Stomatology

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Stomatology
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Burhan
Ahmed
Contents
Chapter 1: Introduction
Chapter 2: Oral-Maxillofacial Clinical Examinations
Chapter 3: Pulpitis
Chapter 4: Dental caries
Chapter 5: Diseases of The periapical Tissues
Chapter 6: Treatment of Diseases of the Dental pulp and the Periapical
Tissues
Chapter 7: Gingival Diseases
Chapter 8: Periodontal Disease
Chapter 9: Oral Mucous Disease
Chapter 10: Nerve Block Anesthesia in Dentistry
Chapter 11: Tooth Extraction
Chapter 12: Maxillo-facial Infection
Chapter 13: Wounds and Injuries of the oral and Maxillofacial region
Chapter 14: Oral & Maxillofacial Trauma
Chapter 15: Malignant tumors on the Oral & Maxillofacial Region
Chapter 16: Temporomandibular Joint Diseases
Chapter 17: Salivary gland diseases
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Chapter
Chapter 1: Introduction
Terminologies
1. Dentistry: is defined as the evaluation, diagnosis, prevention and/or treatment (nonsurgical, surgical or related
procedures) of diseases, disorders and/or conditions of the oral cavity, maxillofacial area and/or the adjacent and
associated structures and their impact on the human body;
2. Stomatology is branch of medicine that relates to the mouth and its diseases; originally practiced by physician;
3. Maxillofacial Surgery: A branch of dentistry that treats diseases and abnormalities of the maxillofacial region by
surgical means.
4.
1. Dental structures of Teeth

a. Enamel
i. covering the crown surfaces.
ii. hardest tissue of human body.
iii. white and translucent.
iv. 96% of the enamel is combined with mineral.
b. Cementum
i. the part covering the root surfaces
ii. The hardness of cementum is similar to that of bone
iii. yellowish
iv. contains 55% of mineral and 45% of organic chemicals
c. Dentine
i. main part of teeth
ii. covered by enamel in crown and by cementum in root
iii. hardness of dentine stands between the enamel and cementum.
iv. contains 70% of mineral and 30% of organic chemical.
v. The center of the dentine is empty and is called as pulp cavity.
d. Pulp
i. soft tissue stayed in the pulp cavity
ii. contains nerve fibres, vessels, lymphatic, fibroblast and odontoblast
iii. main function is to nourish the teeth
iv. Teeth without the nourishment of pulp are more fragile.
2. Periodontal structures of Teeth
a. Alveolar bone
i. provides support for the teeth
ii. made up of the outer cortical plates, trabeculated cancellous bone and the bone of the sockets
b. Periodontal ligament
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Main Points
c.
i. The teeth are attached to the sockets by bundles of connective tissue fibers comprising the
periodontal ligament.
ii. Most of the fibers run apically in an oblique direction from bone to cementum.
iii. Near the crest of the alveolus and near the apex, the main orientation is perpendicular to the root
surface.
Gingivae
i. composed of free gingiva and attached gingiva.
ii. Free gingiva is composed of the interdental papilla and the marginal gingiva.
iii. The attached gingiva attached on the tooth surface and alveolar bone.
Chapter 2: Oral-Maxillofacial Clinical Examinations

1. Describe the regular examinations.
a. Case history collection
i. Chief Complaints
1. Symptom
2. Location
3. Duration
ii. Current history
1. All symptoms
2. Onset, duration and progress of each symptom
3. Any treatment taken and the patients response to that
iii. Previous history
1. Additional History of oral condition
2. Previous treatment and outcome
3. Other medical history
iv. Personal and Family history
1. Personal habits
2. Social history of patients
3. history of the immediate family
b. Inspection
i. Extraoral
1. Face
2. Skin and soft tissue
3. TMJ
4. Lymphatic systems
5. Salivary glands
6. adjacent organs
ii. intraoral
1. Teeth
2. Oral mucosa: lip
tongue
palate
buccal mucosa
floor of mouth
3. Salivary glands
c. Probing: Location, extension, depth, pulp exposure, reaction to probing , etc.
d. Percussion
i. Vertically--------periapical region
ii. Horizontally-----periodontal ligament
e. Palpation
i. Size, extension, hardness, surface, shape, reaction of lesion
ii. Mobility of teeth
f. Smelling
i. Pulp necrosis
ii. Acute necrotic ulcerative gingivitis
g. Bite test
i. Articulation paper----early contact
ii. Pain or sensitivity
iii. Mark for early contact on the occlusion
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Main Points
2. Describe three special examinations.

a. periodontal probing
i. Peridontal pocket
ii. Attachment loss
iii. Subgingival calculus
iv. Bleeding
b. pulp test
i. Vitality of pulp
Cold
Heat
Electricity
c. secretion test: The amount of saliva
3. How to maintain oral hygiene?
a. Dental Plaque Control
i. Mouth rinse
ii. tooth-brushing
iii. interproximal cleaning
iv. scaling
v. dental floss
vi. interdental brush
Chapter 3: Pulpitis
Main Points
1. Pulpitis is a painful inflammation of the dental pulp or nerve.
2. The inflammation causes swelling, when the dental pulp swells, because it's walled off inside the tooth, there's
nowhere to go. The inflammation leads to a vicious cycle of swelling.
3. Etiology
a. Bacteria
b. Physical reason
c. Chemical reason
Pulpitis
Reversible
Irreversible
Acute
Chronic
Closed
Open
Ulcerative
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Hyperplastic
4. Reversible Pulpitis
a. Reversible pulpitis is mild inflammation of the tooth pulp; it is an excessive accumulation of blood in the
pulp resulting vascular congestion.
b. Etiology:
i. Pain is caused by hot, cold, and sweet stimulus lasts for a minute, and the cause removed, it is
stop.
c. Treatment:
i. Pulp capping: It is the protection of slightly exposed healthy pulp by means of an antiseptic and
sedative agent in order to allow the pulp recover and maintain its normal vitality.
5. Irreversible Pulpitis: If a carious lesion causing reversible pulpitis is not treated, the condition will progress to
irreversible pulpitis, a severe inflammation. It may be acute or chronic.
a. Acute Pulpitis: It is the most frequent cause of severe tooth pain.
i. Clinical Manifestation:
1. Persistent pain
2. Poorly localized
3. Night pain
4.
ii. Signs
1.
2.
3.
4.
Temperature stimulus pain

A large carious lesion
A fractured tooth or missing restoration
No reaction to percussion.
Temperature stimulus could make pain.
b. Chronic Pulpitis: It is considered to be a long standing inflammatory of the pulpal connective tissue to
stimulus. Pain usually is dull, throbbing, and intermittent.
i. Chronic ulcerative pulpitis:
1. Symptoms: Pain is slight, dull consciousness, patient complains that when food put into
the caries, make pain.
2. Sign:
a. A large carious lesion.
b. The pulp is exposed. deep probing make bleeding and pain.
c. There are more dental calculus and plaque.
ii. Chronic hyperplastic pulpitis: It occurs almost exclusively in children and young adults, the
great resistance of tissues and reactivity of young people, explains the unique capacity of
proliferation of the pulp tissue.
1. Signs:
a. It is symptompless, except during mastication when pressure of the food bolus
may cause some pain.
b. The affected pulp presents with a mass of granulation tissue leaving the pulp
chamber and often occupying the entire cavity.
6. Pulp necrosis: Death of pulp tissue. A term applied to pulp tissue that is no longer living, may be partial or
complete. Bacterial, chemical, or physical irritation is the reason of pulp necrosis.
a. Signs
i. discolored tooth (greyish-black).
ii. teeth do not respond to either cold or electric pulp tests .
iii. sensitive to percussion .
b. Treatment:
i. Emergency management: The emergency treatment is open the pulp chamber.
ii. The following treatment is root canal therapy (RCT).
Chapter 4: Dental caries

