Group A
Group A
Group A
Caries
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Introduction:
The word caries is derived from the Latin word meaning rot or decay. Dental caries is
an irreversible microbial disease of the calcified tissues of the teeth, characterized by
demineralization of the inorganic portion and destruction of the organic substance of the tooth.
1. Acidogenic theory
2. Proteolytic theory
3. Proteolysis-chelation theory.
1. Acidogenic Theory:
WD Miller in 1882 said Dental decay is a chemicoparasitic process consisting of two stages,
the decalcification of enamel, which results in its total destruction, as a preliminary stage
followed by dissolution of the softened residue of the enamel and dentin. In the first stage
there is destruction which is done by the acid attack whereas the dissolution of the residue
(2nd stage) is carried out by the proteolytic action of the bacterias.
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This whole process is supported by the presence of carbohydrates, microorganisms and dental
plaque.
2. Proteolytic Theory:
Heider, Bodecker (1878) and Abbott (1879) thrown considerable light to this theory.
According to this theory, organic portion of the tooth plays an important role in the
development of dental caries. It has been recognized that enamel contains 0.56 percent of
organic matter out of which 0.18 percent is keratin and 0.17 percent is a soluble protein
Enamel structure which are made of the organic material such as enamel lamella and enamel
rods prove to be the pathways for the advancing microorganisms. Microorganisms invade the
enamel lamella and the acid produced by the bacterias causes damage to the organic pathways.
3. Proteolysis-Chelation Theory:
This theory was put forward by Schatz and his coworkers in 1955. Chelation is a process in
which there is complexing of the metal ions to form complex substance through coordinate
covalent bond which results in poorly dissociated or weakly ionized compound.
Chelation is independent of the pH of the medium. Bacterial attack on the surface of the
enamel is initiated by keratinolytic microorganisms. This causes the breakdown of the protein
chiefly keratin. This results in the formation of soluble chelates which decalcify enamel even
at neutral pH. Enamel contains mucopolysaccharides, lipids and citrate which are susceptible
to bacterial attack and act as chelators.
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1. The Host:
The structure, composition & position of
the teethundoubtedly influences the
initiation and progression of a carious
lesion. Studies on the chemical
composition enamel indicate that the
surface enamel is more resistant to caries
than subsurface enamel. The surface is
lower in carbon dioxide, dissolves at a
slower rate in acids, contains less water
and has more inorganic material than
Figure 1: Local factors affecting incidence of dental caries
subsurface enamel. Significant
differences in fluoride content of sound and carious teeth have been reported. The enamel of
sound teeth contain 0.0111 0.0020% fluoride, while that of carious teeth contain 0.0069
0.0011% fluoride.
The presence of deep, narrow occlusal fissures or buccal or lingual pits tend
to trap food, bacteria and debris, and since defects are especially common in the base of
fissures, caries may develop rapidly in these areas. Conversely, as attrition advances the
inclined planes become flattened, providing less opportunity for caries development.
Teeth are malaligned, out of position or rotated difficult to clean and tend to favor the
accumulation of food and debris which leads to caries.
2. Substrate:
a. Saliva: Saliva is the bodys natural protective mechanism against decay. It contains
salivary proteins which get deposited onto the tooth surface which help the enamel against
acid dissolution. This protective layer is referred to as the pellicle. Salivary proteins also
act as antibacterial agents. Since saliva is rich in calcium, phosphate and fluoride, these
materials help in remineralization of the enamel. Saliva acts as cleaner of teeth as it quickly
washes away food debris from the mouth and to buffer the organic acids that are produced
by the bacteria. When salivary flow is reduced or absent, there occurs the increased food
retention. Since salivary buffering capacity is lost, an acid environment is encouraged
which further promotes the growth of aciduric bacteria. These aciduric bacterias savor the
acid conditions and metabolize carbohydrates in the low-pH environment.
