• Word caries is derived from Latin, meaning “rot” or decay. It is similar to the Greek word “ker” meaning death.
  • Dental caries is defined as a multifactorial, transmissible, infectious oral disease caused primarily by the complex interaction of cariogenic oral flora (biofilm) with fermentable dietary carbohydrates on the tooth surface over time.
  1. Cariogenic (acidogenic) bacteria.
  2. Bacterial plaque.
  3. Stagnation areas.
  4. Fermentable bacterial substrate (sugar).
  5. Susceptible tooth surfaces.
  6. Time.

Relevant acidogenic-aciduric bacterial species are:

  1. Streptococcus mutans.
  2. Bifidobacteria.
  3. Lactobacilli.
  • Mutans streptococci are initiators, bifidobacteria and lactobacilli are more enhancers for progression.
  • Boosters for microbial activity are specific environmental conditions, such as the presence of fermentable dietary sugars and the absence of oxygen.
  • It produces lactic acid from sucrose.
  • It can live at a pH as low as 4.2.
  • It forms large amounts of extracellular, sticky and insoluble glucan plaque matrix.
  • It adheres to pellicle and contributes to plaque formation.
  • Acidogenic.
  • Able to produce a pH low enough (usually pH 5) to decalcify tooth
  • Able to survive and continue to produce acid at low levels of pH.
  • Possess attachment mechanisms for firm adhesion to smooth tooth surfaces.
  • Able to produce adhesive, insoluble plaque polysaccharides (glucans).
  • Rapid production of a high concentration of acid within the plaque temporarily overcomes local buffering.
  • Escape of acid into the saliva is delayed by the diffusion-limiting properties of plaque and its thickness.
  • Diffusion of salivary buffers into plaque hampered by the diffusion-limiting properties of plaque and its thickness.
  • Continued acid production from bacterial intracellular storage polysaccharides after dietary sugar is exhausted.
  • Sucrose forms up to a third of the carbohydrate content of many person’s diets.
  • It promotes colonization of teeth by Streptococcus mutans.
  • Its disaccharide bond alone contains enough energy to react with bacterial enzymes to form extracellular dextran matrix.
  • Its small molecular size allows it to diffuse readily into plaque.
  • Bacterial metabolism of sucrose is rapid.
  • Deposition of structure less cell-free, pellicle of salivary glycoprotein.
  • Further deposition of pellicle enhanced by bacterial action precipitating salivary proteins.
  • Colonisation of the cell-free layer by bacteria, particularly by S. sanguis and S. mutans strains within 24 hours.
  • Progressive build-up of plaque substance by bacterial polysaccharides.
  • Proliferation of filamentous and other bacteria as the plaque matures.

Dental caries is a multifactorial disease in which there is an interaction between three principal factors:

  • A susceptible host tissue (tooth, saliva, other host factors).
  • Microflora with cariogenic potential.
  • A suitable local substrate

A. Early Theories

  1. The Legend of Worms: The earliest reference to tooth decay is probably from the ancient Sumerian text known as the ‘Legend of Worms’ from about 5,000 BC. The idea that caries is caused by worms was possibly prevalent for a long time as evident from the writings of Homer who made a reference to worms as the cause of toothache.

B. Endogenous Theories

  1. Humoral theory: According to Galen, the ancient Greek physician and philosopher “dental caries is produced by the internal action of acird, corroding humors”

Hippocrates also referred to the accumulated debries around the teeth and to their corroding action. He also stated that stagnation of juices in the teeth was cause of toothache.

  1. Vital theory: A vital theory of tooth decay was advanced towards the end of the 18th century which postulated that tooth decay originated like bone gangrene, from within the tooth itself.

C. Exogenous theories

  1. Chemical Theory: It was proposed that an unidentified ‘chymal agent’ was responsible for caries. Robertson in 1835 who proposed that dental decay was caused by acid formed by fermentation of food particles around the teeth.
  2. Parasitic or septic theory: Early microscopic observation of scrapings from teeth and of the carious lesions by Antoni Van Leeuwenhock (1632-1723) indicated that microorganisms were associated with the carious process. In 1843, Edrl described filamentous parasites in the membrane removed from the teeth. Ficinus in 1847 observed filamentous organisms in the enamel cuticle and in carious lesions. Dubos postulated that microorganisms can have toxic effects on tissue.
  3. Miller’s Chemico-Parasitic Theory Or The Acidogenic Theory:
  • Proposed by W D Miller in 1890. Caries is caused by acids produced by microorganisms of the mouth. Dental decay is a chemico-parasitic process consisting of two stages:

A. Decalcification of enamel and dentin (preliminary stage).

B. Dissolution of the softened residue (subsequent stage).

  • Acids resulting in primary decalcification are produced by the fermentation of starches and sugar from the retaining centers of teeth.

4. The proteolytic theory:

  • Organic or protein elements of a tooth are the initial pathway of invasion by microorganisms.
  • Enamel lamellae are pathways for organisms in the progress of dental caries
  • Gottlieb and Gottlieb, Diamond and Applebaum suggested that “Caries is essentially a proteolytic process: the microorganisms invade the organic pathways and destroy them in their advance. Acid formation accompanied proteolysis”
  • Proteolysis in the initiation of dental caries is likely to be of no significance, but its role in the progression of the more advanced carious lesions cannot be ruled out.

5. The proteolysis-chelation theory

  • Simultaneous microbial degradation of the organic components and the dissolution of the minerals of the tooth by the process known as chelation.
  • Chelation process involving the complexing of a metallic ion to a substance through a covalent bond which results in a highly stable, poorly dissociated or weakly ionized compound.
  • The proteolysis-chelation theory resolves the argument as to whether the initial attack of dental caries is on the organic or inorganic portion of enamel by stating that both may be attacked simultaneously.

Dental caries can be classified as:

  • Clinical classification.
  • Classification based on severity and rate of Progression.
  1. Pit and Fissure Caries:
  • Develops on the occlusal surface of molars and premolars, buccal and lingual surface of the molars and the palatal surface of the maxillary incisors.
  • Early carious lesions may appear brown or black and will feel slightly soft and ‘catch’ a fine explorer point.
  • The enamel directly bordering the pit or fissure may appear opaque bluish white as it becomes undermined.
  1. Smooth Surface Caries:
  • The primary type is caries that develops on the proximal surfaces of the teeth or on the gingival third of the buccal and lingual surfaces.
  • Proximal caries usually begins just below the contact point and appears in the early stage as a faint white opacity of the enamel without apparent loss of continuity of the enamel surface .
  • In some cases it appears as a yellow or brown pigmented area, but in either event is usually rather well demarcated.
  • The early white chalky spot becomes slightly roughened owing to superficial decalcification of the enamel.
  • As the caries penetrates the enamel, the enamel surrounding the lesion assumes a bluish-white appearance.
  1. Linear Enamel Caries:
  • An atypical form of dental caries that has been observed in the primary dentition of children in Latin American and Asian countries.
  • Found on the labial surface of the anterior maxillary teeth in the region of the neonatal line, which results from metabolic disturbances such as hypocalcemia or trauma at birth.
  • A variant of this type of caries in the primary teeth of children in the far East has been named odontoclasia.
  • The morphological aspectis atypical and results in gross destruction of the labial surfaces of incisor teeth.
  1. Cervical Caries:
  • Occurs on buccal, lingual or labial surfaces and usually extends from the area opposite the gingival crest occlusally to the convexity of the tooth surface.
  • Typical cervical carious lesion is a crescent-shaped cavity beginning, as a slightly roughened chalky area which gradually becomes excavated.
  • Occurs on any tooth without predilection and is directly related to lack of oral hygiene.
  1. Root Caries:
  • Defined by Hazen and his colleagues as “a soft, progressive lesion that is found anywhere on the root surface that has lost connective tissue attachment and is exposed to the oral environment”.
  • Found in dentitions of the older age groups with significant gingival recession and exposed root surfaces.
  • Root caries initiates on mineralized cementum and dentin surfaces which have greater organic component than enamel tissue.
  1. Acute Dental Caries
  • Caries which runs a rapid clinical course and results in early pulp involvement by the carious process.
  • Found in children and young adults (due to open dentinal tubules and no sclerosis).
  • The process is so rapid that there is little time for reparative dentin formation.
  • In acute caries the dentin is usually stained light yellow rather than the darker brown of chronic caries.
  • Pain is most common feature, but this is not an invariable finding.
  1. Rampant Caries:
  • Characterized by sudden, rapid and almost uncontrollable destruction of teeth, affecting surfaces of teeth that are relatively caries free.
  • Involves the proximal and cervical surfaces of the mandibular incisors.
  • A caries increment of 10 or more new carious lesions over a period of about one year is characteristic of rampant caries.
  • Observed in the primary dentition of young children and the permanent dentition of teenagers.
  1. Nursing Bottle Caries:
  • Also K/a nursing caries, baby bottle syndrome, and bottle mouth syndrome.
  • It is an unfortunate form of rampant caries affecting the deciduous dentition.
  • Present clinically as widespread carious destruction of deciduous teeth, most commonly the four maxillary incisors, followed by the first molars and then the cuspids if the habit is prolonged.

Occurs due to:

  • A nursing bottle containing milk or milk formula, fruit juice or sweetened water.
  • Breastfeeding.
  • Sugar or honey-sweetened pacifiers.
  1. Adolescent Caries:

The acute caries attack in the latter period is usually characterized as adolescent caries.

  1. Chronic Dental Caries:
  • It progresses slowly and tends to involve the pulp much later than acute caries. It is most common in adults.
  • The carious dentin is often stained dark brown.
  • Pain is not a common feature of chronic caries because of the protection afforded to the pulp by secondary dentin.
  1. Recurrent Caries:
  • Occurs in the immediate vicinity of a restoration.
  • Occurs due to inadequate extension of the original restoration, which favors
  • Retention of debris, or to poor adaptation of the filling material to the cavity, which produces a “leaky margin”.
  • Beneath restorations where the carious dentin has not removed before restoration.
  1. Arrested Caries:
  • It is caries which becomes static and does not show any tendency for further progression.
  • The deciduous and permanent dentitions are both affected.
  • Sclerosis of dentinal tubules and secondary dentin formation commonly occur in cases of arrested caries.

Dental caries can be detected by:

  • Visible color and texture change.
  • Tactile sensation using a dental explorer.
  1. Radiographs:
  • Interproximal carious lesion recognized on radiograph as small, triangular radiolucent area of enamel and dentin.
  • Radiographs are not useful for early enamel caries.
  1. Infrared laser fluorescence
  • It uses laser light source and a fiberoptic cable that transmits the light to handheld probe with fiberoptic eye at the tip.
  • The light is absorbed and induces infrared fluorescence which is collected at the probe tip and transmitted through ascending fibers, and processed and presented on a display window as an integer between 0 and 99.
  • Increased fluorescence reflects carious tooth substance particularly for numerical value higher than about 20.
  1. Digital Imaging Fiberoptic Transillumination
  • It provides an intense light beam that is transmitted through a fiberoptic cable to a specially designed probe to permit the use of transillumination on the proximal surfaces of posterior teeth.
  • Digital imaging fiberoptic transillumination is a further advancement of this technology in which the visually observed images are captured using a digital charged coupled device camera and sent to a computer for analysis, using dedicated algorithm.
  1. Quantitative light-induced fluorescence (QLF): Uses the ability of human enamel to show fluorescence under certain conditions. Demineralized enamel shows reduced fluorescence due to scattering, as the fluorescence is attributed to the cross-links between structural proteins.
  2. Electronic Caries Monitor (ECM): Measures the changes in electrical impedance between sound enamel and demineralized tooth structure, as normal teeth have lower electrical conductivity compared to demineralized teeth.

Caries activity refers to the increment of active lesions (new or recurrent lesions) over a slated period of time.

Caries susceptibility refers to the inherent tendency of the host and target tissue, the tooth, to be afflicted by the caries process. This is the susceptibility of a tooth to a caries producing environment.

A caries activity test measures the degrees to which the local environmental challenge (e.g. dietary effect on microbial growth and metabolism) favors the probability of carious lesions. These are:

  1. Lactobacillus Colony Test
  • Use for assessing the caries activity is the Lactobacillus colony count.
  • This method, measures the number of aciduric bacteria in a patient’s saliva by counting the number of colonies which appear on tomato peptone agar plates, a selective medium with pH 5.0, after inoculation of the patient’s saliva and incubation.
  1. Colorimetric Snyder Test
  • Developed by Snyder in 1951 is based on the rate of acid produced when a sample of stimulated saliva is inoculated into a glucose and agar containing

medium of pH 4.7–5.0.