1. Dental caries(tooth decay) is a widespread, chronic, infectious disease that affects the hard tissues of teeth.
a. The clinical feature of the dental caries is the hard tissue like enamel, dentin or cementum has a change
in color, morphology and texture. By the age of 17 years, almost 80% of Americans have a cavity. In
underdeveloped Nations, dental caries are increasing. Caries increases are due to eating sugar increase.
Very little sugar was available when poor. Increase in money appears to increase sugar intake.
2. Etiology:
a. Bacteria:
i. The major bacterial species in the decay process are mutans streptococci and lactobacilli and
actinomycetes
ii. Bacteria, acid, food debris, and saliva combine in the mouth to form a sticky substance called
plaque that adheres to the teeth.
iii. This bacterium can metabolize sucrose, found at high levels in the Western diet, to produce
extracellular polysaccharides that enables bacterial cells to stick to teeth, and lactic acid that
causes demineralization of the enamel of the tooth surface.
iv. If this plaque is not removed thoroughly and routinely, tooth decay will not only begin, but flourish.
The acids in plaque dissolve the enamel surface of the tooth and create holes in the tooth
b. Food:
i. Carbohydrates, provide a rich source of energy for bacteria, especially monosaccharide like
glucose and disaccharides such as table sugar or sucrose. Some bacteria can ferment sugars
within milliseconds and produce organic acids. These acids attack the surface of the enamel and
enter through cracks, leading to the loss of calcium or phosphate ions from the tooth.
c. Host:
i. The important factor of the host are teeth and saliva,there is a protective mechanism in saliva,
which is supersaturated with calcium and phosphates. Saliva also contains bicarbonates and
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Main Points
proteins that can neutralize acids. Saliva is a source for fluoride ions that help to deposit calcium
and phosphate back into the teeth.lack of saliva can accelerate the developing speed of dental
caries.
ii. The different teeth and different surface of the teeth have different ability to get caries. Because
it is impossible to clean inside the deep grooves that are located on the occluding, or chewing,
surfaces of teeth.
iii. patients with exposed root surfaces to be at high risk for developing dental caries because these
surfaces can be demineralized faster than enamel.
iv. The tendency to the development of dental caries depends on several other factors which type of
tooth, location and length of exposure to the oral environment, oral hygiene practices, nutritional
status, previous fluoride exposure, and the oral status of the patient.
d. Time:
i. All the process of tooth decay not happened very fast, it needs period of time to happen. So it is a
widespread, chronic, infectious disease.
ii. Among the primary teeth, there are many more occlusal cavities than any other type of lesion.
Occlusal caries is the most common type of caries on the permanent teeth. Studies show that 4375% of all caries lesions are on the occlusal surfaces of posterior teeth. The incisal, buccal,
lingual, and palatal surfaces are usually resistant to dental caries. This resistance is related to
external factors such as food retention and the formation of dental plaque.
3. Classification:
According to the developing speed:
a. Acute carries: Acute enamel caries is characterized clinically by being white or chalky in appearance.
Arrested enamel caries is yellow to dark brown in color and the caries lesion is soft.
i. Rampant caries: dental caries that involve several teeth, appear suddenly, and often progress
rapidly. It is happened after radiotherapy and Sjogren syndrome.
b. Chronic caries: It is brown in appearance, caries lesion is dry and developing of disease is slow.
i. Arrested caries: in the process of the disease, because the environment of the teeth changed,
caries stop to develop.
c. Secondary caries:
Dental caries occurring around the edges and under restorations around the filling material or wall of the
cavities formed plaque stayed area that makes new caries.
According to the region involved:
a. Pits or fissures caries: Dental caries originating in pits or fissures, usually of the occlusal surfaces of
molars and premolars or on the lingual surfaces of the maxillary incisors, typically occurring as a deep
cavity with a narrow point of penetration.
b. Root Caries: In elder adults with gum disease, the dentin of the roots can be exposed to the oral
environment and may be demineralized through acid attacks. Lesions forming on roots vary in color.
c. Smooth tooth surface caries: This is happened the contact area of neighbor teeth, buccal or lingual
surface and surface of the neck .
According to the depth of the lesion:
a. Superficial caries:
The depth of the lesion is just in the enamel or cementum. In enamel caries it is no reaction to cold, hot,
sweet and sour. Staining is frequently seen on these surfaces and may indicate the presence of carious
lesions, especially in children and adolescents. It is important to note that the majority of stained pits and
fissures may not have tooth decay.
d. Intermediate caries:
The lesion is on the superficial dentin there is hole on tooth, the color of caries is deep brown, it is
sensitive to sweet and sour, cold and hot stimulation can cause pain, but stop to irritate, the pain will stop
quickly.
e. Deep caries:
The caries process reaches deep layer of dentin, Visual breakdown in the tooth surface (i.e. hole) and the
area has soft walls or floor.
A patient may complain of pain after eating or drinking something hot or cold ,this pain indicated that the
pulp is irritated and inflamed. If the carious demineralization continues, bacteria may enter the pulp,
causing more serious infection and even death of the pulp.
4. The prevention and treatment
a. Oral hygiene is necessary to prevent cavities. This consists of brushing at least twice a day and using
floss at least daily and regular professional cleaning (every 6 months). X-rays may be taken yearly to
detect possible cavity development in high risk areas of the mouth.
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b. Dental sealants can prevent cavities. Sealants are thin plastic-like coating applied to the chewing surfaces
of the molars. This coating prevents the accumulation of plaque in the deep grooves on these vulnerable
surfaces.
c. Fluoride is often recommended to protect against dental caries. It has been demonstrated that people
who ingest fluoride in their drinking water or by fluoride supplements have fewer dental caries. Fluoride
ingested when the teeth are developing is incorporated into the structure of the enamel and protects it
against the action of acids.
5. Treatment:
a. Destroyed tooth structure does not regenerate. However, the progression of cavities can be stopped by
treatment. The goal is to preserve the tooth and prevent complications.
b. In filling teeth, the decayed material is removed (by drilling) and replaced with a restorative material such
as silver alloy, gold, porcelain, or composite resin.
c. Crowns are used if decay is extensive and there is limited tooth structure which may cause weakened
teeth. Large fillings and weak teeth increase the risk of the tooth breaking. The decayed or weakened
area is removed and repaired and a covering jacket or "cap" (crown) is fitted over the remainder of the
tooth. Crowns are often made of gold, porcelain or porcelain fused to metal.
d. Before filling permanent material, in intermediate and deep caries ,need to basing other materials under it
to prevent irritating pulp.
6. Tetracycline stained teeth:
Tetracyclines are time dependent and produce visible changes, according to dosage in enamel, dentin and
cementum. With tetracycline, teeth acquire a yellowish color which with time becomes grayish because this
tetracycline is oxidized by the ultraviolet radiation of the sun . If the patient is treated with mynocycline, teeth will
acquire a dark gray to black color especially during dentin cementum and bone formation.
7. Wedge-shaped defect
The gum moves away from the crown of the tooth; exposing the sensitive root surface underneath.
Teeth can become very sensitive, reacting to hot and cold temperatures. This process is accelerated by incorrect
tooth brushing. This is usually by being too vigorous with your brushing or using a hard toothbrush and/or
brushing sideways across the gum line.
This type of tooth-brushing wears away the enamel and causes a wedge shaped defect. If the defect is
deep it can become painful and very unsightly as well as being susceptible to decay
Chapter 5: Diseases of The periapical Tissues
Acute
Periapical
Periodontit
is
Periapic
al
disease
s
Acute
Alveolar
Abscess
Chronic
Periapical
Periodontit
is
1. Acute Periapical Periodontitis:

Acute inflammation of the apical periodontal membrane; coming from the irritations.
a. Causes:
i. Mechanical reasons
1. High filling
2. A foreign object wedged
3. Root canal instruments
4. Occlusal trauma
ii. Chemical reasons: Dental and pulp medicine
iii. Bacterial reasons: Bacteria in the root canal
b. Symptoms
i. Pain
ii. Tenderness of the tooth
c. Diagnosis:
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Main Points
i. History of treatment
ii. Affected tooth---filled, accepted RCT
iii. Tender
iv. Percussion---pain
v. X-ray
2. Acute Alveolar Abscess
a. Definition:
i. Pus in the alveolar bone at the apex of the tooth
ii. Severe local reaction
iii. General reaction
b. Cause: Bacteria in the root canal
c. Symptoms
Tenderness
first stage
Throbbing pain, Swelling of soft tissue
More pain, loose
second stage
Edema, loose
third stage
Throbbing pain, Swelling of soft tissue

