Anda di halaman 1dari 82

Diagnosis And Treatment Plan

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

may be valuable asset in diagnosis)


Chief complaint
Symptoms
Medical history
Dental history
Vital statics include,
Patient name
Age
Sex
Home
Address
Phone number
Marital status
Family status
Occupation
Importance of name:
To recognize the patient
Aids in establishing rapport with the patient.
To maintain record
Importance of age:
Indicates vital statistics
Certain diseases have a predilection at certain age groups.:
Age related periodontal diseases,
1. Chronic periodontitis>30 yrs
2. Aggressive periodontitis <30yrs
Herpetic gingivostomatitis is common in children below 6 years.Age also has
effect on dental procedure and personal care.
To prescribe dosage of drugs
Importance of sex:
Physical and psychological maturation
Certain diseases are common in either males or females.:
Desquamative gingivitis is common in females.
Periodontal disease is higher among males compared to females

Gingivitis is more common in boys than in girls below 12 years.


Importance of address:
Various conditions are endemic to certain areas. Address tells about the presence
of fluoride in drinking water.
Importance of telephone no:
For change of appointment. Immediate consultation may be needed so that urgent
treatment may proceed.
Importance of occupation :
May be a factor in the etiology of certain occupational disease like asbestosis and
erosion.
To have idea about socioeconomic status.
Economic and social status:
People who are under stress are more likely to suffer from psychosomatic disease
like lichen planus and ANUG.
Chief complaint
Common chief complaints
Pain
Sensitivity
Bleeding gums
Halitosis
Swelling
Burning sensation( most probably desquamative gingivitis)
Delayed tooth eruption
Loose teeth
Food impaction
It is patients response to the dentists question
Reason for which patient has come or reason for seeking treatment should be

recorded in patients own words and in chronological order.


Significance :aids in diagnosis and treatment planing
History of presenting illness
Starts from beginning of first symptoms and extend to the time of
examination.When it started symptoms were worse or better.Any
aggravating or relieving factors,duration,relapse,remission etc.
Types of pain
Constant dull gnawing pain
Dull pain after eating
Deep radiating pain
Acute throbbing pain
Sensitivity to hot/cold
Sensitivity to chewing

Burning sensation in gums


Extreme sensitivity to inhaled air

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

osteoporosis, should be cautioned about possible problems related to osteonecrosis of the


jaw after undergoing any form of oral surgery involving the bone.
4. All medical problems (e.g., cardiovascular, hematologic, endocrine), including infectious
diseases, sexually transmitted diseases, and high-risk behavior for human
immunodeficiency virus infection, should be listed.
5. Any possibility of occupational disease should be noted
6. Abnormal bleeding tendencies, such as nosebleeds, prolonged bleeding from minor cuts,
spontaneous ecchymoses, a tendency toward excessive bruising, and excessive menstrual
bleeding, should be cited. These symptoms should be correlated with the medications that
the patient is taking
7. The patients allergy history should be taken, including that related to hay fever, asthma,
sensitivity to foods, sensitivity to drugs (e.g., aspirin, codeine, barbiturates, sulfonamides,
antibiotics, procaine, laxatives), and sensitivity to dental materials (e.g., eugenol, acrylic
resins).
8. Information is needed regarding the onset of puberty and for females, menopause,
menstrual disorders, hysterectomy, pregnancies, and miscarriages.
9. A family medical history should be taken, including that of bleeding disorders and
diabetes.
10. clinician should note any previous occurrences of myocardial infarction, coronary artery
disease, coronary surgery, and cardiac valve repair/replacement so that precautions such as
antibiotic prophylaxis for patients with artifi cial valves can be taken. Periodontal probing
is an invasive procedure that may require prophylactic antibiotics before proceeding.
Some patients are aware of blood pressure abnormalities, but many others are not. Th is is
a good time to obtain a baseline blood pressure reading
11. Diabetes is a major problem in successful management of periodontal diseases. For a
known diabetic, it should be determined whether (1) the disease is controlled and (2) the
patient has visited a physician in the past 3 to 6 months. If the patient is unaware of having
diabetes, questions regarding a personal history of periodontal abscesses and blood
relatives with diabetes may suggest a problem requiring medical evaluation.
12. Infectious diseases, such as hepatitis, acquired immunodefi ciency syndrome (HIV/AIDS),
and tuberculosis (TB), should be included in the questionnaire. Abnormal bleeding is
associated with hepatitis infection. All dentists and dental hygienists are encouraged to
receive active immunization against hepatitis B. HIV infection oft en produces associated
periodontal problems Questioning with regard to this disease must be managed discreetly.
TB is quite prevalent among recent immigrants, and its incidence is resurging among
patients, in general. Strict adherence to infection-control practice recommendations from
the Centers for Disease Control and Prevention and other agencies is required.
13. Hepatitis and cirrhosis are common problems that aff ect dental care. Cirrhosis may impair
a patients healing potential. Recurrent kidney infections may require antibiotic
prophylaxis before periodontal treatment.