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b. Diet: In the earlier times, the primitive man used to eat rough and raw unrefined foods which
had self-cleansing capacity. But in present times, soft refined foods are eaten which stick
stubbornly to the teeth and are not removed easily due to lack of roughage. This is the reason
for higher incidence of dental caries now-a-days than the past. Extensive studies have shown
that foodstu or drink containing fermentable carbohydrate are likely to cause significant
acid production, followed by demineralization of the enamel, but all carbohydrates are not
equally cariogenic. Complex carbohydrates such as starch are relatively harmless because
they are not completely digested in the mouth, but low molecular weight carbohydrates
diuse readily into plaque and are metabolized quickly by the bacteria.
3. The Bacteria:
Dental caries do not occur if the oral cavity is free of bacteria. There are many types of bacteria
in the mouth, the most caries active appear to be Streptococcus mutans, Lactobacillus spp.,
Veillonella spp. and Actinomyces spp. Among these streptococci mutans are most commonly
seen microorganism associated with the dental caries. They are considered main causative
factors for caries because of their ability to adhere to tooth surfaces, produce abundant
amounts of acid, and survive and continue metabolism at low pH conditions. Colonization
with Streptococcus mutans at an early age is an important factor for early caries initiation.
4. Time Period:
The time period during which all above three direct factors, i.e. tooth, microorganisms and
substrate are acting jointly should be adequate to produce acidic pH which is critical for
dissolution of enamel to produce a carious lesion.
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Smooth surface caries: Smooth surface
caries occurs on gingival third of buccal
and lingual surfaces and on proximal
surfaces.
Root caries: When the lesion starts at
the exposed root cementum and dentin, it
is termed as root caries.
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3. Radiation rampant caries: These are
commonly observed after radiotherapy of
malignant areas of the salivary glands. Because
of radiotherapy salivary flow is very much
reduced. This results in radiation rampant caries.
Chronic dental caries: Chronic caries travel
very slowly towards the pulp. They appear dark
in color and hard in consistency.
Figure 4: Rampant caries
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Based on Severity (Fig. 6):
Incipient caries: It involves less than half
the thickness of enamel.
Moderate caries: It involves more than
half the thickness of enamel, but does not
involve dentino-enamel junction.
Advanced caries: It involves the dentino-
enamel junction and less than half distance to
pulp cavity.
Severe caries: It involves more than half
distance to pulp cavity.
Figure 6: Classification of caries based on severity
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1. Smooth Surface Caries:
The first change seen histologically is the loss of interprismatic/interrod substance of
enamel with increased prominence of the rods.
There is also accentuation of the incremental lines of Retzius.
This is followed by the loss of mucopolysaccharides in the organic substance.
As it goes deeper, the caries forms a triangular pattern or cone shaped lesion with the
apex towards DEJ and base towards the tooth surface.
Finally there is loss of enamel structure, which gets roughened due to demineralization,
and disintegration of enamel prisms.
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Zone 2: Dark zone
It lies adjacent and superficial to the translucent zone
Usually present and thus referred as positive zone
Called dark zone because it does not transmit polarized light
Formed due to demineralization.
Zone 3: Body of the lesion
Largest portion of the incipient caries
Found between the surface and the dark zone
It is the area of greatest demineralization making it more porous.
Zone 4: Surface zone
This zone is not or least affected by caries
Greater resistance probably due to greater degree of mineralization and greater fluoride
concentration
It is less than 5 percent porous
Its radiopacity is comparable to adjacent enamel.
Dentinal Caries:
1. Early Dentinal Changes:
Initial penetration of the dentin by caries causes an alteration in dentin, known as
dentinal sclerosis.
In this reaction there occurs the calcification of dentinal tubules which seals off from
further penetration by microorganisms.
When dentinal tubules are completely occluded by the mineral precipitate, section of
the tooth gives a transparent appearance in transmitted light, this dentin is termed as
transparent dentin.
In the earliest stages, when only few tubules are involved, microorganisms may be
found penetrating the tubules, called Pioneer Bacteria.
In early caries, fatty degeneration of Tomes fibers and deposition of fat globules in
these processes act as predisposing factor for sclerosis of the tubules.