  • The medium has bromocresol green as a color indicator, which changes from blue-green at pH 4.7–5.0 to yellow at pH 4.0, indirectly checking the presence of acidogenic and aciduric microorganisms.
  • The acid produced by the oral acidogenic flora is detected by the changes in pH indicator, and is compared to an uninoculated control tube after 24, 48 and 72 hours of incubation.
  1. Swab Test
  • Developed by Grainger et al in 1965.
  • The test involves sampling the oral flora by swabbing the buccal surfaces of teeth with a cotton applicator, which is subsequently incubated in the medium.
  • The pH following 48-hour incubation is read on a pH meter or the color change is read by use of color comparator.
  • A pH of 4.1 and below denotes marked caries activity; 4.2–4.4 is considered active; 4.5–4.6 is considered slightly active; and a pH of 4.6 and above is considered as caries inactive.
  1. Salivary S. mutans Level Test
  • The number of S. mutans forming units per unit volume of saliva is the fundamental basis of this test.
  • The test involves incubation of the sample obtained using tongue blades or a wooden spatula on Mitis Salivarius Agar (MSA), a selective streptococcal medium with increased concentration of sucrose (20%) and 0.2U bacitracin per ml to suppress the growth of most non S. mutans colonies.
  • Agar plates are incubated at 37° C for 48 hours 95% N2– 5% CO2.
  • Levels of S. mutans greater than 105 are indicative of an acceptable cariogenic challenge because colonization does not occur until the level of S. mutans reaches 4.5×104/ml for smooth surface and 103/ml of occlusal fissures.
  1. mutans Dip-slide Method
  • This test classifies salivary samples according to estimates of mutans colonies growing on modified MSA.
  • In this method, the stimulated saliva is collected for five minutes and is poured over the agar coated slide, totally wetting the surface and the excess allowed to drain off.
  • After the slides are dry, the bacitracin disks are placed in the middle of the inoculated agar, about 1 cm from each other. The slide is then incubated in a tube containing a CO2 tablet for 48 hours at 370
  • A zone of inhibition 10–20 mm in diameter is formed around each bacitracin disk. If present, mutans appears as small blue colonies growing within the zone of inhibition.
  • The colony density is compared with a model chart and classified as 0 (negligible), 1 (less than 100,000), 2 (100,000–1000,000) 3 (more than 1000,000) S. mutans CFU/ml of saliva.
  1. Buffer Capacity Test

This test evaluates the quantity of acid required to lower the pH of saliva through an arbitrary pH interval or, in other words, the amount of acid or base necessary to bring color indicators to their end point. Importantly, buffer capacity could be quantitated either using a pH meter or color indicators. This test relates the buffering capacity of saliva and caries activity.

  1. Enamel Solubility Test

The Fosdick calcium dissolution test measures a milligram of powdered enamel dissolved in four hours by acid formed when the patient’s saliva is mixed with glucose and powdered enamel.

  1. Salivary Reductase Test
  • This test measures the activity of the reductase enzyme present in salivary bacteria. Saliva is collected by chewing paraffin and expectorated directly into the collection tube. The sample is then mixed with the dye diazo-resorcinol.
  • The “Caries Conduciveness” reading or color change is done after 15 minutes. No incubation procedures are required.
  1. ALBAN test
  • It is simplified substitute for the Synder test.
  • 60 grams of synder test agar is placed in 1 liter of water and suspension is brought to a boil over a low flame.
  • When thoroughly melted, the agar is distributed using about 5 ml per tube.
  • These tubes should be autoclaved for 15 minutes, allowed to cool and stored in refrigerator.
  • 2 tubes of Alban medium are taken from the refrigerator and the patient is asked to expectorate a small amount of saliva directly in to the tubes.
  • The tubes are labeled and incubated at 98.60 F(370C) for upto 4 days and observed daily for:
  1. Change for color from bluish green(pH 5) to definite yellow (pH 4 or below).
  2. The depth in the medium to which the change has occurred.
  3. Streptococcus mutans screening test
  4. Plaque/tooth pick method:
  • This test involves a simple screening of diluted plaque sample streaked on selective culture media.
  • Plaque samples are collected from gingival thirds of buccal tooth surfaces one from each quadrant and placed in Ringer’s solution.
  • Sample is shaken until homogenized.
  • The plaque suspension is stretched across MSA plates.
  • After aerobic incubation at 370 C for 72 hours, cultures are examines and total colonies in 10 fields are recorded.
  1. Saliva /Tongue blade method
  • This estimates the number of S.Mutans in mixed paraffin-stimulated saliva when cultured in Mutans Salivarius Bacitracin (MSB) agar.
  • The subject chews a piece of paraffin wax for one minute to displace plaque microorganisms, thereby increasing the proportions of plaque microorganisms in saliva.
  • Sterile tongue blade are then rotated in patient’s mouth 10 times so that both sides are thoroughly inoculated by oral flora and pressed on to MSB agar in a disposable contact petri dish.
  • Incubation done at 370
  1. Fosdick calcium dissolution test
  • It measures the milligrams of powdered enamel dissolved in 4 hours by acid formed when the patient’s saliva is mixed with glucose and powdered enamel.
  • Saliva is stimulated by having patient chew gum or paraffin.
  • 25 ml of this saliva is collected and part of it is analyzed for calcium content.
  • Remaining saliva is placed in an 8-inch sterile test tube with about 0.1gm of powdered human enamel.
  • The tube is sealed and shaken for 4 hours at body temperature, after which it is again analyzed for calcium content.
  1. ORA test
  • It is based on the rate of oxygen depletion by microorganisms in expectorated milk samples. In normal conditions the bacterial enzyme, aerobic dehydrogenase transfers electrons or protons to oxygen. Once oxygen gets utilized by aerobic organisms, methylene blue acts as electron acceptor and gets reduced to leucomethylene blue. This reflects the metabolic activity of the aerobic organisms.
  • Mouth is rinsed vigorously with 10 ml of sterile milk for 30 seconds and expectorate is collected.
  • 3 ml of this transferred to screw cap tube with disposable syringe.
  • To this 0.12 ml of 0.1% methylene blue is added, thoroughly mixed and placed on a stand in well illuminated area.
  • Tube is observed every 10 minutes for any color change at bottom using a mirror.
  • Time taken for the initiation of color change within 6mm ring is recorded.

Source of Antibodies in Saliva

  • IgG antibodies from serum.
  • IgA antibodies in salivary secretions.
  • A combined effect of serum and salivary components.

Types of Caries Vaccine

  • Live modified organisms.
  • Inactivated or killed organisms.
  • Extracted cellular fractions, toxoids or combination of these.

Methods of immunization

  1. Periglandular salivary immunization
  • In this method, repeated S.mutans in Freunds adjuvant were administered adjacent to the salivary glands.
  • Resulted in protection but inoculation with similar antigens in sites remote from the salivary glands were less consistently successful.
  1. Parenteral immunization
  • A significant reduction in caries, in experimental rats, was related to an increased level of salivary IgA antibodies to S. mutans, as the serum antibody titre was minimal.
  • It is not certain whether passive transfer of IgA in the milk has a protective value by directly preventing adherence of S. mutans to the tooth or indirectly by being absorbed into the blood circulation and then affecting the tooth via crevicular fluid or saliva.
  1. Oral sub mucous immunization
  • Cells or cell walls mixed with an adjuvant are injected under the mucosa of the buccal sulci of the four quadrants of the mouth.
  • This method of immunization resulted in a significant reduction in caries.
  1. Ingestion of whole S. mutans

This approach is attractive because most people who are moderately infected by S. mutans may swallow several million of these microorganisms per day, apparently without any untoward effects.

  1. Murine monoclonal antibody

Applying murine monoclonal IgG antibody to monkey gingiva,resulted in decreased colonization of implanted S. mutans, reduced caries.

  1. Immune bovine milk

Ingestion of food supplemented with immune bovine milk resulted in diminished S. mutans, less plaque and reduced caries in rodents.


  1. Egg yolk antibody

Involves immunization of hens with GTF, followed by purification of the antibody enriched IgG from egg yolks and the experimental use of this enriched antibody as a dietary additive in rodents.

  1. Replacement Therapy
  • A genetically-modified strain of S. mutans, BCS3-L1, is incapable of producing lactic acid, which dissolves tooth enamel, and aggressively replaces native flora.
  • However, the prospect of introducing GMO into the human body’s flora has raised muted concerns including the prospect that BCS3-L1 might be more harmful than native S. mutans as a causative agent of inflammatory heart disease.
  • Primary dentin is elaborated before the teeth erupt and is divided into mantle and circumpulpal dentin.
  • Mantle dentin is the first calcified layer of the dentin deposited against the enamel, forms the dentinal side of the dentinoenamel junction.
  • Circumpulpal dentin is the dentin formed after the layer of mantle dentin.
  • Secondary dentin is elaborated after eruption of the teeth.
  • It is deposited unevenly on primary dentin at a low rate.
  • Has incremental patterns and tubular structures less regular than those of primary dentin.
  • This deposition of secondary dentin protects the pulp.

Two types of tertiary dentin:

  • Type of tertiary dentin formed by primary odontoblasts following a mild stimulus is called reactionary dentin.
  • Type of tertiary dentin formed by newly differentiated or secondary odontoblasts is termed reparative dentin.
  • The dental pulp is enclosed in a rigid environment comprising three mineralized tissues: dentine, enamel and cementum.
  • Embryologically, the dental pulp derives from neural crest cells.
  • Proliferation and condensation of the cells lead to the formation of a dental papilla, from which the mature pulp is derived.
  • Approximately, 80% of the nerves of the pulp are C fibers and the rest are Aδ fibers.
  • The impulse travels from C or Aδ fiber nerve endings, through the plexus of Raschkow, to the nerve trunk in the central zone of the pulp.
  • The Aδ fibers are enclosed in myelin sheaths while traversing the plexus of Raschkow.
  • The nerve trunk is composed of the myelinated Aδ fibers in the periphery and unmyelinated C fibers in the center.

C nerve fibers

  • C fibers are unmyelinated and fine sensory afferents.
  • C fibers have a diameter of 0.3-1.2 pm and a conduction velocity of 0.4-2 m/s.
  • The conduction of these fibers, which are of smaller diameter than Aδ fibers, is slow.
  • These fibers are probably distributed throughout the pulp tissue.
  • With their receptive fields located in the pulp, C fibers transmit impulses that are experienced as a dull, poorly localized, and lingering pain; they conduct throbbing and aching pain associated with pulp tissue damage.
  • In addition to the nociceptive alarm signaling, the intradental sensory axons play a regulation role in the maintenance and repair of the pulpodentinal complex.
  • Most apical myelinated axons are fast-conducting Aδ fibers with their receptive fields located at the pulpal periphery and inner dentin.
  • The Aδ fibers have a diameter of 2-5 pm and a conduction velocity of 6-30 m/s.
  • The Aδ fibers, with a larger diameter than that of the C fibers, conduct impulses at a higher velocity.
  • These fibers are probably activated by a hydrodynamic mechanism and conduct impulses that are interpreted as short, well-localized, sharp, and pricking pain.
  • The Aδ fibers are distributed in the odontoblastic and subodontoblastic zones and are associated with dentinal pain.
  • Reduces the size of the pulp chambers and root canals (due to deposition of secondary dentin and reparative dentin).
  • Decrease in the diameter of the dentinal tubules (due to continuous deposition of peritubular dentin).
  • Reduction in the fluid content of the dentinal tubules.
  • The fibroblasts are reduced in size and numbers, but the collagen fibers are increased in number and in size.
  • Blood vessels decrease in number and arteries undergo arteriosclerotic changes.
  • Calcific material is deposited in the tunica adventitia and tunica media.
  • Number of nerves is also reduced.

The periradicular tissues consist of the following:

  • Cementum, which covers the roots of the teeth.
  • Periodontal ligament, whose collagen fibers, embedded in the cementum of the roots and in the alveolar processes, attach the roots to the surrounding tissues.
  • Alveolar process, which forms the bony troughs containing the roots of the teeth.
  • The width of the PDL varies from 0.15 to 0.38 mm.
  • Teeth with heavy occlusal loads have wider PDL space.
  • With advancing age, the width of the PDL is reduced.
  • Through dentinal tubules following carious invasion.
  • Through crown or root following traumatic exposure of the pulp.
  • Coronal leakage following restorative procedures.
  • Through external or internal resorption that can lead to pulp exposures
  • From the periodontal tissue through exposed dentinal tubules, lateral and accessory canals, or apical and lateral foramina.
  • By the lymphatic or hematogenous route.
  • Ana-choresis, defined as the localization of transient bacteria in the blood into an inflamed area, such as traumatized or inflamed pulp.