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

Post prandial plasma


<140mg/dl
glucose
Oral glucose tolerance Plasma glucose
test
Non fasting plasma

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%

Effect of the diabetes mellitus on periodontium


A. Bacterial pathogens
Increased glucose content of gcf changed the environment of microflora- qualiatative
changes in bacteria
Subgingival flora composed prilimarily of capnocytophaga, anaerobic vibrios,
actinomyces
B. Impaired nuetrophil function
Impaired chemotaxis
Defective phagocytosis or impaied adherence primary defense against periodontal
pathogens diminished- bacterial proliferation unchecked
C. Increased collagenase activity and decreased collagen and extracellular matrix
formation
In hyperglycemic state numerous proteins and matrix molecules undergone non
enzymatic glycosylation to produce AGEs (accumulated glycosylation end products)
Collagen cross linked by AGE formation
Less soluble and less likely to be repared or replaced
Impairs tissue integrity
Most susceptible to breakdown

Effects of periodontal disease on diabetes.


Periodontal disease has been determined to be a potential risk factor for poor glycemic
control in patients with diabetes.
In hyperglyceminc state,numerous proteins and matrix molecules undergo a nonenzymatic glycosilation ,resulting in advance glycation end products(ADEs).
Macrophages have high affinity receptors for a common structural elements an AGEmodified proteins.Binding of AGE modified protein to the macrophage receptor(RAGE)
initiates a cylcle of cytokine upregulation,with synthesis mostly of IL-1 and TNF alfa.The
synthesis and secretion of cytokines are increased with trigger degradative
cascade,resulting in connective tissue degradation.

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.

Standard antibiotic prophylaxis regimen

Procedures that need prophylaxis


All periodontal procedures involving probing
Subgingival scaling
Gingival curettage
Gingivoplasty,gingivectomy,flap surgery
Management od ischemic disease
A patient on angina episode in dental chair should receive
Discontinue procedure
0.3-0.6 mg nitroglycerine
Reassure the patient
Administer oxygen
If symptoms subside:complete procedure at earliest
If angina signs and symptoms do not resolve with this within 3 min give another
dose of nitroglycerine
A third nitroglycerine tablet may be given 3 min after second

If chest pain is not relieved after 3 tablets of nitroglycerine-indicates MI.


Patient under anticoagulant therapy
If under anticoagulant or antiplatelet therapy traditional management of patient on
anticoagulant or antiplatelet therapy was to discontinue therapy about 3-5(for
antiplatelet)7-10(anticoagulant)days before planned surgical procedure.Recent
evidence and new thoughts regarding this for periodontal surgeries or extractions can
be done without altering the drug therapy,without leading to intraoperative or post
operative complications.
PREGNANCY
MANAGEMENT:

2nd trimester is the safest time for treatment


As uterus increases in size during 3rd trimester obstruction of venacava & aorta
may occur if placed in supine position 8: reduction in cardiac blood supply will
lead to supine hypotension syndrome
Supine hypertensive syndrome :-Prevented by tilting patient to left, elevate right
hip 5 6 .
Appointments should be short
ideally no medications should be presrcibed
Minimum radiation, lead aprons can be used

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

Dry cold, yellow puffy skin

Warm,thin.soft,mosit skin

Tick tongue

Exophthalmos

Drowsiness

Tremor

Loss of hair

Weight loss

Weight gain
Decreased sweating
Hoarse voice
Head ache

Hyperthyroidism is absolute contraindication for use of local anesthetic


containing epinephrine.
Care with sedatives in hypothyroidism, chance for excessive sedation.

CDC CLASSIFICATION OF SMOKERS

Current smoker:-1OO cigarettes smoked over lifetime and now too.


Former smokerz- 100 cigarettes smoked over lifetime and now not smoking.
Non smoker-not smoked 100 cigarettes over lifetime
pack year it is a unit for measuring the amount a person has smoked over a long
period of
time.
Calculation:-number of pack years=packs smoked per day x years as a smoker
OR (Number of cigarettes smoked per day x number of years smoked)/20(1 pack
has 20 cigarettes)

EFFECTS OF SMOKING ON THE PREVALENCE AND SEVERlTY


OFPERIODONTAL DISEASE
Gingivitis

Periodontitis

decreased inflammation and bleeding


on probing
Increase prevalence and severity of periodontal
destruction
Increase pocket depth,attachment loss and bone
loss
Increase rate of periodontal destruction
Increase Prevalence of severe periodontitis
Increase Tooth loss
Increase Prevalence with increased number of
cigarettes smoked per day
Increase prevalence and severity with smoking
cessation