This initial decalcification involves the walls allowing them to distend as the tubules
are packed with microorganisms. Each tubule is seen to be packed with pure forms of
bacteria, e.g. one tubule packed with coccal forms the other tubule with bacilli.
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As the microorganisms proceed further they are distanced from the carbohydrates
substrate that was needed for the initiation of the caries.
Thus the high protein content of dentin must favor the growth of the microorganisms.
Therefore, proteolytic organisms might appear to predominate in the deeper caries of
dentin while acidophilic forms are more prominent in early caries.
Diagnosis:
In order to conserve tooth structure and perform minimally invasive dentistry, carious lesions
must be detected at the earliest possible time. By doing so, caries progress can be arrested,
thus avoiding a more invasive operative intervention. Various methods for diagnosis of dental
caries are:
1. Visual-tactile method
a. Conventional methods
i. Tactile examination
ii. Visual examination.
b. Advances in visual method
i. Illumination
Ultrasonic illumination
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Ultrasonic imaging
Fiber-optic trans-illumination (FOTI)
Wavelength dependent FOTI
Digital imaging FOTI (DIFOTI).
ii. Dyes
iii. Endoscopy filtered fluorescence (EFF).
2. Radiographic methods
a. Conventional methods
i. Intraoral periapical X-rays (IOPA), (Fig. 9) Figure 9: Radiograph showing occlusal caries
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Prevention of Dental Caries:
Method of dental caries control can be classified into two main types:
A. Methods to reduce demineralizing factors:
1. Dietary measures:
a. Sugar substitutes: Xylitol is a five-carbon sugar alcohol with the taste almost identical
to that of table sugar. It is non fermentable, non-cariogenic sugar and has anti-caries effects.
b. Fibrous food: Intake of raw fruits, vegetables and grains helps in increasing the salivary
flow, thereby removal of food debris from the oral cavity. These foods contain natural
phosphates, phytates and non-digestable fibers, moreover they do not stick to teeth, thus
increases caries protective mechanism.
c. Cheese: Cheese is considered as responsible for Increasing the salivary flow, pH, and
Promoting the clearance of sugar. All these factors help in reducing the incidence of caries.
3. Chemical measures:
Substances interfering with carbohydrate degradation through enzymatic alterations:
Vitamin K, Sarcocide
Substances interfering with bacterial growth and metabolism: Chlorhexidine, Iodine,
Urea and ammonium compounds, Nitrofurans.
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Apicoectomy
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Introductions:
An Apicoectomy is a minor oral surgical procedure to remove the tip of the apex of the root
of a dead tooth and associated pathological lesions and then seal the root end with a filling. It
is commonly performed to remove a portion of the root with undbrided canal space or to seal
the canal apically when a complete seal cannot be accomplished with nonsurgical root canal
treatment through the crown approach. The typical sequence of procedures used in
Apicoectomy are Anesthetization, flap design, incision and reflection, apical access,
periradicular curettage, root-end resection, root-end cavity preparation, root-end filling, flap
replacement, suturing and suture removal.
Indications:
Inability to perform nonsurgical endodontic therapy due to anatomical, pathological
and iatrogenic defects in the root canal.
Persistent infections after conventional endodontic treatment.
Need for biopsy.
Need to evaluate the resected root surface for any additional canals or fracture.
For removal of iatrogenic errors like ledges, fractured instruments, and perforation
which are causing treatment failure.
Removal of the un-instrumented and unfilled portion of the root.
Blockage of the root canal due to calcific metamorphosis or radicular restoration.
Severe root curvature.
Horizontal fracture at the root tip with associated periapical disease.
Contraindications:
Local Factors:
Inaccessibility to surgical site because of tooth location
Tooth position adjacent to the spaces such as maxillary sinus or nasal fossa
Unusual bony configuration
Short root length in which removal of root apex further compromises the prognosis.
Proximity to the neurovascular bundles
Severe periodontal diseases.
