Diagnosis may be defined as identifying disease from an evaluation of the history,signs and
symptoms,laboratory tests and procedures.
A thorough periodontal examination is a critically important data collection activity that is
necessary to arrive at a diagnosis and develop a treatment plan.In medically healthy patients with
simple and rather straight forward conditions,the examination can usually be completed by one
visit.For medically compromised person with complex periodontal and dental problems,multiple
visits may be needed to complete the data gathering process.
From this information the clinician has to distinguish between normal and abnormal findings
.Periodontal diagnosis should first determine whether disease is present ,then identify its
type,extent,distribution,and severity,and finally provide an understanding of the underlying
pathologic processes and its cause.
Patient interview
Patient interview include,
The source of referral(important if another dentist or physician referred the patient and
Medical history
Most of the medical history is obtained at the first visit, and it can be
supplemented by pertinent questioning at subsequent visits.
The health history can be obtained verbally by questioning the patient and
recording his or her responses on a blank piece of paper or by means of a printed
questionnaire that the patient completes
The importance of the medical history should be clearly explained, because patients often
omit information that they cannot relate to their dental problems. The patient should be made
aware of the following:
(1) the possible role that some systemic diseases, conditions, or behavioral factors may play in
the cause of periodontal disease
(2) the presence of conditions that may require special precautions or modifications of the
treatment procedure
(3) the possibility that oral infections may have a powerful influence on the occurrence and
severity of a variety of systemic diseases and conditions
The medical history should include reference to the following:
1. If the patient is under the care of a physician, the nature and duration of the problem and
its therapy should be discussed. The name, address, and telephone number of the
physician should be recorded, because direct communication with him or her may be
necessary.
2. Details regarding hospitalizations and operations, including the diagnosis, the type of
operation, and any untoward events (e.g., anesthetic, hemorrhagic, or infectious
complications) should be provided.
3. A list of all medications being taken and whether they were prescribed or obtained over
the counter should be included. All of the possible effects of these medications should be
carefully analyzed to determine their effect, if any, on the oral tissues and also to avoid
administering medications that would interact adversely with them. Special inquiry should
be made regarding the dosage and duration of therapy with anticoagulants and
corticosteroids. Patients who are taking the family of drugs called bisphosphonates (e.g.,
Actonel, Fosamax, Boniva, Aredia, Zometa), which are often prescribed for patients with
14. Patients with seizure disorders may require additional medication before periodontal
treatment. Th ose taking phenytoin (Dilantin) or other anticonvulsant medications oft en
develop an associated gingival enlargement
15. Mouth breathing is a compounding factor for periodontal disease. Asthma attacks may be
triggered by stress; so, careful attention must be paid to stress-reducing protocols
throughout all appointments. Approximately 15% of inhaler-dependent patients are
sensitive to the sulfites present in all local anesthetics containing a vasoconstrictor,
contraindicating their use in these patients. Sinusitis may complicate the differential
diagnosis of periodontal pain in the maxillary posterior area.
16. importance of maintaining periodontal health both before and during pregnancy cannot be
overemphasized. It is significant to note that strong links have been found between
periodontal disease in pregnancy and preterm delivery of low-birth-weight infants.
Although periodontal treatment may be rendered at any time during pregnancy, caution
should be exercised in the first trimester and last half of the third trimester. Pregnancy can
modify periodontal disease. Pregnancy gingivitis oft en does not respond to treatment
until several months after gestation
17. Gastric or duodenal ulcers may complicate periodontal healing because of dietary
restrictions. Gingival changes may accompany colitis.
18. Various types of cancer present complications in periodontal treatment. Leukemia may
be accompanied by gingival enlargement. The prognosis for the more severe or advanced
types of cancer can force modification of usual treatment plans. Radiation therapy may
make surgical treatment inadvisable. The treating physician should be contacted if
chemotherapy is being used or has been used recently.
19. Many medicaments and medications used in periodontal treatment are significant
allergens that may have to be avoided with sensitized patients.
20. Some dermatologic diseases, such as lichen planus, pemphigoid, and pemphigus, have
periodontal components.
21. Some types of arthritis can restrict dexterity required for plaque removal. Corticosteroid
therapy oft en delays healing aft er periodontal treatment. Use of aspirin or nonsteroidal
anti inflammatories (NSAIDs) may increase and/or prolong bleeding during treatment
22. Concerns exist regarding possible infection of total joint replacement prostheses following
invasive dental treatment. The American Dental Association has followed the guidelines
recommended by the American Academy of Orthopaedic Surgeons (AAOS) in 2003 by
recommending antibiotic prophylaxis prior to such treatment for the first 2 years
following replacement surgery or for an extended time frame for immunocompromised
and other high-risk patients. However, the AAOS has since issued a recommendation to
prophylax with antibiotics for an indefinite time following joint replacement surgery.
Consultation with the patients orthopedic surgeon is strongly advised
23. Physical or medical limitations may help explain the etiology of inflammatory periodontal
disease if the patient is unable to perform adequate oral hygiene procedures. Such
limitations will likely also influence therapy prognosis and treatment planning.
24.
25. Heavy smoking, excessive alcohol consumption, and drug use infl uence the periodontal
diagnosis, prognosis, and treatment planning. Vigorous toothbrushing, especially with a
hard brush, may explain root exposure. Self-mutilating (factitious) habits and extra- or
intraoral piercings may alter gingival appearance and contribute to periodontal bone loss.
26. Medications used for the treatment or management of any medical problem may affect
periodontal treatment. Some medications, such as -blockers, may require changes in
anesthetics. Calcium channel blockers and anticonvulsants (see G) may contribute to
gingival enlargement. Antibiotics may produce temporary improvements in periodontal
disease. Previous and current use of bisphosphonates and other antiresorptive medications
(in particular, intravenous use) has been associated with osteonecrosis. Precaution must be
taken when treating patients who regularly take aspirin, NSAIDs, clopidogrel (Plavix),
warfarin (Coumadin), and other blood-thinning medications. Certain dietary
supplements, such as ginseng, ginkgo, garlic, and ginger, can affect blood clotting as can a
diet that is heavy in green tea and green leafy vegetables. A dentist must have a recent
edition of the Physicians Desk Reference or a similar reference to determine possible
eff ects of new medications on the treatment plan. Also useful is a recent edition of
Physicians Desk Reference for Nonprescription Drugs, Dietary Supplements, and Herb.
27. It is imperative to update the medical history of a recall or continuing patient at every
visit. New medical problems, altered status of previously diagnosed medical problems,
and changes in medications can affect periodontal treatment
Diabetes mellitus
Definition : clinically and genetically heterogenous disease characterized by abnormally
elevated glucose levels and deregulation of carbohydrate, protein and lipid metabolism.
Oral manifestations: cheilosis, mucosal drying, cracking, burning tooth and tongue,
reduced salivary flow, alteration of oral microbial flora ( increased candida albicans,
haemolytic streptococci staphylococci, increase dental caries.
Periodontal findings: enlarged gingival, gingival polyps, polyploidy gingival
proliferations, gingival abscess, periodontitis, tooth mobility, destructive diseases, increase
bleeding on probing, delayed post surgical healing of periodontal tissues, increase glucose
levels.