EFFECTS OF SMOKING ON THE ETIOLOGY AND PATHOGENESIS OF


PERIODONTAL DISEASE
Microbiology

No effect on rate of plaque accumulation


Increase incolonization of shallow periodontal
pockets by periodontal pathogens

Immunology

Physiology

Increase in levels of periodontal pathogens in


deep periodontal pockets
Decrease nuetrophil
Decrease IgG2
Altered neutrophil chemotaxis,phagocytosis and
oxidative burst
Increase TNF-a and PGE2 in gingival crevicular
fluid (GCF)
Increase neutrophil collagenase and elastase
elastase in GCF
Increase production of PGE2 by monocytes in
response to
Decrease gingival bleeding
Decrease GCF flow, BOP
Decrease subgingival temperature
Increase time needed to recover from local
anesthesia

EFFECTS OF SMOKING ON THE RESPONSE TO PERIODONTAL THERAPY


Non surgical therapy

Decrease clinical response to scaling and root


Planing
Decrease reduction in pocket depth
Decrease gain in clinical attachment levels
Decrease negative impact of smoking with
level of plaque control

Surgical

Decrease pocket depth after surgery


Decrease deterioration of furcations after
surgery
Decrease in gain in clinical attachement levels
Decreas e bone fill, recession and membrane
exposure after GTR
Decrease pocket depth reduction after DFDBA
Decrease pocket depth reduction and gain
clinical attachement levels after debridement
Conflicting data on the impact of smoking on
implant success

Smoking cessation should be recommended


before implants
SMOKING CESSATION PROTOCOL
Ask :- Patients about their use of tobacco at every visit. Check for oral signs of tobacco use and
mention the observations to the patient to help him or her face facts
Advice :- Non-users to never use tobacco,advice users to quit. Advice, users to quit, advice on
associations between orai disease 8: smoking & benefits of cessation
Assess :- Patient s interest & readiness to participate in tobacco cessation programs
Assist :- Use appropriate techniques to assist patient in tobacco cessation
Arrange : Follow up contacts with the patient

NICOTINE REPLACEMENT THERAPIES


Nicotine Gum,
Nicotine Patch,
Nicotine inhaler,
Nicotine Nasal Spray,
Nicotine Lozenges
Dental history
Current Illness. Some patients may be unaware of any problems, but many may report bleeding
gums; loose teeth; spreading of the teeth with the appearance of spaces where none existed
before; foul taste in the mouth; and an itchy feeling in the gums that is relieved by digging with a
toothpick. There may also be pain of varied types and duration, including constant, dull, gnawing
pain; dull pain after eating; deep radiating pains in the jaws; acute throbbing pain; sensitivity
when chewing; sensitivity to hot and cold; burning sensation in the gums; and extreme sensitivity
to inhaled air.
A preliminary oral examination is done to explore the source of the patients chief complaint and
to determine whether immediate emergency care is required. If this is the case, the problem is
addressed after the consideration of the medical history
The dental history should include reference to the following,

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.

Pathologic-periodontal infection, tongue coating, xerostomia,stomatitis, Faulty restoration,


dentures, oral Ca, candidiasis, apthous ulcers

Systemic& extraoral manifestation, nasal infections, tumours, sinusitis, GERD, bronchitis,


pneumonia, TB, DM, hepatic failures, renal failures, blood dyscrasias, dehydration, pregnancy.

Halitophobia- imaginary breath malodour associated with obsessive compulsive disorder


Pseudo halitosis-caused by foods like ginger, garlic etc
Genuine halitosis- is obvious malodour with intensity beyond socially accepted level perceived.
Extra oral causes
ENT: Acute pharyngitis, Purulent sinusitis, post nasal drip-mucositis
OZENA
Chronic or purulent tonsillitis, tonsilolith, foreign body in respiratory tract or sinus cavity
Bronchi:Chronic bronchitis, Bronchiectasis, bronchial carcinoma

Gastrointestinal tract
o
o
o

Zenkers diverticulum: hernia of oesophageal walls


Gastric hernia
Regurgitation oesophagitis
Intestinal gas production
Liver: insufficiency- cirrhosis-NH3 in blood
Kidney: insufficiency-Chronic glomerulonephritis, uric acid in blood
Systemic metabolic disorder
Type 1 DM- ketone bodies (rotten apple)
Trimethylaminuria: typical fishy odour
Hormonal cause: increased progesterone in menstrual cycle
Medications: METRONIDAZOLE
Arsenic-rotten eggs

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.

Organoleptic rating (Gold Standard) : Rosenberg and MC Culloch


123456-

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

Instruments to determine halitosis


Halimeter- portable volatile sulphide monitor, they measure level of sulphide gas found in patients
breath.
Gas chromatography- detect volatile compounds
Oral chromatography-portable gas chromatography
Dark field-phase contrast microscopy
Saliva intubation test
Electronic nose- artificial nose with the capabilities o human nose. Recognize contents of odour and
analyse chemical make up consist of an assay of electronic sensors &mechanism for pattern recognition.
Perioscan- tannerella forsythia, porphyromonas gingivalis, treponema denticola & capnocytophaga
species they all share trypsin like substrate and can all be measured by (BANA) N- benzoyl-di-arginine 2naphylamide which turns orange red when a drop of fast garnets added to the solution

