REVIEW OF ODONTOGENESIS

LESSON 1 DEVELOPMENTAL ANOMALIES OF THE TEETH

Anomaly is a medical term meaning “different from normal”, or deviates from the normal;
something that is noticeably different.

If a condition results during the formation and development of a dental structure, it is referred
to as a developmental anomaly.

Some abnormalities result from:

A. intrinsic factors - such as heredity, metabolic dysfunction, or mutations; or
B. extrinsic factors - such as physical or chemical trauma, biologic agents, nutritional
deficiencies, stress, habits, or environmental conditions.
C. In many instances anomalies result from a combination of intrinsic and extrinsic factors.

Metabolic dysfunction - Inherited metabolic disorders refer to different types of medical conditions caused by genetic defects
most commonly inherited from both parents — that interfere with the body's metabolism. These conditions may also be
called inborn errors of metabolism.
A metabolic disorder occurs when abnormal chemical reactions disrupt the body's metabolism.

A metabolic disorder occurs when the metabolism process fails and causes the body to have either too much or too little of
the essential substances needed to stay healthy.
Our bodies are very sensitive to errors in metabolism. The body must have amino acids and many types of proteins to
perform all of its functions. For example, the brain needs calcium, potassium, and sodium to generate electrical impulses,
and lipids (fats and oils) to maintain a healthy nervous system.

Metabolic disorders can take many forms. This includes:

• a missing enzyme or vitamin that’s necessary for an important chemical reaction
• abnormal chemical reactions that hinder metabolic processes
• a disease in the liver, pancreas, endocrine glands, or other organs involved in metabolism
• nutritional deficiencies

Mutation – the changing of the structure of a gene, resulting in a variant form that may be transmitted to subsequent
generations, caused by the alteration of single base units in DNA, or the deletion, insertion, or rearrangement of larger
sections of genes or chromosomes.

Biologic agents – A substance that is made from a living organism or its products and is used in the prevention, diagnosis,
or treatment of cancer and other diseases. Biologic agents include antibodies, interleukins, and vaccines. Also called
biological agent and biological drug.
 DEVELOPMENTAL DISTURBANCES
OF THE TEETH

ALTERATIONS IN SIZE
Microdontia
Macrodontia

Microdontia – Hypoplasia of teeth

This term is used to describe teeth which are smaller than normal.

Three types of microdontia:

(1) True Generalized Microdontia or Proportional Microdontia

- all the teeth are smaller than normal. Aside from its occurrence in some cases of
pituitary dwarfism and Down’s syndrome, this condition is exceedingly rare.
The teeth are well formed, they are merely small.

(2) Relative generalized microdontia or Disproportional Microdontia

- normal or slightly smaller than normal teeth are present in jaws that are somewhat larger
than normal, and there is an illusion of true microdontia.

Since it is well recognized that a person may inherit the jaw size from one parent and the tooth
size from the other parent, the role of hereditary factors in producing such a condition is
obvious.

(3) Microdontia involving only a single tooth – Focal or Localized microdontia

- affects most often the maxillary lateral incisor and the third molar. These two teeth are
among those that are most often congenitally missing. Supernumerary teeth; however,
are frequently small in size.

One of the common forms of localized microdontia is that which affects the maxillary lateral
incisor, a condition that has been called the ‘peg lateral’. Instead of exhibiting parallel or
diverging mesial and distal surfaces, the sides converge or taper together incisally, forming a
peg-shaped or cone-shaped crown. The root of such a tooth is frequently shorter than usual.
Conditions Associated with Microdontia:

Down’s Syndrome or Trisomy 21 – genetic disease associated with growth delays

Ectodermal Dysplasia - disorders in which two or more of the ectodermally derived

structures — the skin, sweat glands, hair, nails, teeth and mucous membranes —
develop abnormally.

Chondroectodermal Dysplasia – Ellis-van Creveld Syndrome –

- rare congenital abnormality associated with ectodermal dysplasia

Macrodontia – Hyperplasia of Teeth; Megadontism

Refers to teeth that are larger than normal.

Three types of macrodontia:

(1) True generalized macrodontia or Proportional Macrodontia

- the condition in which all teeth are larger than normal. It has been associated with
pituitary gigantism, but is extremely rare.
- results in crowding of teeth and possibly an abnormal eruption pattern caused by insufficient arch space.

(2) Relative generalized macrodontia or Disproportional Macrodontia

- somewhat more common and is a result of the presence of normal or slightly larger
than normal teeth in small jaws, the disparity in size giving the illusion of macrodontia.
As in microdontia, the importance of heredity must be considered.

(3) Macrodontia of single tooth - Focal or Localized Macrodontia

- relatively uncommon, but is occasionally seen. It is of unknown etiology. The tooth
may appear normal in every respect except for its size.
True macrodontia of a single tooth should not be confused with fusion of teeth, in
which, early in odontogenesis, the union of two or more teeth results in a single large
tooth.