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Vertically fractured tooth
Systemic Factors:
Leukemia or neutropenia in active state leading to more chances of infection after
surgery, and impaired healing
Uncontrolled diabetes mellitus: Defective leukocyte function, defective wound
healing commonly occurs in severe diabetic patients
Recent serious cardiac or cancer surgery
Very old patients: Old age is usually associated with complications like cardiovascular
or pulmonary disorders, decreased kidney functions and liver functions.
Uncontrolled hypertension
Uncontrolled bleeding disorders
Immunocompromised patients
Recent myocardial infarction or patient taking anticoagulants
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of the surgery for the operator. The following general guidelines and principles should be used
during flap design:
The flap should be designed for maximum access to the site of surgery.
Adequate blood supply to the reflected tissue is maintained with a wide flap base.
Avoid severely angled vertical incision
Incisions over bony defects or over the periradicular lesion should be avoided; these
might cause postsurgical soft tissue fenestrations or nonunion of the incision.
The actual bony defect is larger than the size observed radiographically.
A minimal flap, which should include at least one tooth on either side of the intended
tooth, should be used.
Acute angles in the flap must be avoided. Sharp corners are difficult to reposition and
suture and may become ischemic and slough, resulting in delayed healing and possibly
scar formation.
Incisions and reflections include periosteum as part of the flap. Any remaining pieces
or tags of cellular nonreflected periosteum will hemorrhage, compromising visibility.
The interdental papilla must not be split (incised through) and should be either fully
included or excluded from the flap.
Vertical incisions must be extended to allow the retractor to rest on bone and not crush
portions of the flap.
Periradicular Curettage:
The tissue should be carefully peeled out, ideally in
one piece, with a suitably sized sharp curette (Fig. 14).
This process should leave a clean bony cavity. When
the lesion is very large, portions of tissue can be left
without compromising the blood supply to an adjacent
tooth. This should not affect periradicular healing.
Figure 14: Periapical curette
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as possible to still enable maximum visibility to the root apex. In general, the amount of root
removed depends on the reason for performing the root-end resection.
However, sufficient resection must be performed to expose additional canals, apical deltas, or
fractures.
should be filled with a root-end filling material (Fig. 17). Root-end filling materials should be:
Well tolerated by periapical tissues
Adhere to tooth surface
Dimensionally stable
Resistant to dissolution
Bactericidal or bacteriostatic
Not stain tooth or periradicular
tissue
Radiopaque.
Figure17: Placement of restorative materials
after cavity preparation
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Many materials have been used as root-end filling materials. Commonly used root-end filling
materials are Amalgam, Gutta-percha, Gold foil, Titanium screws, Glass ionomers, Zinc
oxide eugenol, Cavit, Composite resins, Polycarboxylate cement, Poly HEMA, Super
EBA, Mineral trioxide aggregate.
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Basic Instruments
used in Oral Surgery
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Instrument Used for Preparing The
Surgical Field:
Swab Holder (Fig. 19):
It is an instrument with long blades, expanded at the
ends, forming an oblong tip. The blades have a central
Fenestration and transverse serrations.
Uses:
1. To hold a swab and clean the area of operation.
2. To swab the throat when there are profuse secretions
in a patients under general anesthesia. Figure19: Swab Holder
2. Blades:
No. 10 (Fig. 20.B) For making
skin incisions
No. 11 (Fig. 20.C) For making
stab incisions (to drain an abscess)
No. 12 (Fig. 20.D) For
mucogingival procedures
No. 15 (Fig. 20.E) For
intraoral surgery.
Figure20: (A) Bard Parker Blade Handle (B) No.10 Blade (C) No.11 Blade
(D) No.12 Blade (E) No. 15 Blade (F) Dissecting Scissors
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Dissecting Scissors (Fig. 20.F):
As the name suggests, dissecting scissors are used to perform soft tissue dissection in the
deeper layers. The scissors have a blunt nose for undermining the tissues and a side cutting
edge for cutting the tissues.
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Tongue Depressor (Fig. 22.D):
The tongue depressor is an L shaped
instrument with a broad smooth blade for
depressing or retracting the tongue.