A.   Anaerobic Gram-negative bacteria

•      Treponema.

•      Dialister.

•      Porphyromonas.

•      Tannerella.

•      Fusobacterium.

•      Prevotella.

•      Centipeda.

•      Veillonella.

B.   Facultative Gram-negative bacteria

•      Neisseria.

•      Capnocytophaga.

•      Haemophilus.

C.   Anaerobic Gram-positive bacteria

•      Actinomyces.

•      Eubacterium.

•      Propionibacterium.

•      Peptostreptococcus.

•      Filifactor.

D.  Facultative Gram-positive bacteria

•      Enterococcus.

•      Actinomyces.

•      Streptococcus.

•      Lactobacillus.

Pulpal pain is described in one of two ways:

  1. Sharp, piercing, and lancinating: This type of painful response is consistent with those usually associated with excitation of the “Aδ” nerve fibers in the pulp.
  2. Dull, boring, gnawing, and excruciating: This painful response is consistent with those resulting from excitation and slower rate of transmission of the “C” nerve fibers in the pulp.
  1. Physical                                                                                                                                                                              A. Mechanical                                                                                                                                                                                            a. Trauma
  • Accidental (contact sports).
  • Iatrogenic dental procedures (during cavity or crown preparation).                                                                                                         b. Pathologic wear (attrition, abrasion, etc.).                                                                                                                                               c. Crack through body of tooth (cracked tooth syndrome).                                                                                                                         d. Barometric changes (barodontalgia).                                                                                                                                                      B. Thermal                                                                                                                                                                                                   a. Heat from cavity preparation, at either low or high speed.                                                                                                                     b. Exothermic heat from the setting of cement.                                                                                                                                           c. Conduction of heat and cold through deep fillings without a protective base.                                                                                         d. Frictional heat caused by polishing a restoration.                                                                                                                                                                                                                                                                                                                                                     C. Electrical (galvanic current from dissimilar metallic fillings).                                                                                                              2.Chemical                                                                                                                                                                                 a. Phosphoric acid, acrylic monomer, etc.                                                                                                                                                   b. Erosion (acids).                                                                                                                                                                                 3. Bacterial                                                                                                                                                                                                 a. Toxins associated with caries.                                                                                                                                                                 b. Direct invasion of pulp from caries or trauma.

      c. Microbial colonization in the pulp by blood-borne microorganisms (anachoresis).

Cracked Tooth Syndrome Incomplete fractures through the body of the tooth may cause pain of apparently idiopathic origin. This is referred to as the “cracked tooth syndrome.”

Also known as aerodontalgia, denotes toothache occurring at low atmospheric pressure experienced either during flight or during a test run in a decompression chamber.

  • Pulpitis is inflammation of the pulp.
  • It may be acute or chronic, partial or total, and the pulp may be infected or sterile.
  1. Inflammatory diseases of the dental pulp                                                                                                                                                A.Reversible pulpitis
    • Symptomatic (acute).
    • Asymptomatic (chronic).                                                                                                                                                BIrreversible pulpitis                                                                                                                                                          a. Acute
  • Abnormally responsive to cold
  • Abnormally responsive to heat                                                                                                                                                                          b. Chronic
  • Asymptomatic with pulp exposure
  • Hyperplastic pulpitis
  • Internal resorption
  1. Pulp degeneration                                                                                                                                                                                      a. Calcific (radiographic diagnosis                                                                                                                                                              b. Others (histopathologic diagnosis)
  2. Necrosis

Reversible pulpitis is a mild-to-moderate inflammatory condition of the pulp caused by noxious stimuli in which the pulp is capable of returning to the uninflamed state following removal of the stimuli.

  • Symptomatic reversible pulpitis is characterized by sharp pain lasting for a moment.
  • Pain occurs on by cold and by cold air.
  • It does not occur spontaneously and does not continue when the cause has been removed.
  • Asymptomatic reversible pulpitis may result from incipient caries and is resolved on removal of the caries and proper restoration of the tooth
  • Made by patient’s symptoms and by clinical tests.
  • The pain is sharp, lasts but a few seconds, and generally disappears when the stimulus is removed.
  • Cold, sweet, or sour usually causes it.
  • Application of cold is an excellent method of locating and diagnosing the involved tooth.
  • No tenderness on percussion.
  • Periapical tissue is normal on radiographic examination.
  • Prevention is important.
  • Use of a cavity varnish or cement base before restoration.
  • Care in cavity preparation and polishing are recommended to prevent pulpitis.

Irreversible pulpitis is a persistent inflammatory condition of the pulp, symptomatic or asymptomatic, caused by a noxious stimulus.

A.   Early stages:

·         Paroxysm of pain may be caused by sudden temperature changes, particularly cold; sweet or acid foodstuffs; and pressure from packing food into a cavity or suction exerted by the tongue or cheek.

·         Pain continues when the cause has been removed, and it may come and go spontaneously, without apparent cause.

·         •Pain is sharp, piercing, or shooting, severe, intermittent or continuous, depending on the degree of pulpal involvement.

·         Pain exacerbates on bending over or lying down (due to change in intrapulpal pressure).

·         There may be the referred to adjacent teeth, to the temple or sinuses when an upper posterior tooth is involved, or to the ear when a lower posterior tooth is affected.

B.   Later stages:

•      Pain is more severe, boring, gnawing, or throbbing, or as if the tooth was under constant pressure.

•      Patients are often kept awake at night by the pain, which continues to be intolerable.

•      Pain is increased by heat and is sometimes relieved by cold, although continued cold may intensify the pain.

•      Apical periodontitis is absent.

  • Inspection reveals deep cavity extending to the pulp or decay under a filling. The pulp may already be exposed.
  • Diffuse, dull, constant pain, characterized by throbbing and gnawing, and the tooth may respond abnormally and severely to heat.
  • Pain lingers after the stimulus is removed, or it can occur spontaneously.
  • On gaining access to the exposure, grayish, scum-like layer over the exposed pulp and the surrounding dentin can be seen.
  • Radiographic examination may not show anything of significance.

Reversible pulpitis, acute alveolar abscess.

  • Consists of complete removal of the pulp, or pulpectomy.
  • In posterior teeth, removal of the coronal pulp or pulpotomy should be performed as an emergency procedure.
  • Pain of irreversible pulpitis is more severe and lasts longer.
  • IN reversible pulpitis, the cause of the pain is traceable to a stimulus like cold water or a draft of air, whereas in irreversible pulpitis, the pain may come without any apparent stimulus.
  • Also k/a “pulp polyp”.
  • It is a productive pulpal inflammation due to an extensive carious exposure of a young pulp.
  • This disorder is characterized by the development of granulation tissue, covered at times with epithelium and resulting from long-standing, low-grade irritation.
  • Slow, progressive carious exposure of the pulp.
  • Large, open cavity; a young, resistant pulp; and a chronic, low-grade stimulus are necessary.
  • Seen only in the teeth of children and young adults.
  • Appearance of the polypoid tissue is clinically characteristic; a fleshy, reddish pulpal mass fills most of the pulp chamber or cavity or even extends beyond the confines of the tooth.(Figure: 1)
  • At times, the mass is large enough to interfere with comfortable closure of the teeth.
  • In early stages of development, it may be the size of a pin.
  • Polypoid tissue is less sensitive than normal pulp tissue and more sensitive than gingival tissue.
  • Cutting of this tissue produces no pain, but pressure thereby transmitted to the apical end of the pulp does cause pain.
  • This tissue bleeds easily because of a rich network of blood vessels.

Figure 1:  Chronic hyperplastic pulpitis

  • Clinical examination.
  • Radiographs show a large, open cavity with direct access to the pulp chamber.
  • Tooth may respond feebly or not at all to the thermal test, unless one uses extreme cold.
  • Gingival polyp is firm with colour similar to adjacent gingival whereas pulp polyp is edematous more reddish in colour.
  • Gingival polyp is not friable whereas pulp polyp is friable.
  • On passing a probe around in gingival polyp its origin can be trace around or adjacent to the tooth whereas in pulp polyp its origin can be trace within the tooth.(Figure:2 A and B)


      Figure 2:

     A- Gingival polyp                     B- Chronic hyperplastic pulpitis

  • Elimination of the polypoid tissue followed by extirpation of the pulp and restoration.
  • Bleeding from hyperplastic pulpal mass can be controlled with pressure.
  • Resorption is a condition associated with either a physiologic or a pathologic process resulting in a loss of dentin, cementum or bone.

Two types:

  • Internal resoption (pulpally derived)
  • Externally (periodontally derived).
  • Internal resorption was first reported by Bell in 1830. Pink tooth of Mummery (1920), so called due to the presence of a pink discolorationon the crown, is named after the anatomist Mummery.
  • Internal resorption is an idiopathic slow or fast progressive resorptive process occurring in the dentin of the pulp chamber or root canals of teeth.

Internal resorption can be categorized by the type/cause as:

  • Inflammatory: Following damage to the predentin subsequent to a bacterial infection or trauma.
  • Transient: Due to another form of trauma induced noninfective, self-limiting root resorption and follow a luxation injury.
  • Progressive: Stimulated by constant inflammation following infection.
  • Replacement/metaplastic: It involves subsequent deposition of mineralized tissue resembling bone or cementum but not dentin.

Etiology is unknown, but such patients often have a history of trauma.

  • Internal resorption in the root of a tooth is asymptomatic.
  • In the crown of the tooth, internal resorption may be manifested as a reddish area called “pink spot.” (Figure:3)
  • Pink spot represents the granulation tissue showing through the resorbed area of the crown.
  • It is a slow, progressive, intermittent process extending over 1 or 2 years.
  • Sometimes it may develop rapidly and may perforate the tooth within a matter of months.
  • Maxillary anterior teeth are commonly involved.

Figure 3: Pink tooth

  • Usually, diagnosed during routine radiographic examination.
  • The radiograph shows a change in the appearance of die wall in the root canal or pulp chamber, with a round or ovoid radiolucent area.(Figure: 4)
  • Resorptive defect is more extensive in the pulpal wall than on the root surface.

Figure 4: Radiographic appearance of internal resorption

  • Extirpation of the pulp.
  • Routine endodontic treatment.

External resorption is a lytic process occurring in the cementum or cementum and dentin of the roots of teeth.

Three types:

  • External surface resorption.
  • External inflammatory root resorption.
  • Exernal replacement resorption or ankylosis.

·         Cysts.

·         Dental trauma.

·         Excessive mechanical forces.

·         Periradicular inflammation.

·         Tumours.

·         Periodontal treatment.

·         Hormonal imbalance.

·         Reimplantation of teeth.

·         Pressure from impacted teeth.

  • External root resorption is asymptomatic.
  • As the root is completely resorbed, the tooth may become mobile.
  • If the external root resorption extends into the crown, it will give the appearance of “pink tooth” seen in internal resorption.
  • In replacement resorption or ankylosis, the root is gradually replaced by bone renders the tooth immobile, in infraocclusion, and with a high metallic percussion sound.
  • Small areas of external surface resorption of cementum cannot detect by radiograph.
  • External inflammatory root resorption can diagnose by radiographs and appears as concave or ragged areas on the root surface or blunting of die apex.
  • Areas of replacement resorption or ankylosis have a resorbed root with no periodontal ligament space and with bone replacing the defects.
  • Treatment of external resorption varies with the etiological factor.
  • External resorption is caused by extension of pulpal disease into the supporting tissues, root canal therapy indicated.
  • External resorption due to by excessive forces from orthodontic appliances can be stopped by reducing those forces.
  • In cases of external cervical root resorption, intervention in the form of surgical exposure of the defect and restoration with a suitable restorative material is treatment.
  • Degeneration is present in the teeth of older people.
  • Occurs due to persistent, mild irritation in teeth of younger people.

Early stage:

  • Pulp degeneration does not cause definite clinical symptoms in early stages.
  • No discoloration.