A variant of this localized macrodontia is the type that is occasionally seen in cases of
hemifacial hypertrophy, in which the teeth of the involved side may be considerably larger than
those of the unaffected side.
Conditions Associated with Macrodontia:

Otodental syndrome - a very rare inherited condition characterized by grossly enlarged

canine and molar teeth (globodontia) associated with sensorineural hearing loss.

Hemifacial hypertrophy (also termed facial hemihypertrophy, facial hemihyperplasia,

or Friedreich's disease) abbreviated as (HFH)
- rare congenital disease characterized by unilateral enlargement of the head and
teeth.

Microdontia
Macrodontia
 ALTERATIONS IN
NUMBER AND ERUPTIONS
Supernumerary
Anodontia
Impaction

Dental lamina – initiates tooth formation

I. SUPERNUMERARY TEETH

Extra or supernumerary teeth in the dentition may be seen in all the quadrants of the jaw;
most probably result from continued proliferation of the permanent or primary dental
lamina to form a third tooth germ.

A supernumerary tooth may have a normal morphology or may be rudimentary and miniature.

Occurrence may be single or multiple, unilateral or bilateral, erupted or impacted, and in one or
both jaws. Multiple supernumerary teeth are rare in individuals with no other associated
diseases or syndromes.

The conditions commonly associated with an increased prevalence of supernumerary teeth

include cleft lip and palate, cleidocranial dysplasia, and Gardner syndrome. Supernumerary
teeth associated with cleft lip and palate result from fragmentation of the dental lamina during
cleft formation.

Gardner syndrome is characterized by the occurrence of multiple impacted supernumerary

teeth.
Supernumerary teeth are found more often in the permanent dentition than in the primary
dentition and are much more commonly seen in the maxilla than in the mandible (10:1).

The anterior midline of the maxilla is the most common site, in which case the supernumerary
tooth is known as a mesiodens.

The maxillary molar area (fourth molar or paramolar) is the second most common site.

Classification of Supernumerary Teeth:

Supernumerary teeth are classified according to morphology and location. In the primary
dentition, morphology is usually normal or conical. There is a greater variety of forms
presenting in the permanent dentition.

• Conical. This small peg-shaped conical tooth is supernumerary and most commonly
found in the permanent dentition.

• Tuberculate. The tuberculate type of supernumerary possesses have more than one
cusp or tubercle. It is frequently described as barrel-shaped and may be invaginated.
Tuberculate supernumeraries are often paired and are commonly located on the palatal
aspect of the central incisors. They rarely erupt and are frequently associated with
delayed eruption of the incisors.

• Supplemental. The supplemental supernumerary refers to a duplication of teeth in the

normal series and is found at the end of a tooth series. The most common supplemental
tooth is the permanent maxillary lateral incisor, but supplemental premolars and molars
also occur.
The majority of supernumeraries found in the primary dentition are of the supplemental
type
Supernumerary Teeth may also be classified as:

• True supernumerary - supernumerary tooth or teeth have normal morphology

• Accessory or rudimentary – miniature tooth

Types of Supernumerary Tooth/Teeth – based on location

• Mesiodens
– most common supernumerary tooth; located between maxillary central incisors;
they give rise to diastema

• Maxillary 4th Molar

– second most common supernumerary tooth

• Peridens
– erupts outside the dental arch

• Mesiomolar or Distomolar

• Paramolars
- erupts on the buccal, lingual, or proximal to one of the molars

• Paramolar Tubercle
- fused with a permanent molar
Other Supernumerary Teeth

Predeciduous Dentition:

• Natal teeth - teeth that appear at the time of birth

- described as hornified epithelial structures without roots, occurring on the gingiva
over the crest of the ridge, which may be easily removed.

Infants occasionally are born with structures which appear to be erupted teeth, usually in
the mandibular incisor area.

• Neonatal teeth - those appearing within 6 months following birth; erupting prematurely in
the first 30 days of life.

Prematurely erupted true deciduous teeth, usually mandibular central incisors, have been
thought to arise either from an accessory bud of the dental lamina ahead of the deciduous
bud or from the bud of an accessory dental lamina.

Prematurely erupted primary teeth should be preserved (provided they cause no injury to
the infant or the mother), and supernumeraries should be extracted.

Postpermanent dentition – supernumerary teeth appearing after the loss of permanent teeth

- Most teeth appearing after extraction of the permanent teeth are believed to arise from
eventual eruption of previously impacted teeth.

Syndromes Associated with Supernumerary Teeth:

• Cleidocranial Dysostosis
• Gardner’s Syndrome
• Down’s Syndrome
• Crouzon’s Syndrome (Craniofacial Dysostosis)

Clinical Significance of Supernumerary Teeth:

• They occupy space

• When impacted, they may block the eruption of other teeth
• May cause delayed eruption or mal-eruption of adjacent teeth
• When supernumerary teeth erupt, they may cause malalignment of the dentition and
may be cosmetically objectionable.
II. ANODONTIA

Anodontia is the congenital absence of teeth, caused by the failure of tooth buds to
develop. It may involve both the deciduous and the permanent dentition.