Lab evaluation
Fasting
Normal
<70mg/dl
Diabetes mellitus
>126mg/dl
Impaired
70-110mg/dl
>200mg/dl
140-200mg/dl
>200mg/dl
At 2 hr
>200mg/dl
glucose
Data from American diabetes association 2003- Carranza 11th edition
Fasting glucose: no caloric intake for atleast 8 hours
HbA1c test give us an idea about blood glucose level over 2-3 months (glycosylated
hemoglobin assay test)
Definition : glycated hemoglobin it is a form of hemoglobin that is measured primarily
to identify the average plasma glucose concentration over prolonged periods of time
Interpretation of HbA1c test
Normal
6.0-6.5%
Good control
6-7%
Moderate control
7-8%
Need treatment
>8%
Hypertension
Defined as having systemic blood pressure greater than or equal to 140mm of hg or
diastolic >90mm of hg or having to use antihypertensive medication
JNC-7
Classification based on etiology
Primary hypertension:when no underlying pathology can be found to explain.
Secondary hypertension:underlying etiology present.
Management of hypertensive patient
First dental visit two BP reading spaced at least 10 min apart is average and used as
baseline value.
Stress should be minimized
Afternoon dental visit are preferred.
Patients systolic BP greater than 180mmHg and diastolic 110mmHg should be limted to
emergency care until hypertension is controlled.
Renal diseases
Dental management of patients with renal disease need to be altered
Physician consultation is necessary to determine stage of renal disease,regimen
for medical management and alterations in periodontal therapy.
In patients undergoing dialysis it is preferable to treat the patient before rather
than after dialysis or transplant.
Management
Consult physician
Monitor BP
Check PTT(20-40 sec)
Check PT(11-13sec)
Check BT (2-6)
Blood urea(dont treat if 60mg/dl)serum creatinine(dont treat if <1.5mg/dl)
Eliminate area of oral infection
Good oral hygiene to be maintained
Drugs which are nephrotoxic or metabolized by the kidney should be
avoided(tetracycline,amino glycoside,phenacetin)
Cardiovascular disease
Ischemic heart disease
Unstable angina:occurs irrwgularly or multiple occasion without predisposing
factors.
Stable angina:angina occurs infrequently associated with exertion or stress.Can
control with rest and medication.
Infective endocarditis
Patients are at high risk of developing IE after dental treatment indiced
bacteremia.
Antibiotic prohylxis recommended.
BRONCHIAL ASTHMA
MANAGEMENT:
Consult physician
Minimize stress
Treatment in afternoon
in case of emergency, discontinue treatment
Make patient erect and straight
Administer O2
Administer bronchodilators(inhalation)
If subsides continue procedure, else seek for hospital care
HEPATITIS
6 types
Hepatitis A,B,C,D,E and G
Universal precautions
HBeAg(+ve)-carrier of disease
Anti HBsAg(+ve)-treat routinely
HBsAg (+ve)-infectious
HBsAgl-veHreat routinely
Min aerosol
High speed hand piece
HBlG
HB vaccine
THYROID PROBLEMS
Hypothyroidism
Hyperthyroidism
Cold intolerance
Heat intolerance
Weakness
Sweating
Fatigue
Tachycardia
Warm,thin.soft,mosit skin
Tick tongue
Exophthalmos
Drowsiness
Tremor
Loss of hair
Weight loss
Weight gain
Decreased sweating
Hoarse voice
Head ache
Periodontitis
Immunology
Physiology
Surgical
1. Visits to the dentist should be listed, including their frequency, the date of the most recent
visit, the nature of the treatment, and oral prophylaxis or cleaning by a dentist or
hygienist, including the frequency and date of most recent cleaning.
2. The patients oral hygiene regimen should be described, including tooth brushing
frequency, time of day, method, type of toothbrush and dentifrice, and interval at which
brushes are replaced. Other methods for mouth care, such as mouthwashes, interdental
brushes, other devices, water irrigation, and dental floss, should also be listed
3. Any orthodontic treatment, including its duration and the approximate date of
termination, should be noted.
4. If the patient is experiencing pain in the teeth or in the gingiva, the manner in which the
pain is provoked, its nature and duration, and the manner in which it is relieved should be
described
5. Note the presence of any gingival bleeding, including when it first occurred; whether it
occurs spontaneously, on brushing or eating, at night, or with regular periodicity; whether
it is associated with the menstrual period or other specific factors; and the duration of the
bleeding and the manner in which it is stopped.
6. A bad taste in the mouth and areas of food impaction should be mentioned
7. Assess whether the patients teeth feel loose or insecure, if he or she has any difficulty
chewing, and whether there is any tooth mobility.
8. Note the patients general dental habits, such as grinding or clenching of the teeth during
the day or at night. Do the teeth or jaw muscles feel sore in the morning? Are there
other habits to address, such as tobacco smoking or chewing, nail biting, or biting on
foreign objects?
9. Discuss the patients history of previous periodontal problems, including the nature of the
condition, and, if it was previously treated, the type of treatment received (surgical or
nonsurgical) and the approximate period of termination of the previous treatment. If, in
the opinion of the patient, the present problem is a recurrence of previous disease, what
does he or she think caused it?
10. Note whether the patient wears any removable prosthesis. Does the prosthesis enhance or
is it a detriment to the existing dentition or the surrounding soft tissues?
11. Does the patient have implants to replace any of the missing teeth?
Intraoral Radiographic Survey
The radiographic survey should consist of a minimum of 14 intraoral films and 4
posterior bite-wing films.
Panoramic radiographs are a simple and convenient method of obtaining a survey view of
the dental arch and the surrounding structure
They are helpful for the detection of developmental anomalies, pathologic lesions of the
teeth and jaws, and fractures as well as for the dental screening examinations of large
groups. They provide an informative overall radiographic picture of the distribution and
severity of bone destruction with periodontal disease, but a complete intraoral series is
required for periodontal diagnosis and treatment planning
Casts
Casts from dental impressions are useful adjuncts during the oral examination. They
indicate the position of the gingival margins (recession) and the position and inclination
of the teeth, the proximal contact relationships, and the food impaction areas. In addition,
they provide a view of the lingualcuspal relationships. Casts are important records of the
dentition before it is altered by treatment. Finally, casts also serve as visual aids during
discussions with the patient, and they are useful for pretreatment and post treatment
comparisons as well as for reference at recall visits. They are also helpful to determine
the position of implant placement if the case will require it.
Clinical Photographs
Color photographs are useful for recording the appearance of the tissue before and after
treatment. Photographs cannot always be relied on for the comparison of subtle color
changes in the gingiva, but they do depict gingival morphologic changes. With the advent
of digital clinical photography, record keeping for mucogingival problems (e.g., areas of
gingival recession, frenum involvement, papilla loss) has become important.
Review of the Initial Examination
If no emergency care is required, the patient is dismissed and instructed about when to
report for the second visit. Before this visit, a correlated examination is made of the
radiographs, photographs, and casts to relate the radiographic changes to unfavorable
conditions represented on the casts. The casts are checked for evidence of abnormal wear,
plunger cusps, uneven marginal ridges, malposed or extruded teeth, crossbite
relationships, and other conditions that could cause occlusal disharmony or food
impaction. Such areas are marked on the casts to serve as a reference during the detailed
examination of the oral cavity. The radiographs, photographs, and casts are valuable
diagnostic aids; however, it is the clinical findings in the oral cavity that constitute the
basis for diagnosis.