More pain, loose
second stage
Edema, loose
third stage
Spread---space infection
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Spread---space infection
d. Diagnosis
i. Subjective history of the tooth
ii. Clinical test---inspection, palpation, percussion, thermal test, electric pulp test
iii. X-ray
3. Chronic Periapical Periodontitis
a. Definition:
i. Long-standing infection
ii. Periapical tissue
b. Cause
i. Developmental sequence of dead pulp
ii. Unsatisfactory pulp treatment
c. Symptoms
i. Symptomless
ii. Fistula
iii. Occlusal discomfort
iv. X-ray
d. Diagnosis:
i. X-ray-strong evidence
ii. Clinical examination
1. affected tooth-discoloration of the crown, caries cavity, filled, leaky filling, trauma, etc.
2. tender to percussion
3. slightly loose
iii. Anamnesis-pain , swollen
e.
4. The different symptoms between the acute pulpitis and acute periapical abscess
a. Acute Pulpitis:
i. Persistent pain
ii. Poorly localized
iii. Night pain
iv. Temperature stimulus pain
b. Acute Periapical abscess:
Tenderness
first stage
Chapter 6: Treatment of Diseases of the Dental pulp and the Periapical Tissues
Main Points
a. Definition
i. A way to protect the healthy pulp by means of an antiseptic and sedative agent
ii. To allow the pulp to recover and maintain its vitality and function
b. Indication (important)
i. Young permanent teeth
ii. Traumatic or accidental exposed
iii. Deep caries cavity
c. Material:
i. Calcium hydroxide
ii. Zinc oxide-eugenol cement
d. Technique
i. a. Decay removed
ii. b. Put calcium oxide over the surface and cover the cavity by ZOE
iii. c. After 2-4weeks, no clinical symptoms, pulp test normal, permanent restoration should be done.
e. Note
i. Successful operation--- Tooth remain comfortable or slightly hypersensitive to thermal change for
a short time
ii. Unsuccessful operation--- abnormal reaction to thermal change or definite pain
2. Pulpotomy
a. Meaning
i. Remove the infected pulp in the pulp chamber and leave the portion in the root canal
b. Indication
i. Young permanent tooth
ii. Apical end is not completely formed
c. Technique
i. Local anesthetic and sterilize the field
ii. Remove caries
iii. Remove the roof
iv. Remove the coronal pulp
v. Put calcium oxide and then ZOE
vi. Observation and permanent restoration
3. What is RCT?
Root canal therapy
a. Objectives
i. Remove the debris
ii. Eliminate the bacteria
b. Indication (important)
i. pulpitis
ii. Periapial periodontitis
iii. Combined periodontic-endodontic lesion
c. Three steps of RCT
Technique ---three steps
i. Root canal preparation
1. Opening the pulp chamber
2. Removing any vital or necrosis pulp tissue
3. Measuring the length of the root canal
4. Enlarge the root canal
5. Washing the root canal
ii. Root canal sterilization
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1. Pulp capping:
1. Root canal sterilization has many method, such as drug sterilization (Ca (OH2),
microwave sterilization, electrolyte sterilization laser light sterilization.
iii. Root canal filling
1. Objective
The root canal system should be obturated to prevent any exchange beween the canal
and the periodontal ligament.
2. Root filling materials
The materials available for filling root canals may be divided into filler and sealers, filler
such as gutta percha , slier, titanium, plastic.
3. When to fill:
The root filling is completed when the tooth is symptomless and the canal dry.
4. The technique of filling:
The basic technique of filling includes lateral condensation technique and vertical
condensation technique.
4. Re- Contamination of the root canal:
a. microleakage of the coronal restoration or periodontal disease uncovering a lateral canal
b. Pulp tissue remnants and/or micro organisms these must be sealed within the root canal
c. ingress of tissue fluids will provide a culture medium for the micro organisms and allow diffusion of toxic
products into the periodontal tissues.
Chapter 7: Gingival Disease

1. What is periodontal tissue? (important)
It is the supporting tissue of the teeth consisting of
a. The gingival (important)
i. Marginal Gingivae
ii. Gingivae papillae
iii. Attached papillae
iv. A gingival mergin
v. A gingival sulcus (0.5-3mm)
b. The periodontal ligament
c. The cementum
d. The alveolar bone
2. Clinical features of normal Gingivae (important)
a. Gingiva color is pink/pale red and stippled
b. Sharp interdental papilla
c. firm
d. Shallow crevices between gums and teeth (<3mm)
e. little GCF(gingival crevicular fluid)
3. Gingivitis
An inflammatory process limited to the mucosal epithelial tissue surrounding the cervical portion of the teeth and
the alveolar processes.
a. Classification
i. Dental Plaque-induced gingivitis
Simple Gingivitis
Most common
1. Cause and Mechanism
a. Initial factor---plaque
b. Local contributing factors
i. calculus
ii. food impaction
iii. overhanging filling margins
iv. Mouth breathing
v. Irregularity in the position of the teeth
vi. improper tilting of the teeth
vii. abnormal tooth contour
2. Histopathological changes
a. the sulcular epithelium, the col area
b. the epithelial attachment
c. the outer gingival epithelium
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Main Points
plaque calculus a disruption of the oral epithelium accumulation of

inflammatory cells
b. Early leasions
i. At approximately 1 week
ii. marked by the change to predominately lymphocytic infiltrates.
iii. Monocytes and plasma cells also may be present.
c. Advanced lesions
i. characterized by the presence of plasma cells and B lymphocytes.
ii. pockets develop where the gingiva separates from the tooth.
iii. Deposition of fibrin and destruction of collagen can be noted
4. Clinical Manifestations: (important)
a. Bleeding
i. The most common complaint is bleeding gums. The patient usually
notices this when toothbrushing or flossing.
ii. Bleeding may be associated with eating, especially foods with a hard
consistency, such as apples or crusted bread. These foods may rub
against gums.
b. Halitosis
c. Alterations in contour and color
i. Color--- red
ii. Contour --- enlargement of the crestal portion of the gingiva,
disengagement of the margin
iii. Texture--- soft, friable
iv. Bleeding
v. Change in GCF
5. Treatment:
a. Oral hygiene instruction
b. Dental Plaque Control
c. Supergingival - Scaling
ii. Puberty-associated gingivitis
iii. Necrotizing ulcerative gingivitis
Vincent's gingivitis
Acute and ulcerative Inflammation occurs in the marginal gingiva and gingival papillae.
1. Cause and Mechanism:
a. Vincent's spirochetes
b. fusiform bacilli
2. Pathology:
a. Electron microscopic examination
b. four zones
i. Zone 1: Bacterial zone, most superficial
ii. Zone 2: Neutrophil - rich zone, contains numerous leukocytes,
predominantly neu - trophils, with bacteria,
iii. Zone 3: Necrotic zone, consists of disintegrated tissue cells, fibrillar
material, remnants of collagen fibers, numerous spirochetes of the
intermediate and large type, with few other organisms.
iv. Zone 4: Zone of spirochetal infiltration
3. Clinical Signs
a. Oral Symptom:
i. a constant radiating, gnawing pain
ii. a metallic foul taste
iii. an excessive amount of "pasty" saliva
b. Oral Signs
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3. Stages:
a. The initial stage
i. an acute exudative inflammatory response begins within 4 or 5 days of
plaque accumulation.
ii. gingival fluid and transmigration of neutrophils increase.
i. Characteristic lesions ----- punched - out, crater - like depressions at the

crest of the gingival that
ii. The surface of the gingival craters is covered by a gray,
pseudomembranous slough demarcated from the remainder of the
gingival mucosa by a pronounced linear erythema.
iii. In some instances, the lesions are denuded of the surface
pseudomembrane, exposing the gingival margin, which is red, shiny and
hemorrhagic.
Other
i. A fetid odor
ii. increased salivation
iii. spontaneous gingival hemorrhage or pronounced bleeding upon the
slightest stimulation
iv. a single tooth or group of teeth, or be wide - spread throughout the
mouth.
v. rare in edentulous mouths, but isolated spherical lesions occasionally
occur on the soft palate.
d. Extra- Oral And Systemic Signs and Symptoms
i. Local lymphadenopathy and slight elevation in temperature are common
features of the mild and moderate stages of the disease.
ii. In severe cases there are marked systemic complications such as high
fever, increased pulse rate , leukocytosis, loss of appetite, and general
lassitude.
iii. Systemic reactions are more severe in children. Insomnia, constipation,
gastrointestinal disorders, headache, and mental depression frequently
accompany the condition.
4. Diagnosis
a. Diagnosis is based upon clinical findings.
b. Bacterial studies are useful in the differential diagnosis between acute necrotizing
ulcerative gingivitis and specific infections of the oral cavity such as
actinomycosis and streptococcal stomatitis.
5. The Principle of Treatment
a. Remove the calculus.
b. Remove the necrotizing gingiva and Irrigate gingiva.
c. take antibiotics
iv. Drug-induced gingival enlargements
1. Definition:
a. Gingival overgrowth (GO)
b. It refers to take some drugs such as Dilantin sodium and cause gingiva
hyperplasia and enlargement in size.
2. Etiology:
a. phenytoin (Dilantin) for the treatment of seizures
b. cyclosporine (a potent immunosuppressant widely used in organ transplant
recipients)
c. numerous calcium channel blocker agents (especially nifedipine)
3. Cause and Mechanism
a. a hyperplastic reaction initiated by the drug
b. Inflammation is a secondary complicating factor
4. Pathology
a. pronounced hyperplasia of connective tissue and epithelium
b. the connective tissue presents densely arranged collagen bundles with an
increase in fibroblasts and new blood vessels.
c. Oxytalan fibers are numerous beneath the epithelium and in areas of
inflammation.
d. Inflammation is common along the sulcal surfaces of the gingiva.
5. Ultrastructural changes
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c.
a. in the epithelium widening of the intercellular spaces in the basal layer,