Treatment

Mechanical reduction of the intra oral nutrients

Tongue ckeaning
Tooth brushing
Full mouth disinfection
Chewing gum

Chemical reduction of oral micro flora load that releases malodour gases

Chlorhexidine- 0.2%, 0.12%


Halite- 0.5%chlorhex, .05%cetyl pyridinium chloride, 0.14%zinc lactate
Essential oils- Listerine rinses
Chlorine dioxide
2 phase oil water rince containing CPC
Triclosan
H2o2
Oxidising lozenges

Conversion of VSCs

Metallic salt sodium


Tooth paste
Chewing gum
Masking malodour-rinses, mouthsprays, lozenges

Masking malodour-rinses, mouth sprays, lozenges

Examination of Oral Cavity


The entire oral cavity should be carefully examined. The examination should include the lips, floor of the
mouth, tongue, palate, and oropharyngeal region, as well as the quality and quantity of saliva. Although
findings may not be related to the periodontal problem, the dentist should detect all pathologic changes
present in the mouth.

Examination of Lymph Nodes


Because periodontal, periapical, and other oral diseases may result in lymph node changes, the
diagnostician should routinely examine and evaluate head and neck lymph nodes. Lymph nodes can
become enlarged and indurated as a result of an infectious episode, malignant metastases, or residual
fibrotic changes.
Inflammatory nodes become enlarged, palpable, tender, and fairly immobile. The overlying skin may be
red and warm. Patients are often aware of thepresence of swollen glands. Primary herpetic
gingivostomatitis, necrotizing ulcerative gingivitis (NUG), and acute periodontal abscesses may produce
lymph node enlargement. After successful therapy, lymph nodes return to normal in days or weeks.

Examination of the Teeth


The teeth are examined for caries, developmental defects, anomalies of tooth form, wasting,
hypersensitivity, and proximal contact relationships.

Wasting Disease of the Teeth


Wasting is definedas any gradual loss of tooth substance characterized by the formation of smooth,
polished surfaces, without regard to the possible mechanism of this loss. The forms of wasting are
erosion, abrasion, attrition, and abfraction.

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.

Proximal Contact Relationships


Slightly open contacts permit food impaction. The dentist should check the tightness of contacts using
clinical observation and dental floss. Abnormal contact relationships may also initiate occlusal changes,
such as a shift in the median line between the central incisors, labial version ofthe maxillary canine,
buccal or lingual displacement of the posterior teeth, and an uneven relationship of the marginal ridges.

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.

Trauma from Occlusion.


Trauma from occlusion refers to tissue injury produced by occlusal forces, not to the occlusal forces
themselves . The criterion that determines if an occlusal force is injurious is whether it causes damage in
the periodontal tissues; therefore the diagnosis of trauma from occlusion is made from the condition of
the periodontal tissues. The periodontal findings are then used as a guide for locating the responsible
occlusal relationships. Periodontal findings that suggest the presence of trauma from occlusion include
excessive tooth mobility, particularly in teeth showing radiographic evidence of a widened periodontal
space ; vertical or angular bone destruction; intrabony pockets; and pathologic migration, especially of the
anterior teeth.
The other method is to test for the movement of teeth that are subject to pressure that the patient
generates. Fremitus, vibration,or micromovement of a tooth can be felt when patients tap their teeth
together. When the patient mimics clenching the teeth and then attempts to move the mandible in
excursions, tooth movement can be observed. The patient placing a finger where the clinician felt tooth
movement helps the patient to appreciate the looseness of his or her teeth

Pathologic Migration of the Teeth


Alterations in tooth position should be carefully noted, particularly with a view toward identifying
abnormal forces, a tongue-thrusting habit, or other habits that may be contributing factors . Premature
tooth contacts in the posterior region that deflect the mandible anteriorly contribute to destruction of the
periodontium of the maxillary anterior teeth and to pathologic migration. Pathologic migration of anterior
teeth in young persons may be a sign of localized aggressive (juvenile) periodontitis.

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.

Dentition with the Jaws Closed


Examination of the dentition with the jaws closed can detect conditions such as irregularly aligned teeth,
extruded teeth, improper proximal contacts, and areas of food impaction, all of which may favor plaque
accumulation.
Excessive overbite, seen most often in the anterior region, may cause impingement of the teeth on the
gingiva and food impaction, followed by gingival inflammation, gingival enlargement, and pocket
formation. The real significance of excessive overbite for gingival health, however, is controversial.
In open-bite relationships, abnormal vertical spaces exist between the maxillary and mandibular teeth.
The condition occurs most often in the anterior region, although posterior open bite is occasionally seen.
Reduced mechanical cleansing by the passage of food may lead to accumulation of debris, calculus
formation, and extrusion of teeth.
In crossbite the normal relationship of the mandibular teeth to the maxillary teeth is reversed, with the
maxillary teeth being lingual to the mandibular teeth. Crossbite may be bilateral or unilateral, or it may
affect only a pair of antagonists. Trauma from occlusion, food impaction, spreading of the mandibular
teeth, and associated gingival and periodontal disturbances may be caused by crossbite.