SECOND VISIT
Oral Examination
Oral Hygiene
The cleanliness of the oral cavity is appraised in terms of the extent of accumulated food debris, plaque,
materia alba, and tooth surface stains Disclosing solution may be used to detect plaque that would
otherwise be unnoticed. The amount of plaque detected, however, is not necessarily related to the severity
of the disease present. For example, aggressive periodontitis is a destructive type of periodontitis in which
plaque is scanty. Qualitative assessments of plaque are more meaningful
Oral Malodor
Oral malodor, also called fetor ex ore, fetor oris, and halitosis, is foul or offensive odor emanating from
the oral cavity. Mouth odors may be of diagnostic significance, and their origin may be oral or extraoral
Breath odour is the subjective perception after smelling someones breath,if unpleasant it is called oral
malodour or halitosis or bad breath
Classification
Genuine halitosis
Physiologic
Pathologic
Oral
Extraoral
Pseudo halitosis
Halitosis
Etiology
90%: oral cavity
10%: Systemic/ Local Factors
As a result of microbial putrification of food debris, cells,saliva and blood within oral cavity
Physiologic- mouth breathing , medication,aging, poor OH, Fasting, tobacco within oral cavity.
Gastrointestinal tract
o
o
o
Mechanism Of Halitosis
Proteolysis of protein to peptide & aminoacids.resultant substrate with cysteine & reduced glutathione
rises to volatile sulphur compounds which are malodour causing substances.
Self examination
Smelling plate and spoon after sweeping the tongue
Smelling toothpick after introducing into interdental area
Smelling saliva , spit on small cap or spoon, licking the wrist &smelling after dried.
No odour
Barely perceptible
Slightly but clearly noticeable
Moderate
Strong offencive
Extremely foul smell
Breath odour
Rotten eggs- VSCs
Sweet odour or dead mice: liver insufficiency
Rotten apple: type 1 DM
Fishy odour: kidney insufficiency, trimethyl aminuria
Treatment
Tongue ckeaning
Tooth brushing
Full mouth disinfection
Chewing gum
Chemical reduction of oral micro flora load that releases malodour gases
Conversion of VSCs
Erosion
Also called corrosion, erosion is a sharply defined, wedge-shaped depression in the cervical area of the
facial tooth surface. The long axis of the eroded area is perpendicular to the vertical axis of the tooth The
surfaces are smooth, hard, and polished. Erosion generally affects a group of teeth. In the early stages, it
may be confined to the enamel, but it generally extends to involve the underlying dentin as well as the
cementum. The etiology of erosion is not known. Suggested causes include decalcification by acidic
beverages or citrus fruits and the combined effect of acid salivary secretion and friction. Sognnaes refers
to these lesions as dentoalveolar ablations and attributes them to forceful frictional actions between the
oral soft tissues and the adjacent hard tissues. Salivary pH, buffering capacity, and calcium and
phosphorus content have been reported as normal in patients with erosion, and the mucin level is elevated
Abrasion
Abrasion refers to the loss of tooth substance induced by mechanical wear other than that of mastication.
Abrasion results in saucer-shaped or wedge-shaped indentations with a smooth, shiny surface. Abrasion
starts on exposed cemental surfaces rather than on the enamel and extends to involve the dentin of the
root. A sharp ditching around the cementoenamel junction appears because of to the soft cemental
surface compared with the hard enamel surface. Continued exposure to the abrasive agent, combined with
decalcification of the enamel by locally formed acids, may result in loss of enamel, followed by loss of
the dentin of the crown.
Toothbrushing with an abrasive dentifrice and the action of clasps are common causes of abrasion;
brushing is the much more prevalent cause. The degree of tooth wear from toothbrushing depends on the
abrasive effect of the dentifrice and the angle of brushing. Horizontal brushing at right angles to the
vertical axis of the teeth results in the severest loss of tooth substance. Occasionally, abrasion of the
incisal edges results from habits such as holding objects (e.g., bobby pin, tacks) between the teeth.
Attrition
Attrition is occlusal wear resulting from functional contacts with opposing teeth. Such physical wear
patterns may occur on incisal, occlusal, and approximal tooth surfaces. A certain amount of tooth wear is
physiologic, but accelerated wear may occur when abnormal anatomic or unusual functional factors are
present.
Occlusal or incisal surfaces worn by attrition are called facets. When active tooth gnashing occurs, the
enamel rods are fractured and become highly reflective to light. Thus, shiny, smooth, and curviplanar
facets are usually the best indicator of ongoing frictional activity. If dentinis exposed, a yellowish brown
discoloration is frequently present . Facets vary in size and location depending on whether they are
produced by physiologic or abnormal wear. At least one significant wear facet has been reported in 92%
of adults, and facet prevalence is almost universal. Facets are usually not sensitive tothermal or
tactilestimulation.
Reversed faciolingual occlusal plane. The normal occlusal plane is sometimes reversed by occlusal wear
so that in the mandible the occlusal surfaces slope facially instead of lingually and in the maxilla they are
inclined lingually. The third molars usually are not affected.Facets generally represent functional or
parafunctional wear, as well as iatrogenic dental treatment through coronoplasty (occlusal adjustment).
Coronoplasty, however, does not appear to contribute to higher ratings of wear.Excessive wear may result
in obliteration of the cusps and the formation of either a flat or a cuneiform (cupped-out) occlusal surface.
Reversal of the occlusalplane of the premolars and first and second molars occurs in advanced stages of
wear. Contrary to earlier thought, attrition of young adults from modern societies is not age related. This
suggests that a significant amount of attrition in young adults is unlikely to occur from functional wear
and is probably the result of bruxing activity. Attrition has been correlated with age in older adults. The
angle of the facet on the tooth surface may be significant to the periodontium. Horizontal
facets tend to direct forces on the vertical axis of the tooth, to which the periodontium can adapt most
effectively. Angular facets direct occlusal forces laterally and increase the risk of periodontal damage.
However, continuous tooth eruption without alveolar bone growth may compensate for gradual attrition,
which is characterized by a lack of inflammatory changes on the alveolar bone surfaces.
Abfraction
A recently studied mechanism of tooth wear, abfraction results from occlusal loading surfaces causing
tooth flexure and mechanical microfractures and tooth substance loss in the cervical area. These four
mechanisms of tooth wearcorrosion, abrasion, attrition, and abfractioncan combine with each other,
resulting in increased degree of tooth wear.
Dental Stains
These stains are pigmented deposits on the teeth. Dental stains should be carefully examined to determine
their origin.
Hypersensitivity
Root surfaces exposed by gingival recession may be hypersensitive to thermal changes or tactile
stimulation. Patients often direct the operator to the sensitive areas. These may be located by gentle
exploration with a probe or cold air.
Tooth Mobility
All teeth have a slight degree of physiologic mobility, which varies for different teeth and at different
times of the day. Mobility is greatest on arising in the morning and progressively decreases. The increased
mobility in the morning is attributed to slight extrusion of the tooth because of limited occlusal contact
during sleep. During the waking hours, mobility is reduced by chewing and swallowing forces, which
intrude the teeth in the sockets. These 24-hour variations are less marked in persons with a healthy
periodontium than in those with occlusal habits such as bruxism and clenching. Single-rooted teeth have
more mobility than multi-rooted teeth; incisors have the most mobility. Mobility is principally in a
horizontal direction, although some axial mobility occurs, but to a much lesser degree.Tooth mobility
occurs in the following two stages:
1. In the initial, or intrasocket, stage the tooth moves within the confines of the periodontalligament
(PDL). This is associated with viscoelastic distortion of the PDL and redistribution of the periodontal
fluids, interbundle content, and fibers. This initial movement occurs with forces of about 100 g and is
about 0.05 to 0.10 mm (50-100 m).
2. The secondary stage occurs gradually and entails elastic deformation of the alveolar bone in response
to increased horizontal forces. When a force of 500 g is applied to the crown, the resulting displacement is
about 100 to 200 m for incisors, 50 to 90 m for canines, 8 to 10 m for premolars, and 40 to 80 m for
molars.