cytoplasmic edema and rarefaction of desmosomes. The mitotic index is
reduced.
6. Clinical Manifestations:
a. A painless, bead - like enlargement
b. The marginal and papillary enlargements unite and develop into a massive tissue
fold covering a considerable portion of the crowns and may interfere with
occlusion.
c. Uncomplicated by inflammation, the lesion is mulberry -shaped, firm, pale pink
and resilient, with a minutely lobulated surface and no tendency to bleed.
7. Diagnosis
a. clinical findings
b. case history and taking- drug history
8. Principle of Treatment
a. a: stop drugs
b. b: keep mouth clean
c. c: gingivoectomy
v. Pregnancy-associated gingivitis:
1. Definition: Women appear gingivitis in pregnancy.
2. Cause and Mechanism:
a. alterations arise in the level of sex (steroid) hormones circulating in their
bloodstream
b. variations in levels of progesterone and estrogen in women may adversely affect
the periodontal tissues in the mouth.
c. Gingivitis in pregnancy is caused by local irritants.
3. Pathology:
a. nonspecific vascularizing proliferative inflammation.
b. marked inflammatory cellular infiltration with edema and degeneration of the
gingival epithelium and connective tissue.
c. The epithelium is hyperplastic, with accentuated rete pegs and varying degrees
of intracellular and extracellular edema and infiltration by leukocytes.
4. Symptom and Sign:
a. The gingiva is inflamed and varies in color from a bright red to a bluish red
sometimes described as "old rose.
b. The marginal and interdental gingival is edematous, pits on pressure, is soft and
friable, and sometimes presents a raspberry- like appearance.
c. there is an increased tendency to bleed.
d. The gingival changes are usually painless
e. In some cases the inflamed gingival forms discrete "tumorlike" masses
5. Diagnosis
a. It is easy to diagnose based on clinical feature and pregnancy case
6. Principle of Treatment
a. OHI
b. Plaque control
c. Non specific treatment just keep the mouth clean and after the birth, most patient
recover the normal.
Chapter 8: Periodontal Disease

1. The gingiva Epithelium
i.
oral epithelium
ii.
oral sulcular epithelium
iii.
Junctional epithelium
2. Signs of Pristine Periodontal Health
i.
Pink gingivae
ii.
Firm gingivae
iii.
Uniform colour
iv.
Presence of stippling
v.
A knife-edged gingival margin
vi.
Intact gingival margin
Page32
Main Points
4. Periodontitis
i.
Causes:
a.initiating agent :plaque
b.local contributing factors
1. Dental Calculus
2. Dental stains
3. Food impaction
4. Trauma from occlusion
a. abnormal jaw relation induce trauma of periodontal tissues and then damage
structure of periodontal tissues .
b. For Example
i. premature contact
ii. excessive loading
iii. non-working-side contacts,etc.
iv. crowding or malalignment
5. Anatomic factors
6. Bad habits:
a. grinding of tooth
b. mouth breathing
c. unilateral mastication
7. Faulty dentistry
c. host contributing factors
1. Genetic factors:susceptibility
2. Hormone:disorder
3. Smoking
4. vasoconstrictionbad blood circulationfunction of immunocell decrease
5. Systemic diseases
a. diabetes
b. AIDS
c. osteoporosis
6. stress
ii.
Clinical Signs of Periodontitis
a. the signs of gingivitis(see above)
b. True pocket (probing depths3mm) attachment loss has occurred.
c. Junctional epithelium disappear and CEJexpose
d. Recession
e. Suppuration
f. Mobility above physiological levels (0.2mm)
g. Drifting of teeth
1. horizontal resorption
2.
vertical resorption
h. Exposure of furcations
i. Radiographic evidence of bone loss
iii. Diagnosis of Periodontitis
a. the signs of gingivitis
b. True pocketing on probing
c. Mobility above physiological levels
Page32
vii.
A flat and triangular interdental papilla
viii.
A probing depth3mm,when 20-25g weight is applied to the probe
ix.
Complete absence of any bleeding to probe
x.
Complete absence of any suppuration
xi.
No recession
xii.
A gingival margin situated just above the CEJ
xiii.
Complete absence of furcation exposure
3. Clinical Signs of Gingivitis
i.
Redness
ii.
Loss of stippling
iii.
Swelling
iv.
Rolling of the gingival margin and loss of the triangular shape of the interdental papilla
v.
Bleeding on gentle probing.
vi.
Recession
iv.
v.
vi.
d. Reaiographic evidence of bone loss

Different Diagnosis
a.Progress:
1. Acute: A short-lived, intense,brisk experience, may often be curable.
2. Chronic: It is a chronic process,have a long time. Chronic diseases are generally
incurable, and management involves the control of symptoms, or the prevention of more
serious complications.
3. Aggressive: Rapidly progressing ,a short period of time;
b.Years of Age
1. Juvenile is a term used to describe a disease whose onset occurred during juvenile
years.
c. Range or Extent:
1. Localised is a term used to designate a disease involving a small number of teeth
2. Generalised is the term used to describe diseases involving the majority of teeth
present in the mouth.
Complications:
a. Gingival recession
b. Caries or sensitiveness of root
c. Periodontal abscesses
d. Furcation involvement
e. Periodontal-Endodontic combined lesions
1. periapical tissue
2. dental pulp
Treatment:
a. control Plaque*
b. Scaling*
c. occlusal therapy
d. stabilization of loosen teeth
e. drug treatment
1. local application
a. Mouthwashoxysol (to rinse periodontal pocket )
b. anti-inflammatory
c. iodine
d. delayed release
2. systemic administration
a. spiramycin
b. arilin
f. Operation*: remove gingival hyperplasia
5. Pocket:
The deep spaces under the gums are called pockets ,caused by exposured cemento-enamel junction , dispeared
junctional epithelium and damaged the crest of alveolar bone.
6. Plaques: the soft and un-mineralized microbial population adhered the surface of teeth or dental restoration.
7. Dental Calculus: it is mainly calcium from the saliva which has formed hard deposits on the teeth and irritates the
gums.
8. How Does Bacterium Cause Disease?
i.
Bacteria (Plaque) normally cause disease when the following basic sequences occur:
a.Acquisition
b.Adherence or retention
c. Initial survival
d.Prosperity and longer-term survival
e.Avoidance of elimination
f. Multiplication
g.Elaboration of virulence factors.
ii.
Local risk factors
iii.
Systemic risk factors
Main Points
1.
Function of mucosa membrane :