Later stage:

  • Tooth may become discolored.
  • Pulp will not respond to stimulation.
  1. Calcific Degeneration
  • In this part of the pulp tissue is replaced by calcific material (pulp stones or denticles).
  • Calcification may occur either within the pulp chamber or root canal.
  • Calcified material has a laminated structure and may be attach or unattach within the body of the pulp.
  • When it occurs as sequelae to a traumatic injury is known as calcific metamorphosis.
  1. Atrophic Degeneration
  • Observed histopathologically in pulps of older people.
  • Fewer stellate cells are present and intercellular fluid is increased.
  • The pulp tissue is less sensitive than normal.
  • No clinical diagnosis exists.
  1. Fibrous Degeneration
  • Characterized by replacement of the cellular elements by fibrous connective tissue.
  • Removal from the root canal, such a pulp has the characteristic appearance of a leathery fiber.
  1. Pulp Artifacts
  • It is probably an artifact caused by poor fixation of the tissue specimen.
  • Fatty degeneration of the pulp, along with reticular atrophy and vacuolization, are all probably artifacts due to unsatisfactory fixation.
  1. Tumor Metastasis
  • Metastasis of tumor cells to the dental pulp is rare, except possibly in terminal stages.

·         Necrosis is death of the pulp.

·         It may be partial or total.

·         Occur due to inflammation, traumatic injury.

·         It is of two types:

A.   Coagulation.

B.   Liquefaction.

In this the soluble portion of tissue is precipitated or is converted into a solid material.

Results when proteolytic enzymes convert the tissue into a softened mass, a liquid or amorphous debris.

It is a form of coagulation necrosis in which the tissue is converted into a cheesy mass consisting chiefly of coagulated proteins, fats, and water.

  • No painful symptoms.
  • Discoloration of the tooth (grayish or brownish).
  • The dull or opaque appearance of the crown.
  • Teeth with partial necrosis can respond to thermal changes (due to presence of vital nerve fibers through the adjacent inflamed tissue).
  • Radiograph shows a large cavity or filling.
  • Thickening of the periodontal ligament.
  • Pulp does not respond to cold, the electric pulp test, or the test cavity.
  • Nerve fibers are resistant to inflammatory changes.

Treatment consists of preparation and obturation of the root canals.

1.   Acute periradicular disease

A.   Acute apical periodontitis (symptomatic periodontitis)

• Vital.

• Nonvital.

B.   Acute alveolar abscess

C.   Acute exacerbation of chronic apical periodontitis (phoenix abscess)

2.   Chronic periradicular diseases

A.   Chronic apical periodontitis

• Chronic alveolar abscess

• Cystic apical periodontitis.

B.   Persistent apical periodontitis.

3.   Condensing osteitis.

4.   External root resorption.

5.   Diseases of the periradicular tissues of non- endodontic origin.

  • Also k/a symptomatic apical periodontitis.
  • It is a painful inflammation of the periodontium as a result of trauma, irritation, or infection through the root canal, regardless of whether the pulp is vital or nonvital.

In vital tooth

•      Abnormal occlusal contacts.

•      Restoration extending beyond the occlusal plane.

•      Wedging of a foreign object between the teeth like toothpick or food.

•      Traumatic blow to the teeth.

In non-vital tooth

A.   Sequelae of pulpal diseases.

B.   Iatrogenic:

•      Root canal instrumentation forcing bacteria or debris inadvertently through the apical foramen.

•      Forcing of irritating irrigants or medicaments through the apical foramen.

•      Extension of obturating material through the apical foramen to periapical tissue.

•      Perforation of the root.

  • Over instrumentation during cleaning and shaping of root canals.
  • Pain and tenderness of the tooth.
  • Tooth may be slightly sore.
  • The tooth may feel extruded.
  • Pain increase on closure and mastication.
  • Pain on percussion.
  • Radiographic examination:

    • Thickened periodontal ligament or a small area of rarefaction in pulp less tooth.(Figure: 5)
    • Normal periradicular structures (in vital pulp).

Figure 5: Thickened periodontal ligament

  • Determine the cause and relieving the symptoms.
  • Adjustment of high points (in hyperocclusion cases)
  • Removal of irritants (in case of nonvital infected pulp).
  • As acute phase has subsided, the tooth is treated by conservative means.
  • Also k/a Acute abscess, acute apical abscess, acute dento-alveolar abscess, acute periapical abscess, and acute radicular abscess.
  • An acute alveolar abscess is a localized collection of pus in the alveolar bone at the root apex of a tooth following death of the pulp, with extension of the infection through the apical foramen into the periradicular tissues.
  • Mere tenderness of the tooth.
  • Pain relieved by continued slight pressure on the extruded tooth to push it back into the alveolus.
  • Later, severe, throbbing pain, with swelling of the overlying soft tissue.
  • The tooth becomes elongated, and mobile.
  • Infection may progress to chronic apical abscess and pus may break through to form a sinus tract.
  • It may further progress on to osteitis, periostitis, cellulitis, or osteomyelitis.
  • Swelling is usually seen in the adjacent tissues dose to the affected tooth. When swelling becomes extensive, the resulting cellulitis.
  • In case of maxillary anterior tooth (cuspid), swelling of the upper lip may extend to one or both the eyelids.
  • In case of maxillary posterior tooth, cheek may swell to an immense size.
  • In the case of a mandibular anterior tooth, swelling can involve lower lip, chin, and sometimes the neck.
  • In the case of mandibular posterior tooth, swelling of the cheek may extend to the ear or even around the border of the jaw into the submaxillary region.()
  • The tissue at the surface of the swelling appears taut, inflamed; pus starts to form beneath it.
  • Palatal swelling form due to involvement of palatal root of maxillary molars and premolars.
  • By clinical examination.
  • Subjective history given by the patient.
  • In the early stages, it may be difficult to locate the tooth due to absence of clinical signs and diffuse, annoying pain.
  • When infection has progressed to the point of periodontitis and extrusion of the tooth; radiograph shows a cavity, defective restoration, thickened periodontal ligament space or evidence of breakdown of bone in the region of the root apex.(Figure: 6B)
  • If the acute alveolar abscess is an exacerbation of a long-standing chronic alveolar abscess, an area of periapical rarefaction seen on radiograph.
  • The affected pulp is necrotic and does not respond to electric current or to application of cold.
  • The tooth may be tender to percussion.
  • Apical mucosa is tender to palpation, and the tooth may be mobile and extruded.

Figure6: A- Extraoral                                    swelling   

               B- Radiographic                          changes in  

                                                                          acute alveolar abscess

Periodontal abscess, irreversible pulpitis.

  • The immediate treatment consists of establishing drainage and controlling the systemic reaction.

Emergency treatment of an acute alveolar abscess, the following procedure is recommended:

  • Complete the access opening painlessly.
  • Irrigate profusely, debride the pulp chamber, but avoid forcing any solution or debris into the periapical tissue.
  • Using a No. 8, 10, or 15 K file or reamer as an explorer, locate the root canal orifices and instrument each root canal within 1 mm of the root apex.
  • Continue to debride and to irrigate while enlarging each root canal.
  • Frequently, a purulent exudate escapes into the chamber.
  • When periapical abscess does not drain through the root canal, use a sterile precurved ISO No. 8 or 10 patency K-file and go beyond the apical constriction to initiate drainage.
  • If the abscess does not drain through the canal in spite of creating canal patency then the canals should be cleaned and shaped to facilitate the placement of a suitable intracanal medicament like calcium hydroxide.
  • If there is excessive drainage of blood and pus through the canals then allow the drainage to take place and irrigate the canals copiously. Place a sterile cotton pack in the access opened pulp chamber.
  • After 1 hour remove the pack can, reirrigate canals before placing calcium hydroxide medicament and sealed with a suitable temporary restoration like IRM or Gavit.
  • Advise the patient to use hot saline rinses for 3 minutes each hour.
  • Advise proper antibiotics and analgesics.
  • When symptoms have subsided, the root canals are opened and reassessed before completing the root canal therapy.
  • Also k/a exacerbating apical periodontitis, Phoenix abscess.
  • It is an acute inflammatory reaction superimposed on an existing chronic apical periodontitis.
  • Initially, the tooth may be tender on palpation.
  • As inflammation progresses, the tooth gets elevated from its socket and becomes sensitive.
  • The mucosa over the radicular area may appear red, swollen and tender to palpation.
  • Radiograph shows well-defined periradicular lesions.(Figure:7)
  • Discoloration of the tooth over a period of time.
  • Lack of response to vitality tests diagnoses a necrotic pulp.
  • Rarely tooth may respond to the electric pulp test (due to fluid in the root canal or in a multirooted tooth).

Figure 7: Well-defined periradicular lesion in acute exacerbation of chronic periodontitis

The treatment is the same as that of an acute alveolar abscess.

  • Also k/a Asymptomatic apical periodontitis and periapical granuloma.
  • It is the symptomless sequelae of acute apical periodontitis.
  • Characterized radiographically by periapical radiolucent changes.
  • A dental granuloma is a misnomer because its tissue is principally chronic inflammatory in composition, and is not a tumor.
  • A granuloma contains “granulomatous” tissue, i.e., granulation tissue and chronic inflammatory cells infiltrating its fibrous connective tissue stroma.
  • It is a cell-mediated response to pulpal bacterial products.
  • Not produce any subjective reaction.
  • Usually, asymptomatic.
  • History of pulpalgia that subsided.
  • Discovered by routine radiographic examination.
  • The area of rarefaction is well defined, with lack of continuity of the lamina dura. (Figure:8)
  • The mucosa over the root apex may or may not be tender to palpation. Tooth does not respond to thermal or electric pulp tests.

Figure 8: Characterisitic periradicular radiolucency with chronic apical periodontitis.

  • Also k/a chronic suppurative apical periodontitis.
  • It is a long-standing, low- grade infection of the periradicular alveolar bone characterized by the presence of an abscess draining through a sinus tract.
  • Infection is in the root canal.
  • It is a natural sequela of death of the pulp with extension of the infective process periapically.
  • Sequela of preexisting acute abscess.
  • Tooth is generally asymptomatic, or only mildly painful.
  • Presence of a sinus tract, which can be either intraoral or extraoral.
  • Sinus tract prevents exacerbation or swelling by providing continual drainage of the periradicular lesion.
  • Pus breaks into the mouth depends on the thickness of alveolar bone and the overlying soft tissues.
  • Confined pus takes the path of least resistance.
  • In upper jaw, this path is along the labial alveolar plate (labial plate thinner than palatal).
  • Suppuration from the upper lateral incisors or from the palatal root of a maxillary molar may occur palatally.
  • In the lower jaw, swelling occurs in the buccal vestibule, but it may occur along the lingual alveolar wall in the case of lower molars because of the position of the roots in their alveoli.
  • A parulis, or gumboil, is a localized accumulation of pus located with the gingival tissues. (Figure :9).
  • It originates from either an acute periapical abscess or an occluded periodontal pocket.
  • The cortical bone is destroyed by the inflammatory process, and the gumboil often appears as a yellowish white bump on the gingiva.
  • The lesion is usually painful, and pain relief occurs when the “boil” ruptures or drains spontaneously.

Figure 9: Elevated white nodule above the maxillary right canine is a parulis, or gumboil.

  • Radiograph taken after the insertion of a gutta-percha cone into the sinus tract shows the involved tooth by tracing the sinus tract to its origin.
  • Radiograph shows a diffuse area of bone rarefaction.
  • The periodontal ligament is thickened, discontinuity of lamina dura.(Figure:10)

Figure 10: Diffuse radiolucency at apical region, thickened periodontal ligament space, discontinuity of lamina dura. A gutta percha tracer point has been placed in the draining sinus to trace the origin of the sinus tract.

  • Elimination of infection in the root canal.
  • Once this end is accomplished and the root canal is filled, repair of the periradicular tissues generally takes place.
  • Also k/a apical periodontal cyst, dental root end cyst.
  • Originate from an epithelial rest of Malassez in periodontal ligaments secondary to inflammation.
  • Most frequently found at the apices of the involved teeth with infected or necrotic pulps.
  • Occur between the third and the sixth decade of life.
  • Males are affected more.
  • Lesion is usually small, slow growing asymptomatic, sometimes exhibit mild pain and sensitivity to percussion.
  • Once infected they may lead to pain and swelling.
  • Root resorption and displacement of teeth may occur.
  • Affected tooth is usually non-vital.
  • Lesions undergo asymptomatic evolution with crepitations followed by erosion and fluctuation of the overlying soft tissue.
  • Bone in the surrounding area will be thinned out with springiness and egg shell crackling, leading to cortical plate expansion.
  • Alveolar process exhibits a paper-like texture on palpation.
  • Appear as round or pear-shaped unilocular radiolucency at the apex of a non-vital tooth.
  • The margin of a radicular cyst is radiopaque with hyperostotic borders, which continues with the lamina dura.
  • Expansion of cortical plates of maxilla or mandible.
  • As cyst becomes secondarily infected, the inflammatory reaction of the surrounding bone may result in loss of cortex.
  • A round shape, a well-defined cortical border, and a size greater than 2 cm in diameter are more characteristic of a cyst.