When a force such as that applied to teeth in occlusion is discontinued, the teeth return to their original
position in two stages: (1) an immediate, springlike elastic recoil and (2) a slow, asymptomatic recovery
movement. The recovery movement is pulsating and is apparentlyassociated with the normal pulsation of
the periodontal vessels, which occurs in synchrony with the cardiaccycle. Many attempts have been made
to develop mechanical or electronic devices for the precise measurement of tooth mobility. Even though
standardization of the grading of mobility would be helpful in diagnosing periodontal disease and in
evaluating the outcome of treatment, these devices are not widely used. As a general rule, mobility is
graded clinically with a simple method. The tooth is held firmly between the handles of two metallic
instruments or with one metallic instrument and one finger , and an effort is made to move it in all
directions; abnormal mobility most often occurs faciolingually. Mobility is graded according to the ease
and extent of tooth movement, as follows:
Normal mobility.
Grade I: Slightly more than normal.
Grade II: Moderately more than normal.
Grade III: Severe mobility faciolingually andmesiodistally, combined with vertical displacement.
Mobility beyond the physiologic range is termed abnormal or pathologic. It is pathologic in that it
exceeds the limits of normal mobility values; the periodontium is not necessarily diseased at the time of
examination. Increased mobility is caused by one or more of the following factors:
1. Loss of tooth support (bone loss) can result in mobility. The amount of mobility depends on the severity
and distribution of bone loss at individual root surfaces, the length and shape of the roots, and the root
size compared with that of the crown. A tooth with short, tapered roots is more likely to loosen than one
with normal-size or bulbous roots with the same amount of bone loss. Because bone loss usually results
from a combination of factors and does not occur as an isolated finding, the severity of tooth mobility
does not necessarily correspond to the amount of bone loss.
2. Trauma from occlusion, or injury produced by excessive occlusal forces or incurred because of
abnormal occlusal habits (e.g., bruxism, clenching), is a common cause of tooth mobility. Mobility is also
increased by hypofunction. Mobility produced by trauma from occlusion occurs initially as a result of
resorption of the cortical layer of bone, leading to reduced fiber support, and later as an adaptation
phenomenon resulting in a widened periodontalspace.
3. Extension of inflammation from the gingiva or fromthe periapex into the PDL results in changes that
increase mobility. The spread of inflammation from an acute periapical abscess may increase tooth
mobility in the absence of periodontal disease.
4. Periodontal surgery temporarily increases tooth mobility for a short period.
5. Tooth mobility is increased in pregnancy and is sometimes associated with the menstrual cycle or the
use of hormonal contraceptives. Mobility occurs in patients with or without periodontal disease,
presumably because of physicochemical changes in the periodontal tissues.
6. Pathologic processes of the jaws that destroy the alveolar bone or the roots of the teeth can also result
in mobility. Such processes include osteomyelitis and tumors of the jaws.
One study has suggested that pockets around mobile teeth harbor higher proportions of Campylobacter
rectus and Peptostreptococcus micros (and perhaps Porphyromonas gingivalis) than nonmobile teeth.
This hypothesis needs further verification.
Sensitivity to Percussion
Sensitivity to percussion is a feature of acute inflammation of the PDL. Gentle percussion of a tooth at
different angles to the long axis often aids in localizing the site of inflammatory involvement.
Examination of periodontium
The periodontal examination should be systematic starting in the molar region in either the
maxilla or mandible and proceeding around the arch. It is important to detect earliest sign of
gingival and periodontal disease. Charts to record periodontal and associated findings provide a
guide for a thorough examination and record of the patients condition. They are also used to
evaluate the response to treatment and for comparison at recall visit.
A Etiological Agents and Clinical Signs of Inflammation. Information collected during a
complete periodontal examination includes assessments of probable etiological agents such as
the presence of plaque and calculus and clinical signs of periodontal inflammation (e.g., redness,
swelling, bleeding on probing, purulent exudate).
Any local factors that make it difficult to perform adequate oral hygiene are also recorded since
control of periodontal infections requires correction or removal of these factors. Commonly
found local factors that can contribute to the pathogenesis of periodontal infections include poor
dental restorations (e.g., subgingival overhangs, poor contours, open interproximal contacts),
crowded/malpositioned teeth, and anatomical dental defects (e.g., coronalradicular grooves).
B Assessment of Periodontal Damage. A periodontal examination also includes a careful
assessment of past damage to periodontal tissues. A mandatory initial assessment of damage is
measurement of the probing depths (PD) at six locations around all teeth.
These locations are the mesiofacial, midfacial, distofacial, mesiolingual, midlingual, and
distolingual. PD is the distance in millimeters from the crest of the gingival margin to the base of
the probe able crevice between the tooth and gingiva. At healthy sites, these crevices are usually
only a few millimeters deep and are the habitat for a diverse community of microorganisms that
make up the normal periodontal microbiota. Bacteria at these sites live in a homeostatic host
microbial relationship. Anything that disrupts this health-associated homeostasis, such as the
complete cessation of all oral hygiene procedures, will up regulate host innate and adaptive
immune responses to the increased microbial challenge.
Th eoverall result is clinically observable inflammation. If the hostmicrobial homeostasis is not
restored (e.g., by resumption of oral hygiene), the gingiva will remain inflamed for prolonged
periods. The persistence of chronic inflammation often leads to tissue destruction that is
clinically manifested by detachment of tissue from the tooth and formation of a periodontal pocket.
PD measurements provide objective assessments of this detachment and the magnitude of the
mucogingival line ) and substract the pocket or sulcus depth from it to determine width of
attached gingival
4. Histochemical test Staining test- paint the gingival and oral muosa with Schillers or
Lugols iodine solution (iodine and potassium iodide solution)alveolar mucosa takes a
brown color due to its glycogen content while glycogen free attached gingival remains
unstained .measure the total width of unstained gingival substract the pocket or sulcus
depth from it to determine width of attached gingival
MEASUREMENT OF THICKNESS OF GINGIVA
Earlier it was measured using traumatic techniques like probes and injection needles. But
now measured atraumatically using the newer ultrasonic device called KRUPP SDM
This uses a pulse echo principle
There are many methods available for assessing plaque and calculus. The presence of
supragingival plaque and calculus can be directly observed and the amount is measured with a
caliberated probe.for the detection of subgingival calculus each tooth surface is carefully
checked to the level of gingival attachment with a no ;17 and 3A explorer. Warm air may be used
to deflect gingival and aid in visualization of calculus.
Although the radiograph may sometimes reveal heavy calculus deposits interproximally and
even on the facial and lingual surface , it cannot be relied on for thorough detection of calculus
GINGIVAL STATUS
COLOUR
Melanin a non hb derived brown pigment responsible after normal pigmentation of skin ,
gingiva , and remainder of oral mucous membrane
Tyrosomes
Tyrosinase ---dihydroxyphenylalanine---melanine
METALLIC PIGMENTATION
Heavy metals like bismuth, silver, mercury, absorbed systematically from therapeutic
use , occupational household environment.
Bismuth, arsenic- black
Silver- violet.
Lead pigmentation cause grey black line along gingival margin (burtonian line)
Mechanism perivascular precipitation of metallic sulfides in subepithelial connective
tissue. Occurs on area of inflammation. Ulcers on areas of permeability of irritated blood
vessels allows sweepage of metals to surrounding tissue.
Melanin pigmentation increases physiologically as well assystemically
Addisons disease
ENDOGENOUS PIGMENTATION
Melanin brown or black
Bilirubin yellow jaundice, iron bluish grey haematochromatosis
EXOGENOUS
Coal +metal dust + coloring agents
Tobacco users also have melanin pigmentation and hyperkeratosis of gingival.