a. Screen
Page32
Chapter 9: Oral Mucous Disease
b. Sensory
c. Taste
d. Digestion
e. Support,supply and connect,etc.
2. A variety of diseases in different types Occurred in the oral mucosa. Including:
a. Infectious diseases
i. Candidosis(Candida albicans;true fungus)
ii. Herpetic stomatitis(herpes simplex virus)
b. Non-infectious diseases
i. Glottitis
c. Precancerous lesion
i. Lichen Planus Leukoplakia
d. Oral manifestation all over the body
i. Aphthae,ulcer
3. Pathologic diagnosis terminology:
a. Macule: A small localized change in the color of skin that is neither raised (elevated) nor depressed.
Macules are never large. They are basically little spots or blemishes in the skin. They are entirely flat and
can only be appreciated by visual inspection; they cannot be seen from the side.
For example: Peliosis or Purpura
macule
papule
b. Papule: A small solid rounded bump rising from the skin that is usually less than 1 centimeter in diameter
(less than 3/8 inch across).Papules may open when scratched and become crusty and infected.
For Example: Lichen Planus
c. PatchDissimilar size and true pustute on the mucosa, white and smooth ,and with coarse or crackit
has a clear margin.
For Example: Leukoplakia
patch
vesicle
d. Vesicle: In dermatology, a vesicle is a small blister, as on the skin. Vesicles also occur on the mucous
membranes, such as the buccal mucosa (the lining of the mouth). Vesicles are less than .5 centimeters in
diameter.
e. Ulcer: An area of tissue erosion, for example, of the skin or lining of the gastrointestinal (GI) tract. Due to
the erosion, an ulcer is concave. It is always depressed below the level of the surrounding tissue.
Page32
For Example: herpetic stomatitis
For Example: Aphthae,etc.
ulcer
erosion
Erosion: An erosion is an eating away of a surface. (Erodere in Latin means to eat out.)For example, a
skin erosion is a loss of part or all of the epidermis (the outer layer) leaving a denuded surface.
For Example: herpetic stomatitis,etc.
g. Nodule: A small solid collection of tissue, a nodule is palpable (can be felt). It may range in size from
greater than 1.0 cm (3/8 inch) to somewhat less than 2 cm (13/16 inch) in diameter. A nodule may be
present in the epidermis, dermis or subcutis (at any level in the skin).
For Example: Paradentoma, fibroma
f.
Atrophy
Rhagades
k. Pseudomembrane: Formed by cellulose, necrotic and exfoliated cellula epithelialis and inflammatory
cell .It cannot erased.
For Example: Aphthae, etc.
Page32
nodule
tumor
h. Tumor: An abnormal mass of tissue. Tumors are a classic sign of inflammation, and can be benign or
malignant (cancerous).
For Example:
i. OptimumParadentoma
ii. Malignancy :Squamous cell carcinoma.
i. Atrophy: Wasting away or diminution. Muscle atrophy is wasting of muscle, decrease in muscle mass.
For Example: Glossitis (papillae of tongue)
j. Rhagades : Line slit on the mucous caused by the missing of flexibility because of inflammation .
For Example: angular Cheilitis
Necrosis: The death of living cells or tissues. Necrosis can be due, for example, to ischemia (lack of
blood flow). From the Greek "nekros" (dead body).
m. GangreneThe death of body tissue due to the loss of blood supply to that tissue, sometimes permitting
bacteria to invade it and accelerate its decay.
4. Lichen Planus
a. Definition: A Chronic inflammatory disease on the skin or mucosa characterized by glistening, violaceous
and angulated papules. It is in precancerous conditions.
b. The etiology is not known completely. May be caused by:
i. Psychosomatic factors : lose one's love, death of family members
ii. Endocrine factors
iii. Immune factors
iv. Infection factors: Hepatitis C
v. Microcirculation factors
vi. Heritage factor: susceptible population
vii. Systemic disease:
c. Symptom and Sign:
i. Chronic and repeated feature
ii. Papules, atrophy,etc.
iii. Symmetrical form, any area, more buccal mucosa, lesion color between rad and white
1. No symptom ,burning sensation by chance.
2. Woman, one's age :over 50
d. Diagnosis: Reasion, Symptom and signs
e. Treatment: Relax
5. Moniliasis (oral candidiasis)
a. Definition:
i. This is an infection of the mouth by a fungus called Candida albicans.
ii. Moniliasis white mouth
b. Etiology
i. Fungus (Candida albicans)
1. Overgrowth of Candida can be caused by factors which reduce the individuals natural
resistance.
ii. Induction Reason
1. Stress
2. Long term use of antibiotics, corticosteroids and anti-cancer drugs
iii. Hormonal changes, etc :This is commonly associated with Diabetes Mellitus, and hormonal
changes occurring in pregnancy
c. Symptom and sign:
i. Acute
ii. Ulcers,pseudomembrane, atrophy,etc.
iii. Form in the mouth, slightly raised lesions, usual on the tongue or inner cheeks.
1. The lesions are painful
d. Treatment:
i. Antifungal medications such as nystatin can be given to treat the infection.
ii. Good oral hygiene helps the healing process. Such as: denture induced candidal infections,etc.
iii. It is important to treat any underlying condition.
iv.
6. Recurrent Aphthous Ulcer, RAU (aphthae)
a. Definition: Recurrent, isolated and natural repair lesion of Ulcer on mucous membrane.
Page32
l.
b. Etiology:
i. Abnormalities of the immune system
ii. Genetic factor
iii. Systemic disease: Iron, Folic acid, or Vitamin B6, B12 and Vitamin C deficiency
iv. Stress,etc.
c. Symptom and sign
i. Commonly acute can occur at any age, female, young people.
ii. Forms as a single ulcer or in clusters
Red halo forms around ulcer, necrosis and Pseudomembrane, etc.
iii. White ulcer that is surrounded by a red area.
A red spot which forms into an ulcer 1-2mm to 1 centimeter in size (may be larger)
They appear on mucosa including the inner cheek, lips, base of gums, and palate.
iv. An initial burning sensation, Painful
natural repair7-14days
d. Classification:
i. Minor aphthous ulcer
iii.
Herpetiform ulcer
ii. Major aphthous ulcer
e. Treatment:
i. alleviate pain
ii. immunization
iii. Oral hygiene is important in order to prevent bacterial infection.
N.B. For lesions that persist for more than 2 weeks, Tetracycline and antibiotics may be given.
7. Leukoplakia:
a. Definition
i. A white spot or patch on the mucous membranes in the mouth (for instance, inside the cheeks, on
the gums or the tongue) that may become cancerous
b. Etiology: The etiology is not known completely
i. The most important of these is the use of tobacco. Old long history smoker
ii. A second important etiological factor is infection of Candida Albicans. Candidal infection in a
long-case history
iii. Systemic disease
c. Symptom and sign
i. Chronic
ii. Patch, etc.
iii. Electron microscope: epithelial dysplasia
iv. pain from ulceration and erosion
1. The dangerous areas: the margin of tongue, The floor of mouth ,mouth corner
d. Diagnosis:
i. Reason, Symptom and signs
ii. Biopsy: epithelial dysplasia
e. Treatment:
i. Remover stimulating factor
ii. Squash vitA paste
iii. Oral hygiene
iv. Operation
v. system diseases
8. Herpetic Stomatitis
a. Definition: Reactivation of herpes simplex virus in the oral tissues, characterized by vesicles and
ulceration.
b. Etilogoy: Herpex Simplex Virus
i. Primary infection (primarily herpes)
Herpetic stomatitis is caused by Herpes Simplex Virus and is seen in children between 6 months
and 5 years,any area in mouth.
Get in touch with patients
ii. Recurrented infection (Recurrent herpes)
Immunodeficiency,
tiredness, etc. adult.
c. Symptoms & Signs
i. Commonly acute
ii. Incubation, blister, erosion, healing
iii. Vesicles on the tongue, buccal mucosa, gums and any area around the mouth.
Page32
1. The vesicles breakdown to form ulcers, etc.

2. The area of erosion is very painful.
3. The mucosa becomes red, swollen and bleeds easily.
4. Microscope: virus
iv. Patients in two main age groups, young children and adults
The initial symptoms are of Malaise with tiredness , generalized muscle aches and a sore throat
v. Secondary bacterial infection may occur with enlarged lymphnodes and difficulty in swallowing.
vi. High fever.
It is self-limiting and lasts between 7 to 10 days.
d. Treatment
i. Antiviral drug
Squash Dendrid
As the child mouth will be sore, a liquid diet will be needed.
Acyclovir may be used.
ii. Tetracycline mouthwash: It has contagious: saliva fluid by eye mouth and skin, etc.
iii. Immunoregulant, transference factor.
The patient can recover without any medication within 10 days.
Chapter 10: Nerve Block Anesthesia in Dentistry