2. Babcocks Tissue Holding Forcep (Fig. 24.B): It has fenestrated blades without
teeth. It is used to hold enlarged lymph nodes or any glandular tissue.
3. Lanes Tissue Holding Forcep (Fig. 24.C): It is a long and stout instrument with
sharp teeth on the blades. It is used to hold tough structures like the skin, coarse muscles.
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Instrument Used to Remove Pathologic Tissues:
Curette (Fig. 27.B.C):
A curette can be single ended or
double ended. The working end may
be in the same plane as the shank or
at an angulation for adequate access
to the pathologic cavity. It is used to
remove tooth particles or debris from
the extraction socket and to enucleate
cysts, periapical granulomas,
intraosseous tumors. Figure 27: (B and C) Lucas curettes, (D) Volkmanns scoop
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concave inner surface. The beaks are sharp. They can be either side cutting (Blumenthal) or
both side and end cutting.
Uses:
1. To nibble sharp bony margins following simple or surgical extraction of teeth, surgical
procedures
2. To peel off thinned out bone present over cystic or tumorous lesions.
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Bone Gouge (Fig. 29.E):
The bone gouge has a round handle and a blade that has a sharp working tip that is concave
on the inner side. It is used to remove cancellous graft material during grafting procedures and
irregular pieces of bone.
Figure 29: (A) Osteotome, (B to D) Chisels, (E) Bone gouge, (F) Mallet
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Instrument Used for Suturing:
Mayo-Hegar Needle Holder (Fig. 30.A): The
needle holder is a straight instrument with a short
working tip. The working tip has cross hatched
serrations with a single vertical serration to grip the
needle. The handle has a catch. Usually a six inch
needle holder is used in Oral Surgery. The instrument
is held between the ring finger and the thumb and the
index and the middle finger support the needle holder.
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Forceps:
They are designed to deliver the teeth from the sockets. Each forceps has two handles, a joint
and two beaks. All the forceps have crosshatching on the handles to allow a firm grip and have
serrations on the inner side of the beaks to allow a better grip on the tooth. The beaks are
applied along the long axis of the tooth, below the CE junction in mandibular teeth, and above
the CE Junction in maxillary teeth. A firm grip on the tooth is established prior to giving any
forceps movements.
Types of Forceps:
1. Maxillary Extraction Forceps (Fig. 32)
a. Maxillary anterior forceps
b. Maxillary premolar forceps
c. Maxillary molar forceps
d. Maxillary anterior root forceps
e. Maxillary posterior root forceps
f. Bayonet forceps Figure 32: Maxillary Extraction Forceps
2. Mandibular Extraction Forceps (Fig. 33)
a. Mandibular anterior forceps
b. Mandibular premolar forceps
c. Mandibular molar forceps
d. Mandibular root forceps
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References:
1. Nisha Garj, Amit Garj. Textbook of Operative Dentistry, 2nd ed.; Chapter-25
2. R. A. Cawson, E. W. Odell Oral Pathology and Oral Medicine, 8th ed.; Chapter-3
3. R. Rajendran, B. Sivapathasundaram. Shafers Textbook of Oral Pathology, 6th ed.;
Chapter-9
4. Textbook of Endodontics by Nisha Garj, Amit Garj; Chapter-25
5. Ingles Endodontics; Chapter-33
6. T. R. Pitt Ford. Hartys Endodontics in Clinical Practice, 5th ed; Chapter-9
7. Louis I. Grossman, Seymour Oliet, Carlos E. Del Rio. Endodontic Practice, 11th
ed.; Chapter-17
8. Prof. Dr. Neelima Anil Malik. Textbook of Oral and Maxillofacial Surgery, 3rd ed.;
Chapter-5
9. S.M Balaji. Textbook of Oral and Maxillofacial Surgery; Chapter-4
10. Dr. Vinod Kapoor. Textbook of Oral and Maxillofacial Surgery, 2nd ed.; Chapter-
1
11. Gustav O. Kruger. Textbook of Oral and Maxillofacial Surgery, 6th ed.; Chapter-3
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