GINGIVAL DEPIGMENTATIONMainly done by chemical, cryosurgical, electrosurgical methods, and lasers
And it appears pale when vascularisation decreases (epithelial keratinization increases) and
during inflammation red color intensifies due to vascular proliferation and reduction of
keratinization.
BLUISH color of gingiva may be
keratinization
due to
Engorged and conjusted blood vessel causes venous stasis and blood flow becomes
sluggish and there will be localized anoreemia ie. Blue hue and extravasation of rbc and
destruction of hb.
SIZE OF GINGIVA
FACTORS CONTRIBUTING TO INCREASE IN SIZE OF GINGIVA ARE
ANUG marginal
HERPETIC GINGIVOSTOMATITIS- diffuse
PATCH LIKE- acute reaction to chemical irritation
An increase in size of the gingiva is a common feature of gingival disease. The accepted current
terms for this condition are gingival enlargement and gingival overgrowth.
Definition- change in size of gingival may be due to Gingival hyperplasiaenlargement of size
of gingival due to increase in number of cells
Gingival hypertrophy due to increase in size if cells
Overgrowth due to increase in size of gingival
Drug induced enlargement except cyclosporine- pale pink in colour
Classification of gingival enlargements
A gingival abscess is a localized, painful, rapidly expanding lesion that usually has a sudden
onset . It is generally limited to the marginal gingiva or the interdental papilla. In its early stages,
it appears as a red swelling with a smooth, shiny surface. Within 24 to 48 hours, the lesion
usually becomes fluctuant and pointed, with a surface orifice from which a purulent exudate may
be expressed. The adjacent teeth are often sensitive to percussion. If permitted to progress, the
lesion generally ruptures spontaneously.
Histopathology. The gingival abscess consists of a purulent focus in the connective tissue
surrounded by a diffuse infiltration of polymorphonuclear leukocytes, edematous tissue, and
vascular engorgement. The surface epithelium has varying degrees of intracellular and
extracellular edema, invasion by leukocytes, and sometimes ulceration.
Etiology. Acute inflammatory gingival enlargement results from bacteria carried deep into the
tissues when a foreign substance (e.g., toothbrush bristle, piece of apple core, lobster shell
fragment) is forcefully embedded into the gingiva. The lesion is confined to the gingiva and
should not be confused with periodontal or lateral abscesses.
DRUG INDUCED GINGIVAL ENLARGEMENT
Painless beadlike enlargement of interdental papilla extending to facial and lingual marginal
gingival.marginal and papillary enlargement unite to form massive field covering portion of
crown along with edema.
Complications
Site- maxillary or mandibular anterior region
Inflammation mulberry shaped, firm, pale pink, resilient, difficult plaque control
Anticonvulsant
Phenytoin, ethantoin , mephentoin , succinimide , methosuccinimide, valporic acid.
Phenytoin stimulates proliferation of fibroblast cells including sulfated glycosaminoglycan,
collagen degradationComplications include megaloblastic anaemia folicacid deficiency
Alternative drugs that can be used are gabapentin carbamezepine .valporic acid
IMMUNOSUPPRESSANTS
Cyclosporine more vascularised and hypersensitive
Complication nephrotoxicity, hypertension, hypertrichosis ,
Alternate drug Tacrolimus
CALCIUM CHANNEL BLOCKER dihydropyridine derivatives , benzothiazene derivatives ,
phenyl alkaline derivative ,
It affects gingival margin interdental papilla and attached gingival of the facial and
lingual surface of mandible and maxilla.
Present as large firm dense, resilient, intensive fibrous tissue that covers the alveolar
ridge and extend over teeth.
Color may be normal or erythematous if inflamed.
h/f bulbous , increased crevicular fluid, dense collagen bundles.
Treatment surgical removal by series of gingivectomies
CONDITIONED ENLARGEMENT- the systemic condition of patient exaggerate the
usual response to dental plaque.. Types of conditioned enlargement can be --PREGNANCY- marginal or generalized, single or multiple tumour like masses , discrete
mushroom like spherical mass protrude from gingival margin often from interproximal
space.
h/f - angiogranuloma both marginal and tumour like enlargement are caused by central
mass of connective tissue.
Newly formed capillaries are diffusely arranged and with edema and chronic
inflammatory exudates.
Treatment spontaneous reduction in the size of gingival enlargement occurs after
delivery. Complete elimination of the residual inflammatory lesion requires the removal
of all plaque deposits and factors that favour its accumulation
PUBERTY
Seen in both males and females and appear in areas of plaque accumulation.
Prominent bulbous interdental papillae
Affect marginal gingival and idp.
Facial gingival is mainly affected
h/p shows degenerative changes and edema.
After puberty there is spontaneous reduction of enlargement ,but it does not
disappear until plaque and calculus are removed.
VITAMIN C DEFICIENCY (scurvy)
PYOGENIC GRANULOMA
non specific conditioned enlargement
exaggerated condition in response to minor trauma
tumour like discrete spherical pedunculated attachment with a broad base
appear as bright red or purple , either friable or firm depending on duration
present with surface ulceration and prulent discharge
treatment surgical excision of lesion and elimination of local irritating factor
SYSTEMIC DISEASES CAUSING GINGIVAL ENLARGEMENT
GRANULOMATOUS DISEASES
WEGENERS GRANULOMATOSIS
Acute granulomatous necrotizing lesion ulceration , gingival enlargement ,tooth mobility,
exfoliation of tooth delayed healing response, reddish purple and it bleedseasily.
h/f scattered giant cell foci of acute inflammation micro abscess, acantholytic
epithelium
NEOPLASTIC
Benign tumorof gingiva
EPULIS generic term used clinically to designate all discrete tumors and tumor like
masses of gingival inflammation
Papilloma
Fibroma
Peripheral giant cell granuloma
Central giant cell granuloma
leukoplakia
gingival cyst
MALIGNANT TUMORS
SCC, Malignant melanoma ,
Sarcoma fibro sarcoma , kaposis sarcoma , lympho sarcoma )
METASTASIS
Adenoma
Lung ca
Papillary hepatocellular ca
Renal cell ca
Hypernephroma
Chondro sarcoma
Testicular tumor
FALSE ENLARGMENT
Not true enlargement
Result of increase in size of underlying areas
Eg pagets disease, fibrous dysplasia , cherubism , ameloblastoma , osteosarcoma.
Underlying tissue cause developmental enlargement
COUNTOUR OF GINGIVA
Normal is scalloped and round. And depends on the shape of tooth , alignment in arch , location
and size of proximal contact and diamension and shape of embrasures. Interdental papilla is
pyramidal and pointed in anterior region and in posterior region it is tent shaprd filling the area.
Various diseased conditions related to gingival contour are
Acute and chronic gingivitis marginal gingival will be rounded or rolled out
Gingival enlargement papilla may be bulbous
STILLMANS CLEFT these are apostrophe shaped indendations which extend from and into
gingival margin along the root surface most frequently on the labial or buccal surface. The
margins of cleft are rolled out underneath linear gap in the gingival and the remainder of gingival
margin is blunt instead of knife edge.
McALLS FESTOON
They are enlargement of marginal gingival with formation of lifesaver like gingival prominence
in relation to canine and premolar facial surfaces. earlier concept was it is.mainly due to TFO.
But now it is due to inflammatory changes of marginal gingiva .
ANUG punched out interdental papilla
INTERDENTAL GINGIVA shape is governed by contour of proximal tooth surface location
and shape of embrasure.