Main Points
Anaesthetic
concentration
onset
duration
method
Maximum
dosage
Toxic effect
Anaesthetic
effect
Procaine
2%
3-5min
45-60min
Infiltration, block
1 g/hr
Lidocaine
2%, 4-5%
3min; 1min
1-2hr; 15min
Infiltration, block; surface
<0.4-0.5 g/hr
Dicaine
1-2%
1min
15min
surface
<0.1 g/hr
1
1
2
2
10
10
4. Advantages of nerve block

a. Larger analgesia area & avoid several injections
b. Less dosage & long--lasting
c. Away from the lesion -- avoid spreading of infection & tumor seeding
d. Less tissue deformity post-injection -- plastic surgery
e. Better Anesthetic Effectiveness
5. Infiltration:
a. Principle: injection of anaesthetic to the area to be treated, relying on the solution diffusing or infiltrating to
the sensory nerves so that the conduction of pain impulses is prevented.
b. Methods: submucous and supra-periosteal
i. sub-periosteal
ii. intra-periodontal
iii. papillary
c. Indications: soft tissue surgery
Page32
1. Trigeminal is the sensory and facial is the motor nerve supply to the brain.
2. Trigeminal Nerve
a. Ophthalmic Division
b. Maxillary Division
i. posterior superior alveolar nerve
ii. middle superior alveolar nerve
iii. anterior superior alveolar nerve
iv. greater palatine nerve
v. naso-palatine nerve
c. Mandibular Division
i. inferior alveolar nerve
ii. incisive nerve
iii. mental nerve
iv. lingual nerve
v. long buccal nerve
3. Local Anesthetics
6. Block Anesthesia
a. Principle: blocking the passage of pain along a nerve trunk by injecting anaesthetic around it at a site
where the nerve is normally unprotected by the bone.
b. Region: Maxillary nerve and its branches
Mandibular nerve and its branches
Posterior Superior
Alveolar Block
(PSA Block)
Infraorbital Block
(IO Block)
Greater Palatine
Block
(GP Block)
Nasopalatine
Block
(NP Block)
Inferior Alveolar
Block
(IA Block)
Lingual Block
Anesthetic Area
Injection Site
Injection
Amount
1.5-2ml
a. Pulp & alveolar process

b. Buccal
-gingiva
-periodontium
- periosteum
Upper lip, side of nose, and lower
eyelid
Mucobuccal fold
distal apex
a. Posterior portion of hard palate

b. Palatal
-mucoperiosteum
-gingiva
-alveolus
Midway between the median palate raphi

and lingual gingival of the molar tooth
In canine partially
slightly superior to the mandibular
foramen inferior to the lingula
Tongue
45- degree
10mm lateral to the alar
45-degree to the skin superiorly/
posteriorly / laterally
90-degree to the palate from the opposite

side
incisive papilla
0.3-0.5ml
0.25-0.5ml
the tip of buccal fat pad

pterygomandibular raphi
1-1.5ml
Lingual nerve lies 10 mm anteriorinferiorly to IA nerve
0.5-1ml
Buccal Block
Mental Block
1-1.5ml
0.5-1ml
st
nd
between the apices of 1 & 2 premolar

1cm beyond the mandible lower border
faces posterosuperiorly
0.5-1ml
Page32
Block Name
7.
1/3
rd
Dominating Nerve
Anterior superior dental nerve
Nasopalatine nerve
Greater palatine nerve
Anaesthesia
Infiltration
Block
4545
Middle superior dental nerve

Infilatration
block
66
Posterior superior dental nerve

Middle superior dental nerve
Infiltration
block
7878
Posterior superior dental nerve

Block
33
and
the
8.
Vagus supply
of the tongue
nerve supply
2/3rd is
supplied by
lingual nerve.
Page32
Mandibular teeth
Mandibular nerve
Block
Complications: (important)
a. Allergy
i. Antigen-antibody reaction
ii. Anaesthetics: ester type mostly
iii. reactions---immediate,
delayed
iv. Manifestation: edema, rash, pyrexia
v. Treatment: antihistamine drugs
corticosteroids
b. Overdose
i. Due to injection of too large an amount of anaesthetic, or inadvertent intravascular injection;
ii. Manifestation: dizziness, headache, nausea, vomiting, convulsion, respiratory inhibition, etc.
iii. treatment: an adequating oxygen supply
anticonvulsant
c. Faint
i. temporary unconscious
ii. triggers: hunger, anxiety, nervousness
iii. manifestation: pale, sweating, cold, feels unwell and lose consciousness
iv. treatment: lower the head, tilting the chair, loosen the tight clothing like collar or belt which may
impede the respiration; oxygen;
d. Infection:
e. Haematoma
Chapter 11: Tooth Extraction

1. Indication:
i.
Dental disease: A tooth that is not restorable by dental procedures;
ii.
Periapical diseases: A tooth that is not amenable to endodontic therapy.
iii.
Periodontal diseases: A tooth that has severe destruction of periodontal tissues and is not amenable to
periodontal treatment;
iv.
Traumatic effect on the tooth or alveolar bone, that is beyond repair.
v.
Impacted tooth, which cause dental caries or root resorption of neighbouring teeth, or pericronitis.
vi.
Resorted deciduous teeth;
Page32
Main Points
2.
3.
4.
5.
6.
7.
vii.
Malposed teeth;
viii.
Supernumerary teeth;
ix.
Treatment consideration: orthodontic consideration, prosthetic consideration;
x.
Problem teeth, which are supposed to be the foci of infection;
Contraindication
i.
local contraindications: acute infection, tumour, irradiated jaws;
ii.
systemic contraindications:
a. Cardiac disease: such as unstable coronary artery disease, uncontrolled hypertension,
uncontrolled arrhythmia, and cardiac decompensation; Usually a post-infarction patient is not
subjected to oral surgery within 6 months.
b. uncontrolled Diabetes;
c. blood disorder: includes serious anaemia, haemophilia, leukaemia;
d. Pregnancy;
e. Menstruation: Tooth extraction is usually not done because of less nervous stability and greater
tendency toward haemorrhage of all tissues;
f. Debilitating diseases of any kind make patient poor risks for further traumatic insults.
Instruments: Instruments for tooth extraction include: forceps, elevators, excavators, chisel, hammer, needle
holders, needles, scissors, bone files, etc.
Forceps extraction procedures
i.
Preparations: anaesthesia, position of patient, sterilization, choice of instrument
ii.
De-attachment of gingival
iii.
Emplace the forceps or elevator
iv.
Movement: buccal-lingually movement and rotatory movement;
v.
Dislocation
vi.
Post-operation instruction
Impacted tooth extraction
Resistance analysis---------soft tissue resistance
-------hard tissue resistance: from bone and tooth
Root removal
i.
closed procedure
ii.
open procedure
iii.
Complications
a. Tooth fracture
f.
Nerve damage;
b. Fracture of alveolar bone;
g.
Displacement of root;
c. Health teeth damage;
h.
Faint;
d. Gingival damage;
i.
Infection: soft tissue and bone infection;
e. Fracture of Mandible;
j.
Bleeding
Dry socket-----acute infection of socket; also a complication of Root Remaoval
i.
Aetiology: micro organism
Triggers: trauma; big post-op wound; smoking; menstruation;
ii.
Clinical features: symptoms: severe pain, which happens 2-3 days post-op; halitosis;
a. general symptoms like fever and lymph nodes enlargement;
b. signs: swollen and inflamed gingiva
1. empty socket, and exposed bone;
iii.
treatment:
a. complete debridement;
b. complete protection of wound;
c. antibiotics
Chapter 12: Maxillo-facial Infection