Figure 11: Periapical cyst

Two types-

  • True cyst: Contains a closed cavity entirely lined by the epithelium.
  • Periapical pocket cyst (bay cyst): The epithelium is attached at the margins of the apical foramen in such a way that the cystic lumen is open to the affected root canal.
  • Lined completely or in part by stratified squamous epithelium.
  • These linings may be discontinuous in part and range in thickness from 1 to 50 cell layers.
  • The lumen of a cyst contains fluid with low concentration of protein and collection of cholesterol clefts (Rushton bodies) with multinucleated giant cells.
  • Chronic inflammatory infiltrate are present subepithelially.
  • Odontogenic keratocyst, lateral periodontal cyst.
  • Extraction, Endodontic therapy and apical surgery.
  • Large radicular cyst need surgical removal or marsupialization.
  • Endodontically treated tooth should be checked periodically with radiographs.
  • Also k/a Phlegmon.
  • Acute cellulitis of the face is an inflammatory condition which involves the  cellular tissue of the side of the face and neck or of the floor of the mouth. 
  • Occurs due to infection by microorganisms that produce streptokinase, hyaluronidase (the spreading factor of Duran-Reynolds) and fibrinolysins, which act to breakdown or dissolve hyaluronic acid, the universal intercellular cement substance, and fibrin.
  • Streptococci are common causative agent (producers of hyaluronidase). Streptococci in their growth phase consume local oxygen and metabolize nutrients to produce an acidic environment, which facilitate the growth of anaerobic microbes (Prevotella and Porphyromonas) that destroy collagen.

Predisposing factors:

  • Dental infection.
  • Sequela of an apical abscess or osteomyelitis
  • Following periodontal infection.
  • Pericoronal infection.
  • Elevated temperature and leukocytosis.
  • Regional lymphadenitis.
  • Painful swelling of the soft tissues involved that are firm and brawny.
  • Swelling is due to inflammatory edema.
  • If the superficial tissue spaces are involved, the skin is inflamed, has an orange peel appearance.
  • If inflammatory spread of infection along deeper planes of cleavage, the overlying skin may be of normal color.

In Maxilla:

It perforates the outer cortical layer of bone above the buccinator attachment and cause swelling of the upper half of the face and soon involves the entire facial area.

In Mandible

  • Perforates the outer cortical plate below the buccinator attachment and cause diffuse swelling of the lower half of the face.
  • Spread to the cervical tissue cause respiratory discomfort.

Extension towards the eye because of the cavernous sinus thrombosis through the veins of the inner canthus of the eye.

  • As the typical facial cellulitis persists, the infection frequently tends to become localized, and a facial abscess may form.
  • When this happens, the suppurative material present seeks to ‘point’ or discharge upon a free surface.
  • Deep neck space infection (DNSI) refers to an infection in the potential spaces and fascial planes of the neck, either with abscess formation or cellulitis.
  • Based on their relationship with the hyoid bone, the deep spaces may be classified as follows:
  1. Spaces localized above the hyoid level (peritonsillar, submandibular, parapharyngeal, buccal, parotid, masticatory/ temporal).
  2. Spaces that involve the entire circumference of the neck (retropharyngeal, danger space, prevertebral and carotid).
  3. Anterior or pretracheal visceral space, below the hyoid bone.
  • DNSI often occur following preceding infections such as dental caries, tonsillitis, pharyngitis, trauma to the head and neck, or among intravenous drug abusers. Infections originating from teeth or their supporting structures, known as odontogenic infections.
  • DNSI are usually polymicrobial in nature. Streptococci, Peptostreptococcus species, Staphylococcus aureus, and anaerobes are the most commonly involved.

Clinical manifestations of DNSI depend on the spaces involved and include:

·         Pain.

·         Fever.

·         Malaise.

·         Fatigue.

·         Swelling.

·         Odynophagia.

·         Dysphagia.

·         Trismus.

·         Dysphonia.

·         Otalgia.

·         Dyspnea.

These infections are potentially life threatening and spread rapidly, leading to severe complications. Complications include:

  • Airway obstruction.
  • Jugular vein thrombosis.
  • Descending mediastinitis.
  •  Pericarditis.
  • Pleural empyema.
  • Cavernous sinus thrombosis.
  • Sepsis.
  • Respiratory distress.
  • Disseminated intra- vascular coagulation.
  • Pleuropulmonary suppuration,
  • Hematogenous dissemination to distant organs.
  1. Cellulitis
  • Is the collection of inflammatory exudate in the tissue space/plane.
  • No pus is seen.
  • Streptococcus is the main culprit. Streptococcus releases enzymes like hyaluronidase which will degrade the connective tissue and facilitates the spread of inflammatory exudate along the tissue plane.
  • Has diffuse margins.
  • Swelling in cellulitis has stretched skin, looks edematous, elevated temperature of overlying skin, firm, brawny and sometimes indurated.
  • Surgical incision does not yield positive results
  • Powerful anti-inflammatories [like diclofenac/ibuprofen] is very much required along with a course of antibiotics.
  1. Space abscess
  • Is the accumulation of purulent material in any given space[pus].
  • Main culprit is Staphylococcus aureus.
  • Has well defined margins.
  • Swelling in space abscess does not have any elevated temperature and is soft and fluctuant on palpation.
  • Surgical incision and drainage is the choice of treatment. Pus/purulent material is drained by opening the locules in which pus is accumulated.
  • Post-surgical antibiotics and analgesics are indicated.

In relation to the lower jaw:

  • Submental space.
  • Submandibular space fossa.
  • Sublingual space.
  • Buccal space.
  • Submasseteric interval.
  • Parotid space.
  • Pterygomandibular space.
  • Pharyngeal space.
  • Peritonsillar space.

In relation to the upper jaw

  • Within the lip.
  • Within the canine.
  • Palatal subperiosteal interval.
  • Buccal space.
  • Maxillary antrum.
  • Infratemporal space.
  • Subtemporalis muscle interval.
  • From the maxillary central and lateral incisor the infection spreads to form labial, palatal abscess or vestibular abscess, sometimes abscesses may form within the lip, which depends upon whether the pus penetrates above or below the muscle attachment.
  • Infections of the canine tooth may result in labial or vestibular abscess if the site of penetration of pus is below the muscle attachment. They form a canine space abscess if the site of penetration of the pus exists above the levator muscle of the upper lip.
  • Infected premolars form abscesses on the buccal or palatal side, and in a long rooted tooth form canine space abscess.
  • Infections from molars form buccal or palatal abscess, if the site of penetration is below the buccinator muscle attachment and a buccal space abscess if the site of penetration of pus is above the muscle attachment.
  • From the mandibular incisor, the infection spreads to form a labial abscess if the pus penetrates above the muscle attachment, and forms a submental space abscess if it is below the muscle attachment.
  • Since all the muscle attachments are well below the mandibular canine root apex, the site of the penetration of the pus is above the muscle attachment, and forms only a labial or vestibular abscess.
  • Premolars may form vestibular abscesses, and lingual perforation may form sublingual abscesses.
  • If the pus from the first molar penetrates above the buccinator attachment, it forms a vestibular abscess on the buccal side, and below the muscle attachment results in a buccal space abscess.
  • A sublingual abscess may be formed if the pus penetrates through the lingual side.
  • In second molars there are four possibilities, namely a vestibular or buccal space abscess if the pus penetrates through the buccal side and sublingual or a submandibular abscess if it penetrates through the lingual side.
  • Infections from the third molars form submandibular or pterygomandibular or submasseteric abscesses.
  • Buccal space is potential space between buccinator and masseter muscle.
  • Boubdaries of buccal space are:
  1. Superior: Zygomatic arch, infraorbital space.
  2. Inferior: Lower border of mandible.
  3. Anterior: Zygomaticus major muscle above and depressor anguli oris muscle.
  4. Posterior: Anterior edge of masseter muscle, pterygomandibular space.
  5. Medial: Buccinator muscle, buccopharyngeal fascia.
  6. Lateral: Skin, subcutaneous tissue.
  • Maxillary molars and premolars if root apices are above the attachment of buccintor muscle.
  • Mandibular molars and premolars if root apices are below the attachment of buccintor muscle.
  • Buccal space infection is dome shaped and periorbital edema develops due to impaired venous and lymphatic drainage.
  • When lower compartment is involved swelling extends from lower border of mandible to infra-orbital rim and from anterior border of masseter to corner of mouth.
  • When upper compartment is involved swelling extends from zygomatic bone to corner of mouth.
  • Obliteration of buccal vestibule depending upon whether the upper or lower compartment is involved.
  • Trismus is usually not present.
  • Drainage of the abscess transorally by placing the incision in the respective buccal vestibule.
  • The maxillary buccal space drains passively with a vestibular incision as it is facilitated by gravity.
  • For mandibular buccal space as the gravity assisted drainage is not possible, liberal incision should be taken and collection should be periodically evacuated by compressing the tissue extraorally.

Canine space or infraorbital spaceis situated over the anterior surface of maxilla in infraorbital area and bounded by:

  1. Superior: Levator labii superioris alaeque nasi, levator labii suprioris, zygomaticus minor.
  2. Inferior: Caninus (levator anguli oris), oral mucosa.
  3. Anterior: Orbicularis Oris, nasal cartilages.
  4. Posterior: Buccinator and buccal space.
  5. Medial: Anterolateral surface of maxilla.    
  • Upper anterior teeth and bicuspid.
  • Skin infection from nose and upper lip.
  • Swelling from lateral nasal groove to anterior boundary of buccal space and from upper lip to preseptal area of the lower eyelid.
  • Cheek swelling and redness.
  • Obliteration of nasolabial folds.
  • Obliteration of labial vestibule due to swelling.
  • Edema of upper and lower eyelid.
  • Intense pain and tenderness secondary to infraorbital nerve edema and inflammation.
  • Edema is more conspicuous in the morning when the patient gets up from sleep (dependent edema) and it gradually gets reduced over a period of time, as the patient is upright.
  • Edema sometimes extends to upper eyelid closing the eye completely.
  • Drainage of canine space abscess is made by making incision parallel to and in depth of maxillary vestibule adjacent to abscessed tooth.
  • Blunt dissection is carried superiorly through the levator angulioris muscle in to canine space.
  • It is important to preserve the infraorbital nerve and its branches.
  • Aggressive antibiotic is important to aid in resolution of the local infection and to prevent the extension into the orbit and brain as it lies in the “danger zone” of face.
  • Temporal pouches are the fascial spaces in relation to temporalis muscle, they are two in number:
  1. Superficial temporal space.
  2. Deep temporal space.
  1. Laterally: Skin, temporal fascia.
  2. Medially: Squamous temporal bone and skull base.
  3. Inferiorly: Superior surface of lateral pterygoid muscle.
  4. Superiorly and posteriorly: Attachment of temporalis to cranium, anterior border.
  5. Anteriorly: Posterior wall of maxillary sinus, pterygomandibular fissure.
  6. Contents: terminal division of internal maxillary artery and mandibular division of trigeminal nerve.
  1. Laterally: Temporalis muscle.
  2. Medially: Lateral surface of temporalis muscle.
  3. Inferiorly: Superior surface of lateral pterygoid muscle.
  4. Superiorly and Posteriorly: Attachment of temporal fascia to cranium, anterior border.
  5. Anteriorly: Attachment of the fascia to orbital process of zygoma.
  • Swelling in temporal area.
  • Trismus (due to involvement of temporalis muscle).
  • Swelling is not very conspicuous due to:
  • Presence of tenacious temporal fascia in superficial pouch involvement.
  • Presence of temporalis muscle and overlying fascia in deep pouch involvement.
  • Superficial pouch infection extends below the zygomatic arch in the massetric area producing a classical “dumbbell” shaped swelling.
  • Deep pouch infection can extend to the infratemporal, lateral pharyngeal and pterygomandibular spaces.
  • Extraoral incision on the temporal region well above the hairline 450 to zygomatic arch.
  • Hemostat is inserted below and above the temporalis muscle.
  • Preserve the facial nerve.
  • Incision can be made above and parallel to zygomatic arch.
  • Temporal fascia is divided to evacuate the contents of superficial pouch and temporalis muscle is pierced open to drain the contents of deep pouch.
  • As abscess cavity heals by fibrosis trismus can occur so post operative physiotherapy is important.

Pharyhgeal spaces include: Lateral pharyngeal space and retropharyngeal space.