TARNOW AND NORLAND classification of interdental gingiva based on anatomic
landmark interdental contact point , apical extent of facialCEJ , coronal extent of
proximal CEJ ,
Occupies the entire embrasure space apical to interdental contact point .
Class 1
Class 2
Class 3
CONSISTENCY
Normal consistency is firm and resilient and is due to collagenous nature of lamina
propria and its contiguity with mucoperiosteum
and it is firmly attach to
mucoperiosteum
Detection of consistency by palapation or by using blunt instrument which may pits on
pressure if it is soft and edematous.- and it is due to loss of collagen fibers in connective
tissue, fluid infiltration , and thinning of epithelium
Conditions showing change in consistency are acute and chronic gingivitis
Acute Gingivitis
Diffuse puffiness and softening
Sloughing with grayish pustules of debris adhering to surface
H/P diffuse oedema , fatty infiltration ad exanthematous necrosis with formation of
pseudomembrane of bacteria , PMNs and degenerated epithelial cells
Vesicle formation- inter cellular and intracellular oedema with degenerated nucleus and,
cytoplasm
Chronic gingivitis
Soggy puffiness that pitson pressur
Marked softness and friaibility of areas of redness and desquamation
Firm , leathery consistency in case of smokers
H/f fluid infiltration and cells of inflammatory exudates , degeneration of connective
tissue epithelium , inflamed engorged capillaries , thinning of epithelium , fibrous and
epithelial proliferation and chronic inflammation
SURFACE TEXTURE
Normal texture is orange peel appearance tested after drying mucosa. Restricted to
attached gingival and central portion of IDP .localized to subpapillary area.
loss of stippling is the earliest sign of gingivitis
absent in infants ,appearsat the age offive
disappears at old age
stimulated by tooth brush
it is due to alternate rounded protuberance and depression of connective tissue ,
papillary projection of connective tissue projects into elevation and depression . it
is the site of gingival fibre attachment.
GINGIVAL POSITION
actual position level of epithelial attachment on teeth
apparent position is level of gingival margin
RECESSION
Refers to exposure of tooth surface by apical shift in the position of gingival
Shallow narrow
Shallow wide
Deep narrow
Deep wide
P .D MILLER -1985
Class 1 marginal tissue recession that does not extent to mucogingival junction, no loss of hard
and soft tissue in interdental area , no tooth malposition
Class 2 marginal tissue recession that extend to or beyond MGJ , no loss of hard and soft
tissue in interdental area , no tooth malposition
Class 3 marginal tissue recession extend to or beyond muco gingival junction . losss of hard
and soft tissue in interdental area
Class 4 marginal tissue recession extend to or beyond MGJ severe loss of hard and soft tissue
interdentally
TYPES
1. Localized
2. Generalized
3. Visible .> CEJ to margin
4. Hidden > CEJ to base of pocket
CLINICAL SIGNS
Exposed rootsurface
Abrasion of cementum exposed by recession
Sensitivity of surface
Hyperemia of pulp
Oral hygiene problems
SIGNIFICANCE OF RECESSION
Exposed root surface suspectible tocaries
Abrasion of cementum exposed bycaries
Hyperemia of pulp
Oral hygiene problems
MANAGEMENT OF RECESSION
Composite restoration
orthodontics
TREATMENT
FREE SOFT TISSUE GRAFTS
Pedicle autograft
Langer s graft
GINGIVAL INDEX
The gingival index provides an assessment of the gingival inflammatory status that can be used
in practice to compare gingival health before and after phase 1 therapy or before and after
surgical therapy. It can also be used to compare the gingival status at recall visits. Attaining good
intraexaminer and interexaminer calibration is imperative in the dental office.
The sulcus bleeding index provides an objective and easily reproducible assessment of the
gingival status. It is extremely useful for detecting early inflammatory changes and the presence
of inflammatory lesions located at the base of the periodontal pocket, which is an area
inaccessible to visual examination. Patients can easily understand this index; therefore, it can be
used to enhance the patients motivation for plaque control.
They are indexes used to assess gingival status
TYPES OF GINGIVAL INDEXES
1. Gingival index
2. Modified gingival index
3. Gingival bleeding index
GINGIVAL INDEX
0
1
2
3
SCORE
0.1 -1
1.1 2
2.1 3
Absence of inflammation
Mild inflammation, slight change in color,
edema, no bop
Moderate inflammation, moderate glazing
,redness , edema , bop
Severe
inflammation,
marked
redness,
hypertrophy , ulceration , tendency to
spontaneous bleeding
Mild gingivitis
Moderate gingivitis
Severe gingivitis
EXUDATION
Presence of an abundant number of neutrophils in the gingival fluid transforms into
purulent exudates
Character ; protein content high
Glucose content low
Specific gravity high
Ph < 7.3
Ldh high
Cells inflammatory and parenchymal cells
Clinically the presence of pus can bedetected by placing the ball of index finger along the lateral
aspect of the marginal gingival and applying pressure in a rolling motion towards the crown.
Visual examination without digital pressure is not enough. The purulent exudate is formed in the
inner pocket wall, and therefore the external appearance may give no indication of its presence.
Exudate formation does not occur in all periodontal pockets, but digital pressure often reveals it
in pockets where its presence is not suspected.
Detection of Pockets. The only accurate method of detecting and measuring periodontal pockets
is careful exploration with a periodontal probe. Pockets are not detected by radiographic
examination. The periodontal pocket is a soft-tissue change. Radiographs indicate areas of bone
loss in which pockets may be suspected, but they do not show pocket presence or depth, and
consequently they show no difference before and after pocket elimination unless bone
has been modified.
Gutta-percha points or calibrated silver points can be used with the radiograph to assist with
determining the level of attachment of the periodontal pockets . They may be used effectively for
individual pockets or in clinical research, but their routine use throughout the mouth would be
difficult to manage. Clinical examination and probing are more direct and efficient.
Bleeding on Probing. The insertion of a probe to the bottom of the pocket elicits bleeding if the
gingiva is inflamed and if the pocket epithelium is atrophic or ulcerated. Noninflamed sites
rarely bleed. In most cases, bleeding on probing is an earlier sign of inflammation than gingival
color changes However, color changes may present without bleeding on probing.
Depending on the severity of inflammation, bleeding can vary from a tenuous red line along the
gingival sulcus to profuse bleeding. If periodontal treatment is successful, bleeding on probing
will cease.
To test for bleeding after probing, the probe is carefully introduced to the bottom of the pocket
and gently moved laterally along the pocket wall. Sometimes bleeding appears immediately after
the removal of the probe; other times, it may be delayed for a few seconds. Therefore, the
clinician should recheck for bleeding 30 to 60 seconds after probing
As a single test, bleeding on probing is not a good predictor of progressive attachment loss;
however, its absence is an excellent predictor of periodontal stability.When bleeding is present in
multiple sites of advanced disease, bleeding on probing is a good indicator of progressive
attachment loss. Armitage
the presence of bleeding on probing in a treated and maintained patient population is an
important risk predictor for increased loss of attachment. (armitage 1996)
The insertion of a soft wooden interdental stimulator in the interdental space produces a similar
bleeding response. This tool can be used by the patient to self-examine the gingiva for the
presence of inflammation.
When to Probe. The probing of pockets is performed at various times for diagnosis and to
monitor the course of treatment and maintenance. The initial probing of moderate or advanced
cases is usually hampered by the presence of heavy inflammation and abundant calculus, and it
cannot be done very accurately. Probing at this stage is also difficult as a result of the discomfort
and pain that occurs when the gingival tissues are inflamed.