Functional Occlusal Relationships


Examination of functional occlusal relationships is an important part of the diagnostic procedure.
Dentitions that appear normal when the jaws are closed may present marked functional abnormalities .

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

habitat for the subgingival microbiota. Reduction in PD is considered a desirable outcome of


periodontal therapy because it is easier to restore and maintain the host microbial homeostasis
at shallow sites than at deep sites. Therefore, full mouth PD measurements provide a preliminary
assessment of a potential target of periodontal therapy.
In addition to PD, assessments of periodontal damage are made that include gingival recession,
clinical attachment level (CAL), and loss of alveolar bone.
C Other items that should be collected as part of a periodontal examination are deviations from
normal periodontal anatomy (e.g., altered gingival contours, lack of keratinized gingiva),
position of the mucogingival junction, tooth hypermobility, furcation involvement, occlusal
relationships, and root morphology/length. Any factor that might affect the development of
periodontal disease or interfere with its successful treatment should be noted. Findings from the
detailed periodontal examination are combined with information obtained from the
medical/dental histories and results of the extraoral and oral exams to arrive at an overall
periodontal diagnosis. The diagnosis is the starting point for thinking about the type of treatment
that is best suited to fit the patients specific needs.
MEASURING THE WIDTH OF ATTACHED GINGIVA
1. Anatomically stretch the lips or cheek to demarcate the mucogingival line while pocket
is being probed. Measure the total width of attached gingival ,(gingival margin to
mucogingival line ) and substract the pocket or sulcus depth from it to determine width of
attached gingival
2. Functionally - tension test stretch the lip or cheek outward to demarcate mucogingival
line and to see for any movement of gingival margins. . Measure the total width of
attached gingival ,(gingival margin to mucogingival line ) and substract the pocket or
sulcus depth from it to determine width of attached gingival
3. Roll test push the adjacent mucosa coronally with a dull instrument to mark
mucogingival line. . Measure the total width of attached gingival ,(gingival margin to

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

PLAQUE AND CALCULUS

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

Normal color of gingival is coral pink

Factors contributing to normal color of gingival is


Vascular supply
Thickness and degree of keratinization
Presence of pigment containing cells

Melanin a non hb derived brown pigment responsible after normal pigmentation of skin ,
gingiva , and remainder of oral mucous membrane

Melanocytes synthesize melaninin premelanosomes or melanosomes.

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

Peutz jeugers syndrome


Albrights syndrome and Vonreckling hausens 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

SYSTEMIC conditions causing gingival pigmentation are


Jaundice
Hemochromatosis
Diabetes mellitus
Pregnancy
Anaemia
Polycythemia
Leukemia
When vascularisation increases gingival appears red (epithelial keratinization decreases)

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

venous stasis, destruction of hb, decreased

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

Based on location and distribution, gingival enlargement is designated as follows:


Localized: Limited to the gingiva adjacent to a single tooth or group of teeth
Generalized: Involving the gingiva throughout the mouth
Marginal: Confined to the marginal gingiva
Papillary: Confined to the interdental papilla

Chronic inflammatory gingival enlargement originates as a slight ballooning of the interdental


papilla and marginal gingiva. In the early stages, it produces a life-preserver shaped bulge
around the involved teeth. This bulge can increase in size until it covers part of the crowns. The

enlargement may be localized or generalized; it progresses slowly and painlessly, unless it is


complicated by acute infection or trauma
Histopathology of chronic enlargement
Chronic inflammatory gingival enlargements show
the exudative and proliferative features of chronic inflammation . Lesions that are clinically deep
red or bluish red are soft and friable with a smooth, shiny surface, and they bleed easily. They
also have a preponderance of inflammatory cells and fluid, with vascular engorgement, new
capillary formation, and associated degenerative changes. Lesions that are relatively firm,
resilient, and pink have a greater fibrotic component with an abundance of fibroblasts and
collagen fibers

Etiology. Chronic inflammatory gingival enlargement is caused by prolonged exposure to dental


plaque. Factors that favor plaque accumulation and retention include poor oral hygiene, irritation
by anatomic abnormalities, and improper restorative and orthodontic appliances.
In mouth breathers gingival will be red and oedematous , surface dehydration , it will be seen
more anteriorly
Acute inflammatory enlargement

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 ,

Alternate drug used is isradipine


Hyperplastic tissues are often removed by gingivectomy or undisplaced flap
IDIOPATHIC GINGIVAL ENLARGEMENT
(hereditary gingival hyperplasia, elephantiasis)

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)

Causes haemorrhage collagen degeneration oedema of connective tissue


Marginal gingival appears bluish red friable soft with smooth shiny surface.
Spontaneous bleeding occurson slight provocation
There may be surface necrosis with pseudomembrane formation.
PLASMA CELL GINGIVITIS
Also called atypical gingivitis or plasma cell gingivostomatitis
Seen in oral aspect of attached gingival
Allergic in origin chewingum , dentifrices
Gingival appears red friable and sometimes granular which bleeds easily.
chelitis and glossitis
cessation of exposure to allergen resolves the lesion

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

LEUKEMIA .- diffuse or marginal , localized or generalized , enlargement .


chance of infection bleeding and ulceration present.
Appear as Bluish red slimy surface moderate firm friable haemorrhage ,
Seen in acute myeloid leukemia
h/f immature and proliferating leukocytes
,edematous and degenerated connective tissue
Acute necrotizing inflammation with a pseudomembranous meshcord of fibrous pmns
and bacteria.