  • It is a potential inverted cone shaped space with its base at the skull and its apex at the greater cornu of hyoid bone.
  • Styloid process divides it in to anterior and posterior compartment and a short layer of condensed fascia called aponeurosis of Zuckercandl and Testut.
  • If anterior compartment become infected patient exhibit pain, fever, chills, medial bulging of lateral pharyngeal wall, deviated uvla, dysphagia and trismus.
  • If posterior compartment become infected there is no trismus and visible swelling but respiratory obstruction, septic thromophlebitis of internal jugular vein can occur in later stages.

The lateral pharyngeal space is bounded:

  1. Anteriorly: By the buccopharyngeal aponeurosis, parotid gland and the pterygoid muscles.
  2. Posteriorly: By the prevertebral fascia.
  3. Laterally: By the carotid sheath.
  4. Medially: By the lateral wall of the pharynx.


  1. Anterior compartment: lymph nodes, ascending pharyngeal, facial artery, loose areolar connective tissue.
  2. Posterior compartment: carotid sheath, glossopharyngeal nerve, spinal accessory nerve, hypoglossal nerve, cervical symphathetic trunk.

Common sites of origin of infection include:

  • Teeth, tonsils and adenoids.
  • Parotid gland and lymph glands draining the nose and pharynx.
  • Thrombosis of internal jugular vein or of peritonsillar veins.
  • Metastatic tumors with secondary infection of the internal jugular lymph node chain.
  • Iatrogenic introduction of organisms during infiltration for mandibular nerve block.
  1. Anterior lateral pharyngeal space:
  • Trismus (due to infection to medial pterygoid muscle).
  • Induration and swelling at angle of jaw.
  •  Fever
  • Pharyngeal bulging (due to thin fasciomuscular wall between pharynx and the compartment).
  1. Posterior lateral pharyngeal space:
  • Posterior tonsillar pillar deviation.
  • Retropharyngeal swelling.
  • May show neurologic involvement of cranial nerves IX through XII and of the cervical sympathetic chain with ipsilateral Horner syndrome.
  • Thrombosis of internal jugular vein with sepsis may cause abrupt rises and falls in temperature and chills.
  • Venous blowouts are common than arterial.
  • Swelling of lateral posterior pharyngeal wall and parotid space.
  • Immediate hospitalization.
  • Incision and drainage.
  • Maintenance of airway.
  • Removal of causative agent.
  • Antibiotic therapy initiated empirically and adjusted when results of culture and antibiotic sensitivity tests have been obtained.

It is a potential midline space between the pharyngobasilar fascia which attaches the pharyngeal constrictors to the base of the skull and prevertebral fascia.

The retropharyngeal space is bounded:

Anteriorly: By the wall of the pharynx.

Posteriorly: By the prevertebral fascia.

Laterally: By the lateral pharyngeal space and carotid sheath.

Superiorly: By base of skull.

Occurs due to:

  • Otologic.
  • Pharyngeal or nasopharyngeal infections can directly spread to retropharyngeal space.
  • Upper respiratory infections.
  • Odontogenic infections.
  • Cervical osteomyelitis.
  • Foreign body introduction.
  • Regional trauma.
  • Spread by the lymphatics.
  • Odontogenic or oropharyngeal infections yield combinations or anerobic and aerobic gram positive and gram negative bacteria predominantly Bacteroides fragilis or streptococcus species.
  • Staphylococcus aureus, Coccidiodes immitis and Mycobacterium tuberculosis are most common implicated in retropharyngeal abscesses secondary to vertebral osteomyelitis.

·         Fever.

·         Sialorrhea.

·         Stiff neck.

·         Sore throat.

·         Dysphagia.

·         Possible stridor.

·         Leukocytosis.

·         Occasional lateral neck edema and swelling.

·         Dyspnea.

·         CT scan is effective in diagnosis.

Maintenance of patent airway by:

  • Elective tracheostomy.
  • Fiberoptic intubation or blind.
  • Awake nasotracheal intubation.
  • Initial antibiotics should be aggressive and based on gram stain from an aspirate or productive incision and drainage.
  • Extraoral approach affords the greatest control and manipulation of the affected spaces.
  • It present below the mandible.
  • It is also called digastrics triangle as it is bound anterioposteriorly by anterior and posterior bellies of digastrics muscle, respectively.
  1. Anterior: Anterior belly of digastrics muscle.
  2. Posterior: Posterior belly of digastrics muscle, stylohyoid muscle, stylopharyngeous muscle.
  3. Superior: Medial aspect of mandible and attachment of mylohyoid muscle.
  4. Inferior: Anterior and posterior bellies of digastrics muscle.
  5. Medial: Mylohyoid, hyoglossus,styloglossus.
  6. Lateral: Skin, superficial fascia, platysma, superficial layer of deep cervical fascia, anterior bellies of digastrics muscle.

This space encloses the submandibular salivary gland and lymph nodes. 

  • Odontogenic infection from mandibular posterior teeth either direct spread or spread through lymphatics.
  • Septic fractures.
  • Infections from submandibular salivary glands due to sialolithiasis.
  • Rarely hematogenous infection.
  • Swelling involving the submandibular area, which is diffuse in beginning and tends to get localized.
  • Swelling extends from lower border of mandible to hyoid bone, superioinferiorly.
  • Muscles become spastic.
  • Trismus
  • Swelling shows signs of inflammatory swelling (redness, raised temperature, tenderness). Initially the diffuse swelling is firm in consistency and pits on pressure due to cellulites but as abscess get localized bimanual palpation elicts fluctuations.
  • Constitutional sign and symptoms are present in acute phase.
  • Submandibular lymph nodes are enlarged, tender and firm in consistency.
  • Surgical drainage.
  • Incision and drainage done through standard submandibular incision taken I cm below and behind the inferior border of mandible to avoid the damage to marginal mandibular branch of facial nerve.
  • Superficial abscesses are drained through stab incision.
  • Deep abscesses drained by dissecting the tissue layer wise to open the skin, superficial fascia , platysma and deep fascia.
  • It is a potential space exsist in chin.
  • Submental space infection may spread easily to either or both submandibular spaces.

Boundaries of submental space:

  1. Anterior: Inferior border of mandible.
  2. Posterior: Hyoid bone.
  3. Superior: Mylohyoid muscle.
  4. Inferior: Skin, superficial fascia,platysma, deep cervical fascia.
  5. Medial: Anterior bellies of digastrics muscles.
  6. Lateral: Investing fascia.
  • Infection from lower anterior teeth.
  • Infected symphyseal or parasymphyseal fractures.
  • Extension of submandibular space infection.
  • Suppuration in submental lymph node.
  • Swelling below the chin producing double chin appearance.
  • Skin become erythematous, tense, glossy and tender to touch.
  • Local temperature is raised.
  • Once infection gets localized, fluctuations may be elicited.
  • Percutaneous surgical drainage.
  • Transverse incision is given in the skin below the symphysis of mandible.
  • Blunt dissection carried out by inserting a sinus forceps in upward and backward direction. Drain is inserted.

Located within the mandibular body (V- shaped space), bounded by:

  1. Anterior: Lingual aspect of mandible.
  2. Posterior: Body of hyoid bone.
  3. Superior: Mucosa of floor of mouth.
  4. Inferior: Mylohyoid muscle.
  5. Medial: Anterior bellies of digastrics muscles.

Lateral: Investing fascia. 

  • Odontogenic infection from mandibular anterior teeth.
  • Infection of submandibular and sublingual salivary glands.

Extension of submandibular, submental or pterygomandibular spaces.

·         Congestion and edema of floor of the mouth.

·         Elevation and protrusion of tongue.

·         Laryngeal edema.

·         Breathlessness (due to laryngeal edema) in supine position and relax in sitting position.

·         Dysphagia.

  • Incision is made close to the lingual cortical plate, lateral to sublingual plica, as lingual nerve which is deeply placed and is less likely to be damaged by this approach.
  • The sinus forceps is then inserted and opened to evacuate the pus.
  • Formed by splitting of investing fascia into superficial and deep layers.
  • The superficial layer lies along lateral surfaces of masseter and lower half of temporalis muscles.

Infection occurs due to:

  • From third molars.
  • Caries induced dental abscess.
  • Contaminated inferior alveolar nerve blocks.
  • Direct trauma or through surgery in the area.

·         Swelling around the ramus of mandible.

·         Pain.

·         Tenderness.

·         Fever.

·         Difficulty in deglutition.

Masticatory space comprises of following four spaces:

·         Pterygomandibular space.

·         Submasseteric space.

·         Temporal space.

·         Infratemporal space.

Pterygomandibular space bounded by:

  1. Laterally by: Anterior border of ramus of mandible.
  2. Medially: Medial pterygoid muscle.
  3. Superiorly: Infratemporal surface of greater wing of sphenoid and zygomatic arch, lateral pterygoid muscle.
  4. Inferiorly: Pterygomasseteric sling.
  5. Anteriorly: Buccinator and superior laryngeal constrictor muscles.
  6. Posteriorly: Deep portion of parotid gland.


Mandibular nerve, lingual nerve, inferior alveolar artery and vein, mylohyoid nerve and vessels.

  • Contaminated needles/solution used while giving pterygomandibular block.
  • Septic fractures of mandibular ramus.
  • Infections from mandibular third molars.
  • Trismus (due to edema and inflammation of medial pterygoid muscle).
  • Swelling of anterior tonsilar pillar.
  • Deviation of uvla to opposite side.
  • Infection may spread into infratemporal portion of deep temporal space by passing superiorly around lateral pterygoid muscle.
  • Incision is placed along the anterior border of the coronoid process and the sinus forcep is passed medial to the ramus of mandible to enter and drain the pterygomandibular space, transorally.
  • Extraoral submandibular “Risdon’s incision” is placed and the dissection is carried out medially to detach the insertion of medial pterygoid muscle from the angle of mandible to drain the pterygomandibular space.
  • Present lateral to ascending ramus of mandible.
  • Bounded:
  1. Laterally by: Masseter muscle and fascia covering it.
  2. Medially by: Lateral surface of ascending ramus.
  3. Inferiorly: It extends up to the insertion of masseter at the angle of mandible.
  4. Superiorly: It extends up to the origin of masseter at the inferior border of zygomatic arch. So infection of this space can extend to infra temporal fossa.
  • Mandibular third molar infection.
  • Septic fracture at angle of mandible.
  • Extension of infection from adjoining tissue planes in the infratemporal space, temporal pouch abscess, sublingual space infection.
  • Suppurative parotitis.
  • Hematogenous spread.

·         Fever.

·         Malaise.

·         Body ache.

·         Trismus (due to spasm of masseter muscle).

·         Swelling is inconspicuous as infection lies below the muscle.

·         Infection gets localized due to anatomical barrier formed by muscle.

·         Swelling is firm in consistency, tender on palpation, raised local temperature (when infection is diffuse).

·         When infection gets localized and still present below the masseter, deep seated fluctuations can be elicited by bimanual palpation.

·         When infection becomes superficial by perforating through the fibers of masseter and comes to lie below the superficial fascia and skin, swelling becomes fluctuant due to laudable pus.

·         Submassetric space infection can extend to submandibular space.

  • Incision and drainage can be done both intraorally and extraorally.
  • Intraorally incision is placed in the retromolar area along the anterior border of ramus and dissection done along lateral border of ramus.
  • Extra oral procedure consists of placing standard Ridson’s submandibular incision I cm below and behind the inferior border of mandible and curling around the angle.

Ludwig angina is defined as acute non suppurative, necrotizing cellulitis involving the submandibular, sublingual and submental spaces bilaterally.