The purpose of this initial probing, together with the clinical and radiographic examination, is to
determine whether the tooth should be saved or extracted. After the patient has performed
adequate plaque control for some time and the calculus has been removed, the major
inflammatory changes disappear, and an accurate probing of the pockets can be performed. The
purpose of this second probing is to accurately establish the level of attachment and the degree of
involvement of roots and furcations. Data obtained from this probing provides valuable
information for treatment decisions. Later during periodontal treatment, probings are done to
determine changes in pocket depth and to ascertain healing progress after different procedures.
Probing Around Implants. Because implants are susceptible to bone loss, probing around them
becomes part of examination and diagnosis. A traditional periodontal probe may be used under
light force (e.g., 0.25 N) without damaging the periimplant mucosal seal.
Automatic and Electronic Periodontal Probing. The use of the periodontal probe is the classic
method to detect pocket depth and loss of attachment. However, it presents some problems in
terms of reproducibility of the measurements. Accuracy and reproducibility depend not only on
root morphology and tissue changes but also, on the probing technique, the probing force, the
size of the probe, the angle of insertion of the probe, and the precision of the probes calibration
Probing Force. One of the main problems of reproducibility has been the variation of probing
force. The development of pressuresensitive probes has helped to overcome this. , forces up to
30 g, the tip of the probe remains within the junctional epithelium,5 whereas forces of up to 50 g
are necessary to reach the bone level.
Probe Angulation. Standardization of the probe tip (i.e., <1 mm) and the addition of registration
stents to maintain reproducible probe angulation have been used ., commercially available,
computer-assisted technology has been used to improve probing accuracy and reproducibility. In
addition to more accurate measurement, the data derived from automatic probing can become
part of the electronic record. Once incorporated, clinical changes and patterns of disease activity
can be easily determined. These records also provide feedback to the patient.
The Florida Probe System consists of a probe handpiece, a digital readout, a foot switch, a
computer interface, and a computer. The end of the probe is 0.4 mm, and it reciprocates through
a sleeve that provides a reference by which measurements are made.
These measurements are made electronically and transferred automatically when the foot switch
is pressed or when a voice command is given. Constant probing force is provided by coil
springs inside the probe handpiece and a digital readout . This method combines the advantages
of a constant probing force with precise electronic measurement and computer storage of data,
thereby eliminating the potential errors associated with visual reading and the need for an
assistant to record the measurements.
The automatic probe appears to underestimate deep probing depths but to show less variability
than conventional probing. The automatic probe also has the problem of providing little tactile
sensitivity, thereby making it more difficult to walk the probe.
Electronic systems such as the Interprobe and the Periprobe provide constant probing force and
computer storage of data, but their reproducibility is only slightly better than that of conventional
methods.
The lack of standardization between probings by different individuals and at different times by
the same individual depend not only on root morphology and tissue changes but also on the
probing technique, the probing force, the size of the probe, the angle of insertion of the probe,
and the precision of the probes calibration. For measurements of clinical attachment loss, it is
necessary
to
identify
the
location
of the CEJ.
PERIODONTAL STATUS
POCKET
DEFINITION
As a pathologically deepened gingival sulcus.
Periodontal Pockets. Examination for periodontal pockets must include their presence and
distribution on each tooth surface, the pocket depth, the level of attachment on the root, and the
type of pocket (i.e., suprabony or infrabony).
Signs and Symptoms. Although probing is the only reliable method of detecting pockets,
clinical signs such as color changes (i.e., a bluish-red marginal gingiva or a bluish-red vertical
zone that extends from the gingival margin to the attached gingiva); a rolled edge separating
the gingival margin from the tooth surface; or an enlarged, edematous gingiva may suggest their
presence. The presence of bleeding, suppuration, and loose, extruded teeth may also denote the
presence of a pocket
Periodontal pockets are generally painless, but they may give rise to symptoms such as localized
or sometimes radiating pain or the sensation of pressure after eating that gradually diminishes. A
foul taste in localized areas, sensitivity to hot and cold, and toothache in the absence of caries is
also sometimes present.
CLASSIFICATION
1) based on morphology
- gingival pocket
- periodontal pocket
2) based on relationship on alveolar crest
- superabony ( supracrestal/ supraalveolar)
- intraboney ( infrabony, subcrestal, intraalveolar)
3) Based on number of surface involved.
- Simple
- Compound
- Complex
- Spiral
4) Based on nature of soft tissue
- Edematous
- Fibrotic
5) Based on disease activity
- Active
- Inactive
CLINICAL FEATURES
PATHOGENESIS OF POCKET
DETECTION OF POCKETS
-
WHO probe, CPITN probe: CPITN- C, CPITN-E, Nabers probe, MichiganO probe
PROBING TECHNIQUE
-
The probe should be inserted parallel to the vertical axis of teeth and walk
circumferentially around each surface of each tooth to detect areas of deepest
penetration.
To detect interdental craters( obliquely placed)
Level of pocket depth below which clinical attachment loss will occur as a result of
treatment procedure performed.
CONTENT OF POCKET
-
GENERATION OF PROBE
-
Force of introduction
Shape and size of probe tip
Angle of insertion
Direction of introduction
LOSS OF ATTACHMENT
-
Level of attachment is the distance between the base of pocket and fixed point on the
crown (CEJ)
Determination of LOA
-
Probing depth is the distance between base of pocket and gingival margin.
LOA is the distance between base of pocket and CEJ.
WHEN TO PROBE?
-
Read out
CONVENTIONAL
CRITERIA
PROBING
1mm
0.1mm
12mm
10mm
Non standardized
Constant and standard
Non invasive
Non invasive or light weight
Easy to use
Easy to use
Easy to access any location Easy to access any location
around all teeth
around all teeth
Subjective
A guidance system to ensure
proper angulation
Easily sterilized
Complete sterilization of all
Simple SS instrument
portion entering mouth
No biohazard
Depending on voice dictation Direct electronic readings
Digital output
FURCATION
DEFINITION:
Area of complex anatomic morphology difficult or impossible to debride by routine
periodontal instrumentation.
FURCATION ARROW
-
A radiolucent shadow over mesial/ distal root or proximal Furcation area; usually
seen in maxillary first molar; indicative of furcaton.
PARTS OF FUCATOIN
-
CLASSIFICATION
1) Tarnow and Fletcher (1984)- vertical Furcation
- Grade A: vertical loss of 1 to 3 mm
- Grade B: vertical loss of 4 to 6 mm
- Grade C: vertical loss of 7 mm
2) Lindhe and Nyman (1983)- horizontal Furcation
- Grade 1: loss of inter-radicular bone <1/3rd (initial)
- Grade 2: loss of inter- radicular bone>1/3rd but not through and through.
- Grade 3: through and through loss of inter- radicular bone (total)
3) Glickmans classification
- Grade 1: incipient or early stage
- Grade 2:Cul-de-sca with definite horizontal component
- Grade 3: bone not attached to dome
- Grade4: through and through
Bacterial plaque and inflammatory consequences that result from its long term
presence.
In maxillary molars, the mesial Furcation entrance is located much closer to palatal
thn buccal tooth surface. Thus mesial Furcation should be probed from palatal aspect
of tooth.
The distal Furcation entrance of a maxillary molar is generally located midway
between buccal and palatal surfaces and therefore it could be probed from either
buccal or palatal aspect of tooth.
PATHOLOGICAL MIGRATION
-
Refers to tooth displacement that results when balance among factors that maintain
physiologic tooth position is disturbed by periodontal disease.