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

Tip of IDP located between interdental contact


point and and level of CEJ on proximal surface
of teeth
Tip of IDP located at or apical to the level of
CEJ on proximal tooth surface
Tip of IDP located at or apical to the level of
CEJ midbucally

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

Degree of Gingival Recession. During periodontal examination, it is necessary to record the


data regarding the amount of gingival recession. This measurement is taken with a periodontal
probe from the CEJ to the gingival crest, and it is drawn on the patients chart

RECESSION
Refers to exposure of tooth surface by apical shift in the position of gingival

Severity of recessin is determined by actual position


2 types localized and generalized
Etiology
age 8 percent in children, 100 percent over 50 yrs due to minor trauma or minor
pathologic involvement
faulty tooth brushing technique
gingival ablation
gingival inflammation
abnormal frenal attachment
iatrogenic dentistry
TFO deep over bite gingival inflammation gingival recession
ANATOMIC excessive attrition of teeth , tooth malformation, gingival ablation
PATHOLOGIC abnormal frenal attachment , gingival inflammation
IATROGENIC TFO , movement in labial direction ,
HABITS faulty tooth brushing technique
PHYSIOLOGIC AGE
FACTORS AFFECTING SUSCEPTIBILITY TO GINGIVAL RECESSION
Position of teeth
Root bone angle
Mucodental curvature of tooth surface
Poorly designed tooth material
CLASSIFICATION OF GINGIVAL RECESSION
{SULLIVAN AND ATKINS -1968}

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

Major etiological factors for recession

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

Monitoring and prevention

Useof desensitizing agents varnishes and dentin bonding agents

Composite restoration

Pink porcelain or composite

Removable gingival veneers

orthodontics
TREATMENT
FREE SOFT TISSUE GRAFTS

Free gingival autograft

Free connective tissue autograft

Pedicle autograft

GTR REGENERATIVE PROCEDURES

Langer s graft

Pouch and tunnel technique

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

It was given by LOE AND SILNESS in 1963


Teeth used for assessing index are 16 ,12 ,24, 36, 32, 44

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

MODIFIED GINGIVAL INDEX (LOBENE ,WEATHERFORD , ROSE ,


LENNIN 1986 )
Elimination of gingival probing to access presence or absence of bleeding
Refining of scoring system for mild and moderate inflammation
INDICES TO CHECK GINGIVAL BLEEDING
Gingival bleeding index
Eastman interdental bleeding index
Sulcular bleeding index

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.

IMPORTANCE OF GINGIVAL BLEEDING


1.
2.
3.
4.

First clinical sign of inflammation


Objective sign
Intensity of inflammation
Measure outcome of treatments
ETIOLOGY OF GINGIVAL BLEEDING
LOCAL CAUSE tooth brush trauma , impaction of hard food , gingival burns , presence
of plaque and calculus, mechanical trauma , biting on solid food
SYSTEMIC CAUSE vitamin c deficiency, vit k deficiency ,multiple myeloma , platelet
disorders ,pregnancy , medication.
DETECTION OF BLEEDING
1. Probe is introduced to bottom of pocket
2. Gently move laterally along pocket wall
3. Recheck for bleeding 30 60 sec after probing
4. Force used is 0.25 N
MICROSCOPIC FEATURE OF BLEEDING
1. Enlargement and dialation of capillaries
2. Thinning and ulceration of sulcular epithelium cause rupture of vessel
while probing

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

Bluish red thickness marginal


A bluish red vertical zone from the gingival margin to the alveolar mucosa
Gingival bleeding and suppuration
Tooth mobility
Diastema formation
Localized pain/ pain deep in the bone

PATHOGENESIS OF POCKET

The initial lesion in development of periodontitis is inflammation of gingival in response


to a bacterial challenge.
Changes are associated with different preparations of bacterial cells in dental plaque.
Pocket formation starts as an inflammatory change in connective tissue walls of gingival
sulcus. The cellular and fluid inflammatory exudate causes degeneration of surrounding
connective tissue including gingival fibers.
Just apical to the junctional epithelium collagen fibers are destroyed and area becomes
occupied by inflammatory cells and edema
Collagen loss- 2 mechanisms

1) Collagenases and other enzymes secreted by fibroblast, PMNs, macrophages destroy


collagen. These enzymes that degrade collagen and other matrix macro molecules
( matrix metalloproteinase)
2) Fibroblast phagocytes collagen fibers by extending cytoplasm processes to alignmentcementum interface and degrade collagen fibrils