1. Introduction:
2. Aetiology
3. clinical features
a. Redness
b. Swelling
c. Abscess formation
d. Pain
e. dysfunction
Page32
Main Points
4. complications
a. Sepsis
b. Brain infection
c. Infection of other organs
d. Shock
5. treatment
a. Systemic
b. Local
6. Pericronitis
a. Definition: inflammation around crown of partially erupted tooth wisdom teeth (third molars) most often
affected.
b. Aetiology:
i. Impaction of tooth
ii. Pericoronal pocket
iii. Plaque and food debris
iv. Diminished resistance
c. Clinical features:
i. Existence of impacted wisdom tooth and peri-coronal pocket
ii. Inflammation of soft tissue around the crown
iii. Symptom:
1. soreness or pain
2. difficulty in opening mouth and swallowing
3. occasionally, there can be trismus or pain on biting
4. halitosis
iv. Signs
1. Redness and edema around flap overlying erupted tooth
2. pus in the pocket
3. formation of abscess
4. Regional lymphadenopathy of head and neck
5. fever
d. Pathology:
i. Oral mucosa may ulcerated
ii. Moderately dense collagenic tissue and edematous granulation tissue
iii. inflammatory cells
e. Spread:
i. cellulitis
ii. Osteomyelitis
iii. Sepsis
f. Treatment:
i. Local
1. rinse and mouth wash
2. irrigation of pocket
3. abscess incision
4. wisdom tooth extraction
5. excision of pocket
ii. Systemic---antibiotics
Chapter 13: Wounds and Injuries of the oral and Maxillofacial region
1. Abrasion: a wound produced by the rubbing or scarping off of the covering surface; usually superficial, and
produces a raw, bleeding surface;
a. Character: Irregular wound edge, foreign body, pain, oozing & yellowish plasma oozing
b. Management: Debridement, remove foreign body, Dry wound, drain when infected
2. Contusion: a bruise, usually produced by an impact from a blunt object without breaking the skin causes a selflimiting subcutaneous haemorrhage.
a. Character: petechiae, swelling, pain
b. Management:
Page32
Main Points
4.
5.
6.
7.
8. Fracture of roots:
a. Symptom: no obvious symptom
b. Signs:
i. pathological mobility of tooth
ii. X-ray: fracture line on root
c. Classification:
i. horizontal or diagonal fracture
ii. cervical 1/3 , middle 1/3, apical 1/3 fracture
d. Treatment:
i. crown repair after RCT
Page32
3.
i. Hemostasis
ii. Pain-killer
iii. Prevention of infection
iv. Hematoma resorption
v. Re-establishment of function
Laceration: a wound resulting from a tear usually produced by some sharp objects. It may be shallow or deep
and may involve underlying vessels and nerves
a. Character
i. Irregular wound edge, saw-toothed
ii. Big laceration w/wo necrotic tissue & open fractures
b. Management
i. Debridement
ii. Wound Closure
Penetrating wound:
a. a puncture-type wound
b. produced by a sharp subject
c. usually deep and frequently involve other structures
d. may be small or large, depending on the subject producing the wound.
Gunshot, Missile and war wounds:
a. belong to penetrating wounds
b. vary greatly in character, depending on the speed, shape, and striking angle of the projectile
Procedures for closure of the wounds
a. Cleansing
i. scrub skin with a surgical detergent
ii. wash the debris form the wound with constant stream of water
iii. Investigate and cleanse all areas
iv. Remove any foreign bodies encountered
v. Flush through the wound with hydrogen peroxide
b. Debridement
i. a radical debridement is not indicated
ii. Only the necrotic, obviously nonviable tissue need be removed
iii. Rough, irregular, ragged, or macerated margins should be excised to diminish the ultimate
amount of scar formation
c. Hemostasis
i. Clamp and tie vessels with ligatures
ii. suture
iii. electrocoagulation
d. Supportive therapy
i. Drain
ii. Dressing
iii. Prevention or treatment of various infection
Fracture of the Crown:
a. Symptom:
i. depends on the extent of fracture and if pulp exposed;
ii. no symptom or sensitive to heat or cold or spontaneous pain;
b. Signs:
i. fracture of enamel or/and dentine, with or without pulp exposure
c. Treatment:
i. repair the crown
ii. RCT for fracture with pulp exposure
11.
12.
Chapter 14: Oral & Maxillofacial Trauma

Main Points
Page32
9.
10.
ii. splint
iii. tooth extraction
Displacement of tooth from the socket is called tooth luxation.
Fracture of Mandible:
a. Symptoms:
i. Pain with movement of mandible
ii. Inability to masticate
iii. Tismus
iv. Numbness
v. Salivation
b. Signs:
i. Swelling
ii. Malocclusion
iii. Abnormal mobility with bimanual palpation
iv. Ecchymosis of gum or oral mucosa
v. Soft tissue injuries may be seen
vi. X-ray: fracture of mandible, displacement of mandible
c. Treatment:
i. Reduction
ii. Fixation:
1. arch bars
2. splint
3. internal rigid fixation
Fracture of Maxilla
a. Classification:
i. LeFort fracture( Horizontal fracture)
ii. LeFort fracture ( Pyramidal fracture)
iii. LeFort fracture ( Transverse fracture)
b. Clinical features: pain
i. swelling
ii. deformity
iii. dysfunction
iv. Ecchymosis and bleeding
v. Radiograpy
c. Complications
i. Malunion
ii. Diplopia
iii. Persistent periorbital edema
iv. Poor occlusion
v. Dimness of vision
Zygoma fracture:
a. Classification:
i. Fracture of the arch
ii. Fracture of the suture lines surrounding the body of zygoma
b. Symptoms and Signs:
i. Swelling
ii. Dimpling of the skin over the arch
iii. Depression or flattening of the upper cheek
iv. Hemorrhage into the sclera of the eyes
v. Nasal hemorrhage
vi. Depressed level of eye
vii. Paresthesia over the cheek
viii. Trismus
ix. X-ray: fracture and displacement of zygoma
c. Treatment:
i. Conservative treatment
ii. Surgery
3. Describe the ways of hemastasis.

a. Judge bleeding situation
b. Choose the way to stop bleeding
4. What is debridement?
In oral hygiene and dentistry, debridement refers to the removal of plaque and calculus that have accumulated on
the teeth. Debridement in this case may be performed using ultrasonic instruments, which fracture the calculus,
thereby facilitating its removal, as well as hand tools, including periodontal scaler and curettes, or through the use
of chemicals such as hydrogen peroxide.
Page32
1. Describe the characteristics of OMF Trauma?

a. Rich blood supply
i. Tend to hematoma, edema Respiratory Tract Asphyxia
ii. Ability to anti-infection, regeneration wound healing
iii. Debridement Time: extend to 24 48 h
b. Relationship btw tooth & OMF trauma
i.
Increase infectious incidence
ii.
Malocclusion caused - Diagnosis
iii.
Occlusion regained - Treatment
c. Cranio-cerebral trauma
i.
Cerebral concussion
ii.
Cerebral contusion
iii.
Intracranial hematoma
iv.
Skull base fracture --- panda eyes . leakage of cerebrospinal
d. Cervical trauma
i. Bleeding
ii. Paralysis
e. Effect on breathing
i. Leading difficulty breathing asphyxia
f. Effect of on digastric system
i. Mouth opening diet
ii. mastication, swallowing worse oral hygine
g. Multi-sinus contamination
i. Oral cavity
ii. Nasal cavity
iii. Pharyngeal cavity
iv. Orbit
v. Paranasal sinus
All of the above factors lead to bacteria, increased temperature and humidity which further leads to
infection.
h. Damage to specific structure
i. Parotid Gland Salivary fistula
ii. Facial N. Facial paralysis
iii. Trigeminal N. Regional numbness
i. Facial Defect
i. Facial contour
ii. Psychological trauma
2. Describe the etiology, clinical features and management of asphyxia.
a. Clinical features:
Dysphoria, sweating, inhaling respiration Difficult to inhale, hypopnea, nasal alar movement, labial
cyanosis Three concave signsRapid breathing, weak pulse, decreased BP Pupils diluted, No
reflection to light
b. Etiology
i. Tissue dislocation Upper airway Obstructive Asphyxia
ii. Swelling, Foreign body, Blood, saliva, Vomiting Low Airway Inspiratory Asphyxia
c. Management:
i. Clear foreign body in upper airway
ii. Suspend maxilla
iii. Intubation
iv. Hold the tongue out
5. Describe the common site of dental alveolar process fracture, and their clinical manifestation.
Chapter 15: Malignant tumors on the Oral & Maxillofacial Region

Main Points
1.
Erythroplakia is the clinical diagnostic term A chronic red mucosal macule which cannot be given another
specific diagnostic name and cannot be attributed to traumatic, vascular or inflammatory causes, i.e. it is a
diagnosis of exclusion.
2. Lichen planus: White striations on the left buccal mucosa. White rough lesions forming a network or striated
pattern with an underlying red mucosal base, present on the buccal mucosa.
3. Symptoms of Oral Cancer:
The two most common symptoms of mouth cancer are:
a. An ulcer in the mouth that will not heal 80 out of every 100 people with mouth cancer (80%) have this
symptom
b. Discomfort or pain in the mouth that will not go away
Other symptoms can include
a. A white or red patch in the mouth or throat that will not go away
b. A lump or thickening on the lip, or in the mouth or throat
c. Difficulty or pain with chewing or swallowing
d. A feeling that something is caught in the throat
e. Unusual bleeding or numbness in the mouth
f. Loose teeth for no apparent reason
g. Difficulty moving the jaw
h. Speech problems
i. A lump in the neck
j. Weight loss
k. Bad breath (halitosis)
4. Types of lingual Carcinoma:
a. Exophitic carcinoma
b. Invasive carcinoma
c. Ulcerative carcinoma
Chapter 16: Temporomandibular Joint Diseases