DRIFTING
-
RUSSELS RULE
-
1
2
4
6
Criteria
Negative: neither overt area
of inflammation nor loss of
function
Mild gingivitis; overt area of
inflammation I
Gingivitis:
inflammation
completely circumscribe the
tooth
Use only when radiographs
are available
Gingivitis
with
pocket
formation:
epithelial
Radiographic features
Normal
INTERPRETATION
0-0.2 clinically normal
0.3-0.9- simple gingivitis
1-1.9- beginning of destructive periodontal disease
2-4.9- established periodontal disease
5-8- terminal disease
PERIODONTITIS
CHRONIC PERIODONTITIS
Infectious disease resulting in inflammation within the supporting tissues of the teeth,
progressive attachment loss and bone loss.
AGGRESSIVE PERIODONTITIS
Primary factors
Otherwise clinically healthy patient.
Rapid attachment loss and bone destruction.
Amount of microbial deposits inconsistent with disease severity.
Familial aggregation of diseased individuals.
Gingival abscess
Periodontal abscess
Pericoronal abscess
ABSCESSES OF PERIODONTIUM
ABSCESS
ETIOLOGY
A) Extension of inflammation from perio pocket to supporting periodontal tissues.
B) Lateral extension of inflammation from inner surface of perio pocket into connective
tissue of pocket wall.
C) Formation of pocket with tortuous course around the root.
D) Incomplete removal of calculus.
E) Trauma to tooth or perforation of lateral wall in endo therapy may occur in absence of
periodontal disease.
GINGIVA ABSCESS
Localized acute inflammatory lesion from microbial plaque, trauma, foreign body impact.
PERICORONAL ABSCESS
Inflammation of soft tissue, operculum covering partially erupted tooth.
Mandibular 3rd molar: associated with plaque, food impaction, and trauma.
CLASSIFICATION OF PERIODONTAL ABSCESS BASED ON ETIOLOGY
1) Periodontal related abscess: when acute infection originates from bacteria present in
subgingival biofilm in a deepened periodontal pocket.
2) Non periodontal related abscess: when acute infection originates from bacteria of
another location.
ETIOLOGY OF ABSCESS
Extension of chronic lesion.
Post therapy abscess( post scaling, post surgical, post antibiotic)
Non periodontitis related abscess: foreign body impaction in gingival sulcus, root
morphology alteration, tooth perforation or fracture, poorly controlled diabetes mellitus.
ACUTE ABSCESS:
CHRONIC ABSCESS:
Dull pain
Localized inflammation
Slight tooth dilacerations
Intermittent exudation
Fistulous tract associated with deep pocket
PERIODONTAL ABSCESS:
PULPAL ABSCESS:
Large restoration
Non vital tooth
Localized swelling
Fistula
Severe pain, difficult to locate
Sensitivity to percussion
Prichard established the following four criteria to determine adequate angulation of periapical
radiographs:
1. The radiograph should show the tips of molar cusps with little or none of the occlusal surface
showing.
2. Enamel caps and pulp chambers should be distinct.
3. Interproximal spaces should be open.
4. Proximal contacts should not overlap unless teeth are out of
line anatomically
Periodontitis
Radiographic changes in periodontitis follow the pathophysiology of periodontal tissue
destruction and include the following:
1. Fuzziness and disruption of lamina dura crestal corticationcontinuity is the earliest
radiographic change in periodontitis and results from bone resorption activated by extension of
gingival inflammation into the periodontal bone. Depicting these early changes depends greatly
on the radiographic technique, as well as on anatomic variations(thickness and density of
interdental bone, position of adjoining teeth). No correlation has been found between crestal
lamina dura in radiographs and the presence or absence of clinical inflammation, bleeding on
probing, periodontal pockets, or loss of attachment. Therefore it can be concluded that the
presence of an intact crestal lamina dura may be an indicator of periodontal health, whereas its
absence lacks diagnostic relevance.
2. Continued periodontal bone loss and widening of the periodontal space results in a wedgeshaped radiolucency at the mesial or distal aspect of the crest . The apex of the area is pointed in
the direction of the root.
3. Subsequently, the destructive process extends across the alveolar crest, thus reducing the
height of the interdental bone. As increased osteoclastic activity results in increased bone
resorption along the endosteal margins of the medullary spaces, the remaining interdental bone
can appear partiallyeroded .
4. The height of the interdental septum is progressively reduced by the extension of inflammation
and the resorption of bone
5. Frequently a radiopaque horizontal line can be observed across the roots of a tooth. This
opaque line demarcates the portion of the root where the labial or lingual bony plate has been
partially or completely destroyed from the remaining bone-supported portion
Zero radiography
Determination of Prognosis
The prognosis is a prediction of the probable course, duration, and outcome of a disease based on
a general knowledge of the pathogenesis of the disease and the presence of risk factors for the
disease. It is established after the diagnosis is made and before the treatment plan is established.
The prognosis is based on specific information about the disease and the manner in which it can
be treated, but it also can be influenced by the clinicians previous experience with treatment
outcomes (successes and failures) as they relate to the particular case.
Prognosis is often confused with the term risk. Risk factors are those characteristics of an
individual that put the person at increased risk for developing a disease. In contrast, prognosis is
the prediction of the course or outcome of a disease. Prognostic factorsare characteristics that
predict the outcome of disease once thedisease is present.
Types of Prognosis
Although some factors may be more important than others when assigning a
prognosis, consideration of each factor
may be beneficial to the clinician. Historically, prognosis classification schemes
have been designed based on studies evaluating tooth mortality. One scheme
assigns the following classifications:
Poor prognosis: 50% attachment loss, Class II furcation involvement (location and
depth make maintenance possible
but difficult).
Questionable prognosis: >50% attachment loss, poor crown-toroot ratio, poor root
form, Class II furcations (location and depth make access difficult) or Class III
furcation involvements; >2+ mobility; root proximity.
In contrast to schemes based on tooth mortality, Kwok and Caton have proposed a scheme based
on the probability of obtaining stability of the periodontal supporting apparatus. This scheme is
based on the probability of disease progression as related to local and systemic factors
Prognosis can be divided into overall prognosis and individual tooth prognosis. The
overall prognosis is concerned with the dentition as a whole. Factors that may
influence the overall prognosis include patient age; current severity of disease;
systemic factors; smoking; the presence of plaque, calculus, and other local factors;
patient compliance; and prosthetic possibilities . The overall prognosis answers the
following questions:
The individual tooth prognosis is determined after the overall prognosis and is
affected by it.6 For example, in a patient with a poor overall prognosis, the dentist
likely would not attempt to retain a tooth that has a questionable prognosis because
of local conditions.
Treatment plan
After the diagnosis and prognosis have been established, the treatment is planned.
The plan should encompass short- and long-term goals.
The short-term goals are the elimination of all infectious and inflammatory
processes that cause periodontal and other oral problems that may hinder the
patients general health. Basically, the short-term goals are to bring the oral cavity
to a state of health. This may require periodontal procedures, as well as other
dental therapy, such as endodontics and correcting oral mucous membrane
pathology. Referral to other dental and medical specialties will be necessary.
The treatment plan is the blueprint for case management. It includes all procedures
required for the establishment and maintenance of oral health and involves the
following decisions:
Need for emergency treatment (pain, acute infections)
Teeth that will require removal
Periodontal pocket therapy techniques (surgical or nonsurgical)
Endodontic therapy
The need for occlusal correction, including orthodontic therapy
The use of implant therapy
The need for caries removal and the placement of temporary and final
restorations
Prosthetic replacements that may be needed and which teeth will be abutments if
a fixed prosthesis is used
Decisions regarding esthetic considerations in periodontal therapy
Sequence of therapy