  • Odontogenic infections(direct spread or through lymphatics).
  • Septic fractures.
  • Salivary gland infections.
  • Hematogenous conditions.
  1. Predisposing factors
  •  Immunosupression.
  • Steroid therapy.
  • Diabetes.
  • Debilitating conditions.
  1. Causative organisms
  • Beta hemolytic streptococci.
  • Infection tends to spread rather than localizing, due to liberation of exotoxins by streptococci which breakdown the intercellular cementing substance which facilitates spread of infection along tissue planes.
  • E.coli.
  • Anaerobic organisms.
  • Characterized by acute course producing bilateral swelling due to cellulites of submandibular, sublingual and submental space.
  • Overlying skin appears tense (due to accumulation of inflammatory exudates in interstitial compartment), glossy, hyperemic and having “wood like” consistency or brawny induration.
  • Swelling of submental space produces “double chinned” appearance.
  • Tenderness present on palpation.
  • Due to mounting interstitial fluid pressure edema rapidly spreads along the facial plane, breaking the tissue barriers and go on to involve adjoining spaces.
  • Involvement of sublingual space leads to edema and congestion of the floor of the mouth and tongue gets lifted and protrudes out.
  • Infection of sublingual space rapidly spreads along it to its base, which is present at the hyoid bone.
  • Posterior inferior to the base of the sublingual space lays the larynx and edema extends to the larynx causing the edema of epiglottis and cords which leads to acute respiratory obstruction  due to which death can occur due to asphyxia.
  • Treatment is primarily surgical.
  • In laryngeal edema – tracheostomy.
  • Surgical decompression of tissue planes.
  • Two separate incisions are given bilaterally in the submandibular area and one in submental area is commonly practiced.
  • Decompression of the sublingual space is important that achieved by piercing open the mylohyoid muscle.
  • Sublingual space also decompressed by placing the incision on the floor of the mouth; parallel to lingual vestibule.
  • Choice of the antibiotic is usually the penicillin group.
  • Crystalline penicillin in a dose of 10 to 20 lacs IU IV, every 6 hourly.
  • Alternatively, ampicillin 2 to 4 g/day is divided doses or third generation cephalosporins can be given to make the spectrum of the antibiotics wider aminoglycosides like gentamycin 1 to 4 mg/kg of body weight or amikacin 500 mg every 8 hourly.


Usual adult dosage

Usual pediatric dosage


250-500 mg every 8 hours

20-40 mg/kg/day in divided

doses every 8 hours

Amoxycillin with Clavulanic acid

500-875 mg every 12 hours

25-45 mg/kg/day in doses

divided every 12 hours


500 mg every 6 h

2g1hpre-op (joint prophylaxis)

25–50 mg/kg/day divided into 4 doses


2g every 4 hourly or

3g every 6 hourly



 2g every 4-8 hourly



2g every 8 hourly



2mg/kg loading and then 3-5 mg/kg/day

Up to 2 years 2-2.5 mg/kg every 8 hrs.


15 mg/kg/day



300–450 mg every 6 h

10–30 mg/kg/day divided into 3 or 4 doses


400 mg daily

Not established


500 mg enteric coated every 8 h 333 mg enteric coated every 6 h 250 mg (base) every 6 h

30–50 mg/kg/day divided into 2–4 doses


7.5 mg/kg every 6 hours (maximum 4 g/24 hours)

30/mg/kg/day in divided doses every 6 hours

  • The word “osteomyelitis” originates from the ancient Greek words osteon (bone) and muelinos (marrow) and means the infection of the medullary portion of the bone.
  • Osteomyelitis is an inflammatory condition of the bone that originates as an infection of the medullary space and eventually extends into the cortical bone and periosteum. The bone infection becomes active in the calcified portion of the bone and will produce pus in the medullary cavity and beneath the periosteum, which compromises the blood supply. This initiates ischemia of the bone, which results in necrosis.
  • Osteomyelitis is more commonly observed in the mandible because of its poor blood supply as compared to the maxilla.
  • Dense mandibular cortical bone is more prone to damage and, therefore, to infection at the time of tooth extraction.

·         The odontogenic infections are coomon in occurrence, however majority of them do not lead to osteomyelitis.

·         The chances of precipitation of osteomyelitis are enhanced if there is an underlying local or systemic pathological of condition.

Predisposing factors:

1.   Condtions compromising the host defence are:

·         Diabetes.

·         Anemia/sickle cell anemia.

·         Tuberculosis

·         Malnutrition.

·         Agranulocytosis.

·         Leukemia.

·         Chronic alchohalism

·         Febrile illness.

2.   Conditions compromising jaw vascularity are:

·         Radiation.

·         Paget’s disease, osteopetrosis, osteoporosis.

·         Fibrous dysplasia.

·         Peripheral vascular disease.

·         Malignancy.

·         Sickle cell anemia.


·         Odongenic infections.

·         Trauma

·         Infections derived from periostitis.

·         Following gingival ulcerations, lymphnodes infected from furuncles, lacerations and peritonsilar abscess.

·         Infections derived from hematogenous route: Fruncule on face, wound on skin,upper respiratory tract infection, middle ear infection, mastoiditis, systemic tuberculosis.

Historically accepted classification based on clinical course:

  • Acute.
  • Sub acute.
  • Chronic.

Infective                                                                                                                                                                                                    A. Specific

  •  Tuberculosis.
  •  Syphillis.
  • Actinomycosis                                                                                                                                                                      B.Nonspecific
  •  Pyogenic.
  •  Necrosis.

      Hudson’s classification:

  1. Acute forms of osteomyelitis (suppurative and non suppurative include)
  2. Contiguous focous
  •  Trauma.
  •  Surgery.
  • Odontogenic infections.
  1. Progressive
  •  Burns.
  •  Sinusitis.
  • Vascular insufficiency.                                               C. Hematogenous (metastatic): Developing skeleton(children).                                                      2. Chronic forms of osteomyelitis                                                                                                         A. Recurrent multifocal
  • Developing skeleton(children).
  • Escalated osteogenic activity(age< 25 years).                                                                                B. Garre’s
  • Unique proliferative subperiosteal reaction.
  • Developing skeleton(children to young adults).                                                                                                                                                                                                                                                                                                                                                                                                                    C. Suppurative and non suppurative
  • Inadequately treated forms.
  • Systematically compromised patients.
  • Chronic refractory osteomyelitis.            D. Diffuse sclerosing
  • Fastidious organisms.
  • Compromised host/pathogen interface
  • Osteomyelitis is initiated by acute inflammation, hyperemia, increased capillary permeability and filtration of granulocytes. Tissue necrosis occurs as proteolytic enzymes are released and vascular thrombosis ensues.
  • As the pus accumates the intermedullary pressure increases resulting in vascular collapse, venous stasis and ischemia. Pus travels through the haversian and nutrient canals and accumulates beneath the periostium, elevating it from the bone and thereby further reducing the vascular supply.
  • Compression of neurovascular bundle accelerates thrombosis and ischemia and results in osteomyelitis induced (inferior alveolar in case of mandible) nerve dysfunction.
  • Intensive periosteal elevation occurs more frequently in children, presumably because the periostium is bound less firmly to bone than in adults.
  • If pus continues to accumulate the periostium is penetrated and mucosal and cutaneous abscesses and fistulas may develop. If this condition is treated with antibiotics alone without appropriate surgical intervention, the condition may progress to chronic form.
  • Inflammation regresses, granulation tissue forms a new blood vessels lyse the bone, the separating fragment of necrotic bone (sequestra) from viable bone.
  • Small section of bone may be lysed completely, whereas larger ones may be isolated by a bed of granulation tissue in a sheath of new bone (involucrum).
  • Sequestra may be revascularised, remain quiescent, reabsorbed or be infected chronically and require surgical removal before the infection subsides completely.
  • Occasionally the involucrum is penetrated by channels (cloacae) through which pus escapes to an epithelial surface. Bone surrounding a sequestrum sometimes appears radiographically as less densely mineralized than sequestrum itself, because increased vascularity of adjacent vital bone creates a relative demineralization. Ischemia causes increase in CO2 level which attracts calcium due to change in pH. Calcium deposition leads to increase in mineralization of the sequestrum (dystrophic calcification). Secondly, the calcium mobilization from the devitalized bone does not take place and hence the sequestrated bone appears more opaque on the x-ray.
  • As reparative mechanism the periosteal apposition also take place and the periosteal reaction is evident on x-ray. The lifting of periostium at the edges of the body defect produces a triangular elevation called the Codman’s triangle.

The initial radiological picture of an acute osteomyelitis is alteration and thinning of a trabecular pattern while as the more opaque sequestrum is separated from the normal bone by radiolucent area (involucrum) and associated periosteal reaction is the picture in chronic osteomyelitis. Sequestra formation leads to undermining of the bone and renders it weak. Such a weak bone is liable to fracture (pathological fracture).

It is a serious sequel of periapical infection that often results in a diffuse spread of infection throughout the medullary spaces.

·         Affect people of all ages and has a strong male predilection.

·         It is common in the mandible than in the maxilla (due to poorer vascular supply to the mandible).

·         The typical signs and symptoms are rapid onset, pain, swelling of the adjacent soft tissues, fever, lymphadenopathy, and leukocytosis.

·         Trismus.

·         The associated teeth may be mobile and sensitive to percussion.

·         Purulent drainage also may be present.

·         Sometimes paresthesia of the lower lip.

White blood cell count is frequently elevated.

 Histopathological findings:

  • Medullary spaces are filled with inflammatory exudates.
  • The osteoblasts bordering the bony trabeculae are generally destroyed.
  • Trabeculae may lose their viability and begin to undergo slow resorption.

Radiographic findings:

  • Radiograph may fail to reveal any change for 4-8 days, until the inflammation has resulted in sufficient dissolution of bony tabeculae, conventional radiographs are interpreted as normal.
  • Slight decrease in the density of the involved bone, with a loss of sharpness of the existing trabeculae. In time the bone destruction becomes more profound, resulting in an area of radiolucency in one focal area or in scattered regions throughout the involved bone.Later, the appearance of sclerotic regions becomes apparent.
  • Sequestra may be present but usually are more apparent and numerous in chronic forms.
  • Acute osteomyelitis can stimulate either bone resorption or bone formation. Portions of cortical bone may be resorbed.
  • An inflammatory exudate can lift the periostium and stimulate bone formation. Radiographically, this appears as a thin, faint, radiopaque line adjacent to and almost parallel or slightly convex to the surface of the bone.
  • A radiolucent band separates this periosteal new bone from the bone surface.
  • Clinical sign and symptoms are less severe than acute condition.
  • Duration of disease is longer as compared to acute variety.
  • Deep seated, dull pain, anorexia and fever (1010 F to 1020 F).
  • Teeth in the involved area become loose and tender on percussion.
  • Pus exudates through gingival and cutaneous fistulas.
  • Fetid oral odor may be present due to pus.
  • Cellulitis of the cheek over the involved area.
  • Expansion of the bone due to periosteal reaction.
  • Infection gets localized to form an abscess in the adjoining soft tissue.
  • Regional lymphnodes gets enlarged, discrete, soft and tender.
  • Leukocytosis is not consistent findings.
  • Occlusal radiograph shows erosion of cortex but not extensive involvement of adjacent cancellous bone.

Chronic osteomyelitis is a bone disease that is characterized by inflammatory processes, including necrosis of mineralized and marrow tissues, suppuration, resorption, sclerosis, and hyperplasia.

  • Chronic suppurative osteomyelitis may develop in inadequately treated acute osteomyelitis.
  • The primary cause of chronic osteomyelitis is usually microbiologic, and it results from an odontogenic infection, postextraction complication, inadequate removal of necrotic bone, early termination of antibiotic therapy, inappropriate selection of antibiotics, diagnostic failure, trauma, inadequate treatment for fracture, or irradiation to the mandible.

Clinical features are similar to those of acute osteomyelitis except that all signs and symptoms are milder.

·         Local pain.

·         Fever.

·         Swelling.

·         Purulent discharge.

·         Intraoral and skin fistula.

·         Unhealed soft tissue in the oral cavity.

·         Neuropalsy in the involved area.

·         Pathologic fracture.

·         Trismus.

  • “Moth-eaten” appearance (enlargement of medullary spaces and widening of Volkmann’s canals).
  • Island that is “Sequestrum” (avascular necrotic bone, which harbors microorganisms) with evidence of trabecular pattern and marrow spaces.(Figure:12)
  • CT findings included sclerosis and defect in the trabecular bone. Changes of bone width and thickening of the cortical plate are accompanied with longer disease duration.
  • Radioisotope bone scanning reveals strong uptake and can be used to identify occult areas of involvement. Positron emission tomography is a better modality for the delineation of areas of different metabolic activity.
  • Scintigraphy with bone-seeking radiopharmaceuticals is used when multifocal systemic disease is suspected.
  • Magnetic resonance imaging in short inversion time inversion recovery sequence is highly effective for the evaluation of bone marrow and surrounding soft tissue in terms of the detection of osteomyelitis in the mandible and the identification of inflammation spreading to soft tissue. Magnetic resonance imaging shows larger areas of abnormality than plain radiography or CT.
  • A
  •  B
  • Also k/a osteomyelitis maxillaries neonatorum.
  • It was first described by Rees in 1847.
  • It occurs within first 9 months of life and as early as 1 week after birth.
  • Hematogenous infection.
  • Perinatal trauma to oral mucosa from obstertrician’s finger, mucus suction bulb and un hygienic condition during child birth.
  • Infection involving maxillary sinus.
  • Unhygienic human or artificial nipples.