As consequence of collagen loss, apical cells of JE proliferate along root, extending


finger like projections.
The coronal portion of JE detaches from root as apical portion migrates.
PMNs invade coronal end of JE and increase the number.
As PMNs increases, tissue loses cohesiveness and detach from tooth surface.
Thus sulcus bottom shifts apically and oral sulcular epithelium occupies increased
portion of sulcular (pocket) lining.
Degenerative changes in JE at base are less severe than in lateral walls as migration of JE
requires healthy viable cells.
The degree of leukocytes infiltration of JE is independent of volume of inflamed
connective tissue.
As inflammation continues, the gingiva increases in bulk and crest of gingiva margin
extends coronally. The epithelium of lateral walls of pocket proliferates to form bulbous,
cordlike extrusions into inflamed connective tissue.

HISTOPATHOLOGIC FEATURES OF PERIODONTAL POCKET

The discoloration is caused by circulatory stagnation.


Flaccidity by destruction of gingival fibers and surrounding tissues.
Smooth shiny surface by atrophy of epithelium and edema.
Pitting on pressure by edema and degeneration.
Ease of bleeding results from increased vascularity, thinning and degeneration of
epithelium and proximity of engorged vessels to inner surface.
Pain on tactile stimulation is caused by ulceration of inner aspect of pocket wall.
Pus occurs in pocket with suppurative inflammation of inner wall

DETECTION OF POCKETS
-

By walking the probe when inserted into pocket.

TYPES OF PERIODONTAL PROBE


-

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)

CRITICAL PROBING DEPTH


-

Level of pocket depth below which clinical attachment loss will occur as a result of
treatment procedure performed.

CONTENT OF POCKET
-

Debris consisting principally of microorganisms and their products, gingival fluid,


food remnants, salivary mucin, desquamated epithelial cells and leukocytes.

SIGNIFICANCE OF PUSS FORMATION


-

Puss is a common feature of periodontal disease, but it is only a secondary sign.


It does not reflect the extend of destruction and inflammation severity.
It reflects the underlying inflammatory process

GENERATION OF PROBE
-

1st - conventional (Williams probe)


2nd - pressure sensitive (Vine-Valley probe)
3rd - computer aided (Florida probr)
4th - records sequential probe positions along sulcus.
5th - ultrasound probe

FACTORS AFFECTING PROBING


-

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
-

LOA=PPD (PROBING POCKET DEPTH)


LOA=PPD+R (RECESSION)
LOA=PPD-E (ENLARGEMENT)

Probing depth Vs 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?
-

Initial probing of moderate or advanced cases are usually hampered by presence of


heavy inflammation.
Second probing is to establish level of attachment and degree of involvement of roots
and furcations.
Later in periodontal treatment probing is done to determine the changes in pocket
depth

NIDCR CRITERIA FOR PROBING


LIMITATION
Precision
Range
Probing force
Applicability
Reaction
Angulation
Security

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

and recording in writing

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
-

Fornix, entrance, dome

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

ETIOLOGY OF FURCATION INVOLVEMENT


-

Bacterial plaque and inflammatory consequences that result from its long term
presence.

FACTORS CONTRIBUTING IN DEVELOPMENT OF FURCATION INVOLVEMENT


-

Local anatomic factors( root trunk length; root morphology)


Local development anomalies( cervical enamel projection)
Dental caries
Pulpal depth

WHICH TOOTH IS AFFECTED BY FURCATION INVOLVEMENT?


-

Mandibular first molar( due to reduction root trunk)

PROBES USED FOR DETECTION OF FURCATION AREAS


-

Nabers probe( coloured coded markings at 3,6,9 and 12mm)

METHOD OF DETECTION OF FURCATION IN MAXILLARY MOLAR


-

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.

CLASSIFICATION OF CERVICAL ENAMEL PROJECTION


-

Grade 1: CEPs extends from CEJ towards Furcation entrance


Grade 2: CEPs approaches entrance of Furcation, does not enter Furcation
Grade 3: CEPs extends horizontally into Furcation

MANAGEMENT OF FURCATION INVOLVEMENT


-

Grade1: scaling and root planning, odontoplasty


Grade 2: osteoplasty, odontoplasty
Severe grade 2, grade 3, grade 4: tunneling, root resection, hemi section,
bicuspidisation

PATHOLOGICAL MIGRATION AND DRIFTING

PATHOLOGICAL MIGRATION
-

Refers to tooth displacement that results when balance among factors that maintain
physiologic tooth position is disturbed by periodontal disease.

DRIFTING
-

A physiologic tendency towards mesial migration: premolars drift distally; common


with missing teeth are not replaced.