1. Symptoms of TMJ disorder
i.
jaw pain
ii.
chronic generalized facial pain (either a sharp pain or a dull ache)
iii.
headaches
iv.
earaches
Page32
Main Points
v.
a loud roaring in the ears
vi.
clicking or popping sounds when the jaw is opened
vii.
difficulty in opening and closing the jaw
viii.
difficulty, discomfort, or pain when biting or chewing
ix.
neck, shoulder, chest, and back pain
x.
toothache
xi.
dizziness
2. Classification of TMD
i.
Masticatory muscles dysfunction
ii.
Internal derangement, ID
iii.
Inflammatory disorders
iv.
OsteoarthrosisOA
3. TMJ Dislocation
i.
Classification of the TMJ dislocation
a. Acute forward dislocation
b. Recurrent dislocation
c. Habitualdislocation
ii.
Clinical features:
a. Inability to close the mouth
b. Drooling because of inability to close the mouth
c. Difficulty speaking
d. Jaw may protrude forward
e. Teeth may not align normally
f. Bite feels "off" or crooked
4. Ankylosis of the TMJ
i.
Definition:
The union of two or more separate bones to from a single bone; the close union of bones or other
structures in various animals.
(n.) Stiffness or fixation of a joint; formation of a stiff joint.
ii.
Classification:
a. internal ankylosis of the TMJ: fibrous, fibro-osseous, or osseous ankylosis
b. intermaxillary contracture
Chapter 17: Salivary gland diseases

1. The acinus of salivary gland have three types:
a. serous acinus
b. mucous acinus
c. mixed acinus
2. Acute pyogenic parotitis
Page32
Main Points
3.
4.
5.
6.
a. Etiology
i. main infected bacteria is staphylococcus aureus ( which spreads on the surface of the skin and
mucous widely)
ii. retrograde infection through the duct of the glands.
iii. after big trauma and big operation
b. Symptoms:
i. Swelling of the face (particularly in front of the ears, below the jaw, or on the floor of the mouth)
ii. Dry mouth
iii. Abnormal tastes, foul tastes
iv. Mouth or facial pain, especially when eating
v. Decreased ability to open the mouth
vi. Fever
Mumps (Epidemic parotitis)
a. Definition: Mumps is an acute contagious, viral disease that causes painful enlargement of the salivary
or parotid glands.
b. Symptoms:
i. face pain
ii. swelling of the parotid glands
iii. fever
iv. headache
v. sore throat
vi. swelling of the temples or jaw (temporomandibular area)
vii. testicle pain
viii. testicle lump
ix. scrotal swelling
c. Treatment:
i. no specific treatment for mumps.
ii. Antivirus and antibiotics
Chronic Recurrent Parotitis, Chronic Sialoadenitis
a. Definition:
These conditions form part of the spectrum of chronic inflammatory conditions of unknown origin. All
share a common precursor event that is reduced salivary secretion rate and subsequent stagnation of
salivary flow. These conditions are all more common in the parotid gland because of thicker saliva, which
is more susceptible to bacterial infection than submandibular saliva.
b. The causes are unknown
c. Symptoms & Signs:
i. swelling of the glands,
ii. a dry mouth
iii. Recurrent swelling and pain of the gland
iv. Purulent discharge
Sjogrens Syndrome (Benign lymphoepithelial lesions)
a. Introduction:
i. Systemic autoimmune disease
ii. Exocrine gland
1. salivary gland---xerotomia(dry mouth)
2. lacrimal gland---keratoconjunctivitis sicca(dry eye)
iii. Sicca syndrome
b. Clinical features:
i. Xerotomia--Dry mouth
ii. Gland enlargement
Salivary Gland Stones (Sialolithiasis/Salivary Calculi)
a. Definition: Salivary stones represent grit blocking salivary ducts, thus preventing saliva drainage and
causing gland enlargement.
b. Occurrence: 80% of stones occur in the submandibular gland, with 20% occurring in the parotid gland. In
most cases, multiple stones are found, but multiple gland involvement only occurs in about 3% of
patients.
c. Etiology:
i. Sialolithiasis
ii. Trauma
iii. Infection
iv. Foreign body
Page32
Page32
d. Symptoms & Signs:

i. Recurrent pain and swelling of the involved glands is often associated with eating.
ii. Infection may occur with repeated episodes of obstruction and swelling.
iii. Stones may be palpable in the involved duct and the gland may be tender.
e. Manifestations:
i. Intermittent swelling of the gland
ii. Aggravating with taking food
iii. Acute infection
7. Pleomorphic Adenoma (Mixed tumor)
a. This is a benign tumor that usually does not spread outside the boundaries of normal salivary tissue
unless its capsule or outer shell has been damaged or it has become malignant which is rare.
b. 90% of all parotid tumours, 60% of submandibular tumours and 40% of minor salivary gland
tumours.
c. Symptoms & Signs:
i. They present as a painless slowly growing lump in the parotid (in front of or below the ear), or
submandibular gland (just below the lower jaw).
ii. Occasionally if large and involving the deep lobe they may have a significant intra-oral component
pushing the tonsil towards the midline for parotid tumours or the tongue upwards for
submandibular tumours.
iii. Weakness of the facial nerve is not a feature of this condition but suggests a possible malignant
tumour or may be as a result of technically difficult surgical removal.
8. Warthin's Tumour (Adenolymphoma)
a. Warthin's tumour is a benign tumour that does not spread outside the boundaries of normal
salivary tissue.
b. Clinical Features:
i. Occurs only in the parotid gland
ii. The second most common benign tumor of parotid gland
iii. May be unilateral or bilateral
iv. Occurs as a painless, sometimes fluctuant mass
v. May be associated with acute onset of pain and a sudden increase in size (papillary cystadenoma
lymphomatosum syndrome)
vi. Retrograde infection
vii. Ear symptoms (tinnitus, deafness, earache)
viii. Facial nerve paralysis
ix. The ability to concentrate sodium pertechnetate (99mTc) is suggestive of Warthin tumor
9. Adenoid cystic carcinoma
a. Adenoid cystic carcinoma (ACC) is an uncommon form of malignant neoplasm that arises within
secretory glands, most commonly the major and minor salivary glands of the head and neck.
Other sites of origin include the trachea, lacrimal gland, breast, skin, and vulva.
b. Signs & Symptoms:
i. mass
ii. pain and/or nerve paralysis
iii. it seldom metastasizes to regional lymph nodes.
iv. Distant metastasis is the most common presentation of treatment failure. Lung liver and bones

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.:>BurhanAhmed.:. BurhanAhmed.:. BurhanAhmed.:. BurhanAhmed.:. BurhanAhmed.:. BurhanAhmed.:. BurhanAhmed.:. BurhanAhmed.:. BurhanAhmed.:. BurhanAhmed.:.

1. Dental structures of Teeth

Chapter 2: Oral-Maxillofacial Clinical Examinations

2. Describe three special examinations.

Temperature stimulus pain

Chapter 4: Dental caries

Chapter 5: Diseases of The periapical Tissues

1. Acute Periapical Periodontitis:

Throbbing pain, Swelling of soft tissue

Chapter 7: Gingival Disease

plaque calculus a disruption of the oral epithelium accumulation of

i. Characteristic lesions ----- punched - out, crater - like depressions at the

a. in the epithelium widening of the intercellular spaces in the basal layer,

Chapter 8: Periodontal Disease

d. Reaiographic evidence of bone loss

Function of mucosa membrane :

Chapter 9: Oral Mucous Disease

For Example: herpetic stomatitis

For Example: Aphthae,etc.

1. The vesicles breakdown to form ulcers, etc.

Chapter 10: Nerve Block Anesthesia in Dentistry

4. Advantages of nerve block

a. Pulp & alveolar process

a. Posterior portion of hard palate

Midway between the median palate raphi

90-degree to the palate from the opposite

the tip of buccal fat pad

Lingual nerve lies 10 mm anteriorinferiorly to IA nerve

between the apices of 1 & 2 premolar

Middle superior dental nerve

Posterior superior dental nerve

Posterior superior dental nerve

Chapter 11: Tooth Extraction

Chapter 12: Maxillo-facial Infection

Chapter 14: Oral & Maxillofacial Trauma

3. Describe the ways of hemastasis.

1. Describe the characteristics of OMF Trauma?

Chapter 15: Malignant tumors on the Oral & Maxillofacial Region

Chapter 16: Temporomandibular Joint Diseases

Chapter 17: Salivary gland diseases

d. Symptoms & Signs:

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