  • Staphylococcus aureus.
  • Hemophilus influenza.
  • Streptococci.
  • Pneumococci.
  • Neisseria gonorrhoeae.
  • Coliform bacilli.
  • Sudden onset, very acute course.
  • General constitutional symptoms, high grade fever.
  • Facial cellulitis centered around orbit, intercanthal swelling, palpebral edema, closure of eye, conjunctivitis, proptosis.
  • Inability to suckle and dehydration.
  • Subperiosteal abscess in alveolar region.
  • Fistulae or pus draining tracts on alveolar mucosa.
  • Sloughing out of bone and teeth buds.
  • Radiographic manifestations occur in later stage.
  • Sequestrum formation.
  • Necrotic tooth germ.
  • Broad spectrum antibiotics.
  • Culture and sensitivity test.
  • Incision and drainage of fluctuant abscess.
  • Irrigation of sinus tract with normal saline, 5% povidine iodine and hydrogen peroxide.
  • Supportive therapy such as parenteral feeding.
  • Sequestrectomy followed by orthodontic treatment to aid in the development of arch and maintenance of occlusion.
  • Two weeks postoperative intravenous antibiotics followed by additional 6 weeks administration of oral antibiotics.
  • Also known as chronic non-suppurative sclerosing osteomyelitis, chronic osteomyelitis with proliferative periostitis and periostitis ossificans.
  • First described by Carl Garre in 1893 as irritation induced focal thickening of periosteum and cortical bone of tibia.
  • It is a non-suppurative inflammatory process, where there is peripheral subperiosteal bone deposition caused by mild irritation and infection.
  • Seen exclusively in children or young adults.
  • When it affects the jaw, this generally originates from an infection of low virulence, such as dental decay, mild periodontitis, dental eruption or previous dental extraction in the lesion area.
  • Mandible is more often affected than the maxilla.
  • Appear as hard nontender swelling of jaw in inferior border of mandible below first molar, but lateral expansion may also occur.
  • Subsequent facial asymmetry.
  • Lesion is usually asymptomatic with no accompanying general and local signs of inflammation, although the clinical picture may vary widely.
  • Early lesions show a shadow of thin cortex shell of bone over the cortex.
  • No trabecular shadows in radiolucent space between the shell of new bone and cortex.
  • As infection persist the cortex thickness and becomes laminated with alternating radiopaque-radiolucent layers giving the onion skin appearance.(Figure:13 )
  • Adjacent cancellous bone may remain normal in appearance, become sclerotic or show some areas of osteolytic change within the sclerosed spongiosa.

Figure 13: Multiple layers of new bone on the buccal aspect of the mandible, resulting in an onion-skin appearance.

Fibrous dysplasia, Infantile cortical hyperostosis, syphilitic osteomyelitis, fracture callus, Ewing’s sarcoma.

  • The main treatment goal for Garre’s osteomyelitis is to eliminate the etiologic factor, most frequently by extraction of the causative tooth.
  • Endodontic therapy should be considered as the main treatment goal.
  • Also k/a condensing osteitis.
  • Condensing osteitis is the response to a low-grade, chronic inflammation of the periradicular area as a result of a mild irritation through the root canal.
  • What are the clinical features of chronic focal sclerosing osteomyelitis?
  • This form of osteomyelitis arises most commonly in children and young adults. Rarely in older individuals.
  • Commonly involved tooth is the mandibular first molar, which presents a large carious lesion.
  • There may be no signs or symptoms of the disease other than mild pain associated with an infected pulp.
  • Appears in radiographs as a localized area of radiopacity surrounding the affected root. The entire root outline is nearly always visible, with an intact lamina dura.
  • Periodontal ligament space is widened and this is an important feature in distinguishing it from the benign cementoblastoma. The border of this lesion, abutting the normal bone, may be smooth and distinct or appears to blend into the surrounding bone in contrast to focal cemento-osseus dysplasia, which has radiolucent border.
  • It is an area of dense bone with reduced trabecular pattern.
  • The mandibular posterior teeth are most frequently affected.
  • Results of vitality tests may be in the “normal” range.

Figure 14: Increased area of radiopacity surrounding the apices of mandibular molar

  • Removal of the irritant stimulus is recommended.
  • Endodontic treatment should be initiated if signs and symptoms of irreversible pulpitis are diagnosed.

Chronic diffuse sclerosing osteomyelitis is a condition analogous to the focal form of the disease and also apparently represents a proliferative reaction of the bone to a low-grade infection.

  • It may occur at any age, but is most common in older persons.
  • Occurs in edentulous mandibular jaws or edentulous areas and does not exhibit any gender predominance.
  • Disease of an insidious nature that it presents no clinical indications of its presence.
  • On occasion there is an acute exacerbation of the dormant chronic infection and this result in vague pain, unpleasant taste, and mild suppuration.
  • Spontaneous formation of a fistula opening onto the mucosal surface to establish drainage.
  • Diffuse patchy, sclerosis of bone often described as ‘cotton-wool’ appearance.(Figure:15)
  • This radiopaque lesion may be extensive and is sometimes bilateral.
  • Border between the sclerosis and the normal bone is often indistinct.

Figure 15: Diffuse area of increased radiopacity

  • Caused by inhalation of infected airborne droplets containing the M. tuberculosis bacillus, which is an aerobic, slender, non-motile, non-encapsulated, non-sporing, rod-shaped organism, ranging from 2 to 5 μm.
  • Tuberculous osteomyelitis is rare and constitutes less than 2% of skeletal TB. Jaw involvement is even rarer.

The spread of infection may be by direct transfer from infected sputum, through an extraction socket or mucosal opening associated with an erupting tooth or by regional extensions of soft tissue lesions to underlying bone or by hematogenous spread.

  • The mandibular involvement is more frequent than maxilla and alveolar and angle regions have greater affinity.
  • Tuberculous osteomyelitis commonly affects the adults; however, in some cases children are also affected.
  • Chapotel described four clinical forms of TB of the mandible:
  1. First is the superficial or alveolar form that involves the alveolar process.
  2. Second is the deep or central form in which the angle of the mandible is involved.
  3. Third is the diffuse form characterized by progressive extensive necrosis of mandible that might involve the TMJ.
  4. Fourth one is acute osteomyelitis form.
  • TB of the jaw causes slow necrosis of the bone and formation of a sub-periosteal abscess (lumpy jaw) appearing as a painless, soft swelling.
  • This sub- periosteal abscess may burst resulting in single or multiple sinuses intraorally or extraorally.
  • Pathological fracture of mandible or sequestration may also occur.

The radiographic picture of tuberculous osteomyelitis usually presents as a blurring of bone details leading to diffuse radiolucent picture and cortical plate erosion. It can also present as mixed radiopaque-radiolucent appearance or “worm-eaten” appearance of bony lesions with fistulae formation through which small sequestra are exuded.

  1. Type I: Lumpy jaw; mandible or maxilla is involved and extraoral swelling is present without intraoral or extraoral draining sinuses.
  2. Type II: Nonhealing extraction sockets with/without intraoral or extraoral draining sinus/sinuses.
  3. Type III: Intraoral or extraoral draining sinus/sinuses in the orofacial region and an osteomyelitic bony lesion.
  4. Type IV: TB lymphadenitis of the head face neck region without any features of type I, II, III, or V.
  5. Type V: Lesion of other sites in and around the oral cavity, e.g., maxillary antrum, salivary glands, gingiva, orofacial muscles, tongue, etc.

For diagnosis and treatment refer to bacterial infections of oral cavity.

  • Syphilitic osteomyelitis or gumma seen in tertiary syphilis.
  • Maxilla is more affected than mandible.
  • Gummatous perforate on of palate can lead to oroantral or oronasal communication.
  • Sequestra are called filiary sequestra because they are fine.
  • Syphilitic osteomyelitis can be congenital but occurs between age of 30 to 40 years.
  • Occurs in shaft of long bones and affect the skull.
  • Majority of cases there is hyperostosis.
  • It forms bone dependent bone destruction and new bone formation in which there are areas of mottling.
  • Affected bone shows marked periosteal changes, outline medulla becomes obliterated.
  • Filiary sequestra may be present in old cases.

Diagnosis based on:

  • History of exposure.
  • Presence of primary chancre previously.
  • Positive KTVDRL test.

Crystalline penicillin 10 to 20 lacs IU 6 hourly for 2 weeks and later with long acting penicillin 6 to 12 lac IU, once in a week or biweekly for 3 to 4 months.

  1. Pitts NB, Zero DT, Marsh PD, Ekstrand K, Weintraub JA, Ramos-Gomez F, Tagami J, Twetman S, Tsakos G, Ismail A Dental caries. Nat Rev Dis Primers. 2017 May 25;3:17030. doi: 10.1038/nrdp.2017.30.
  2. Conrads G, About I. Pathophysiology of Dental Caries Monogr Oral Sci. 2018;27:1-10. doi: 10.1159/000487826. Epub 2018 May 24.
  3. Cawson’s essentials of oral pathology and oral medicine 8th edition 2008, published by Elsevier Limited.
  4. Chandra SB, Krishna VG Diseases of dental pulp Grossman’s Endodontic Practice Twelfth Edition 2010 published by Wolters Kluwer (India) Pvt. Ltd.,   page 74-95.
  5. Chandra SB, Krishna VG Diseases of periradicular tissues. Grossman’s Endodontic Practice Twelfth Edition 2010 published by Wolters Kluwer (India) Pvt. Ltd.,   page 97-129.
  6. White S.C, Pharoah M.C. Inflammatory lesions of jaws. Oral Radiology- principles and interpretation; 2011:6th 367-80.
  7. Thomas P, Pillai RK, Ramakrishnan BP, Palani J An Insight into Internal Resorption ISRN Dentistry Volume 2014, Available from
  8. OP – Pulpal and Periapical Dz. Available from: and+ Periapical+Dz/
  9. Case Study Acute apical periodontitis. Available from:
  10. Abbott PV, Yu C. A clinical classification of the status of the pulp and the

root canal system. Australian Dental Journal Supplement 2007;52:(1 Suppl):S17-S31.

  1. Rajendran and Sivapathasundharam. Spread of oral infection. Shafer’s Textbook of Oral Pathology,7thpublished by Elsevier Inc.2012;503-15.
  2. Deshmukh J,Shrivastava R,Bharath KP, Mallikarjuna R Giant radicular cyst of the maxilla BMJ Case Rep. 2014; 2014: bcr2014203678. Published online 2014 May 2. doi: 1136/bcr-2014-203678
  3. Louis M. Lin LM, Ricucci D, Kahler B Radicular Cysts Review JSM Dent Surg 2017;2:1-3.
  4. Resnik RR, Cillo JE. Osteomyelitis. Available from:
  5. Marc Baltensperger, Gerold K. Eyrich. Osteomyelitis of the Jaws published by Springer Science & Business Media, 2008 page 60-74.
  6. Mehra H, Gupta S, Gupta H, Sinha V, Singh J Chronic Suppurative Osteomyelitis of Mandible: A Case Report. Craniomaxillofac Trauma Reconstr. 2013;6:197–200.
  7. Suma R, Vinay C.Shashikanth M. C, Subba Reddy V. V. Garre’s sclerosing osteomyelitis. 2007; 25:30-33.
  8. Chapotel S. Tuberculose mandibularie. Rev Odent 1930;51:444‑
  9. Agarwal S, Caplivski D, Bottone EJ. Disseminated tuberculosis presenting with finger swelling in a Patient with tuberculous osteomyelitis: A case report. Ann Clin Microbiol Antimicrob 2005;4:18.
  10. Bansal R, Jain A, Mittal S. Orofacial tuberculosis: Clinical manifestations, diagnosis and management. Journal of Family Medicine and Primary Care July 2015;4:335-41.
  11. Borle RM Text book of oral and maxillofacial surgey published by jaypee brothers 2014 page no. 329-62.
  12. Kataria G, Saxena A, Bhagat S, Singh B, Kaur M, Kaur G. Deep Neck Space Infections: A Study of 76 Cases. Iran J Otorhinolaryngol. 2015;27: 293–299.
  13. Gregoire C How are odontogenic infections best managed? J Can Dent Assoc 2010;76:a37.
  14. Peedikayil FC. Antibiotics in Odontogenic Infections – An Update. Journal of Antimicrobial Agents. J Antimicro 2: 117. doi:10.4172/2472-1212.1000117.
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