ETIOLOGY OF PATHOLOGICAL MIGRATION


-

Weakened periodontal support


Trauma from occlusion
Changes in forces exerted on teeth
Pressure of tongue
Pressure from granulation tissue of periodontal pocket

RUSSELS RULE
-

When in doubt assign lower score

RUSSELS PERIODONTAL INDEX


Score
0

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

Early notch like resorption of


alveolar crest
Horizontal
bone
loss
involving entire alveolar

attachment broken; there is


pocket
formation;
no
interface with function. Tooth
is firm in socket
Advanced destruction with
loss of masticatory function;
tooth may be loose; may be
drifted; dull or percussion;
depressible in socket

crest upto root lenght

Advanced bone loss>1/2


root/ intrabony pocket with
periodontal
widening
rootresorption/
apex
rarefraction

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.

Localized periodontitis- < 30 % of the sites assessed in the mouth demonstrate


attachment loss/ bone loss
Generalized periodontitis- > 30 % of the site assessed in the mouth demonstrate
attachment loss/ 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.

Localized aggressive periodontitis( secondary factors)


Circum pubertal onset of disease.
Localized 1st molar/ incisor disease with proximal attachment loss on at
least 2 permanent teeth one of which is a 1st molar, and involving no more
than 2 teeth other than 1st molars and incisors.
Robust serum antibody response to infective agents.

Generalized aggressive periodontitis: ( secondary factors)


Usually affecting person under 30 yrs of age.
Generalized proximal attachment loss affective at least 3 teeth other than
first molars and incisors.
Pronounced episodic nature of periodontal destruction.
Poor serum antibody response to infective agents.

PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC DSISEASES

NECROTIZING PERIODONTAL DISEASES

Gingival abscess
Periodontal abscess
Pericoronal abscess

PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS

Necrotizing ulcerative gingivitis


Necrotizing ulcerative periodontitis

ABSCESSES OF PERIODONTIUM

Associated with hematological disorder leukemia, acquired neutropenia


etc
Associated with genetic disorder down syndrome, hypophosphatasia etc
Not otherwise specified.

endodontic- periodontal lesions


periodontal-endodontic lesions
combined lesions

DEVELOPMENTAL OR ACQUIRED WITH ENDODONTIC LESION

Localized tooth related factors that predispose to plaque induced gingival


diseases or periodontitis.
Mucogingival deformities and conditions around teeth.

Mucogingival deformities and conditions on edentulous ridges


Occlusal trauma

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.

CLASSIFICATION OF PERIODONTAL ABSCESS


1) Abscess on supporting periodontal tissue along lateral aspect of root.
2) Abscess on soft tissue wall of a deep periodontal pocket.

PERIODONTAL ABSCESS (LATERAL ABSCESS/ PARTIAL ABSCESS)


With untreated periodontal disease, with deep pockets, tooth perforations or fractures,
foreign body impact, poorly controlled diabetes.
Multiple periodontal abscess- periodontoplasia

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:

Painful, red, edematous, smooth, ovoid


Increase tissue resistance
Swelling of gingival tissue
Exudation on gentle pressure
Sensitivity to percussion
Mild to severe discomfort
Elevation in socket
Periodontal pocket
Tenderness
Tooth dilacerations
Exudation
Inc. temperature
Fever and regional lymphadenopathy

CHRONIC ABSCESS:

Dull pain
Localized inflammation
Slight tooth dilacerations
Intermittent exudation
Fistulous tract associated with deep pocket

PERIODONTAL ABSCESS:

Pre-existing periodontal pocket


Angular bone loss
Furcation involvement
Vital tooth
Gingival swelling
Fistula
Dull/ localized pain
Sensitivity to percussion may or may not present

PULPAL ABSCESS:

Large restoration
Non vital tooth
Localized swelling
Fistula
Severe pain, difficult to locate
Sensitivity to percussion

Radiographic Aids in the


Diagnosis of
Periodontal Disease
Radiographs are valuable for diagnosis of periodontal disease, estimation of severity,
determination of prognosis, and evaluation of treatment outcome. However, radiographs are an
adjunct to the clinical examination, not a substitute for it.

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

Radiographic Appearance of Periodontal Disease

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:

Good prognosis: Control of etiologic factors and adequate periodontal support


ensure the tooth will be easy to maintain bythe patient and clinician.

Fair prognosis: Approximately 25% attachment loss and/or Class I furcation


involvement (location and depth allow
proper maintenance with good patient compliance).

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.

Hopeless prognosis: Inadequate attachment to maintain health,


comfort, and function.

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

This scheme is as follows:

Favorable prognosis: Comprehensive periodontal treatment and maintenance will


stabilize the status of the tooth. Future loss of periodontal support is unlikely.

Questionable prognosis: Local and/or systemic factors influencing the periodontal


status of the tooth may or may not
be controllable. If controlled, the periodontal status can be stabilized with
comprehensive periodontal treatment. If not,
future periodontal breakdown may occur.

Unfavorable prognosis: Local and/or systemic factors influencing the periodontal


status cannot be controlled. Comprehensive periodontal treatment and
maintenance are unlikely toprevent future periodontal breakdown.

Hopeless prognosis: The tooth must be extracted.

Overall Versus Individual Tooth Prognosis

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.

Rationale of Periodontal Treatment

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