Types of Anodontia:

• True anodontia, or congenital absence of teeth, may be of two types:

▪ Complete anodontia - all teeth are missing, may involve both deciduous and
permanent dentition

Hereditary ectodermal dysplasia is a rare inherited condition in which complete or

partial anodontia is a prominent feature; the few teeth that are present may be
deformed, frequently cone-shaped.

▪ Partial anodontia – also called hypodontia or oligodontia

- involves one or more teeth and is a rather common condition

Although any tooth may be congenitally missing, there is a tendency for certain teeth
to be missing more frequently than others.

• Pseudoanodontia – teeth are clinically absent because of impaction or delayed

eruption

• False Anodontia – teeth have been exfoliated or extracted

X-ray radiation of the face at an early age affects normal growth and development of tooth
buds which are extremely sensitive to X-ray radiation. They may be destroyed completely by
relatively low dosages. Teeth already forming and partially calcified may be stunted by X-ray
radiation.
III. IMPACTION - teeth are prevented from erupting

Impaction of teeth is a common event that most often affects the mandibular third molars and
maxillary canines. Less commonly, premolars, mandibular canines, and second molars are
involved. It is rare to see impactions of incisors and first molars.

Etiology of impaction:

• obstruction or lack of space due to crowding or from some other physical barrier;

• premature loss of deciduous teeth with subsequent partial closure of the area they
occupied;

• abnormal eruption path, presumably caused by unusual orientation of the tooth germ;
- Rotation of tooth buds result in teeth which are ‘aimed’ in the wrong direction because their
long axis is not parallel to a normal eruption path

• ankylosis - the fusion of a tooth to surrounding bone

- usually occurs in association with erupted primary molars. It may result in impaction
of a subjacent permanent tooth.
The reason for ankylosis is unknown, but it is believed to be related to periapical inflammation and
subsequent bone repair. With focal loss of the periodontal ligament, bone and cementum become
mixed, causing fusion of the tooth to alveolar bone.

Causes of Impaction:

▪ Irregularity in the position and the pressure of an adjacent tooth

▪ Inflammatory changes in the bone due to exanthematous disease in children
▪ Density of surrounding or overlying bone
▪ Undue retention of temporary teeth
▪ Acquired disease – necrosis due to infection or abscess
▪ Long, continued chronic disease resulting to density of overlying mucous membrane
▪ Lack of space due to underdeveloped jaw
▪ Premature loss of temporary teeth
Classification of Impacted Mandibular Third Molars:

I. Pell & Gregory's Classification

A. Based on the relationship between the impacted mandibular 3rd molar to

the ramus of the mandible and the 2nd molar;

- based on the space available between the distal of the 2nd molar and the anterior
border of the ascending ramus of the mandible.

Class 1. There is sufficient space available between the anterior border of the ascending
ramus & the distal aspect of the 2nd molar for the eruption of the 3rd molar.

Class 2. The space available between the anterior border of the ramus &
the distal aspect of the of the 2nd molar is less than the mesio-distal width of the
crown of the 3rd molar. It denotes that the distal portion of the 3rd molar crown
is covered by bone of the ascending ramus.

Class 3. The 3rd molar is totally embedded in the bone of the anterior border of the
ascending ramus because of the absolute lack of space. It is obvious
that Class 3 teeth present more difficulty in removal as a relatively large
amount of bone has to be removed and there is a risk of damage to IAN or
fracture of the mandible.
B. Based on the relative depth in bone

Position A.
The occlusal plane of the impacted tooth is at the same level as the occlusal
plane of the 2nd molar.
The highest portion of impacted 3rd molar is on a level with or above the occlusal
plane.

Position B.
The occlusal plane of the impacted tooth is between the occlusal plane & the cervical
margin of the 2nd molar.
The highest portion of impacted 3rd molar is below the occlusal plane but above
the cervical line of the of 2nd molar.

Position C.
The impacted tooth is below the cervical margin of the 2nd molar.
The highest portion of impacted 3rd molar is below the cervical line of the of 2nd molar.

Position A Position B Position C

Clinical Pathology:

Pericoronitis Resorption / Hypercementosis

II. Winter’s Classification
The classification is based on the inclination of the mandibular impacted 3rd molar to the
long axis of the 2nd molar.

Mesioangular impaction. The third molar lies obliquely in the bone, the crown pointing in a
mesial direction, usually in contact with the distal surface of the root or crown of the second
molar. This is the most common type of impaction.

Distoangular impaction. The third molar lies obliquely in the bone, the crown of the tooth
pointing distally toward the ramus, the roots approximating the distal root of the second
molar.

Vertical impaction. The third molar is in its normal vertical position, but is prevented from
erupting by impingement on the distal surface of the second molar or the anterior border of
the ramus. Thus, in most cases of this type, there is simply lack of space for eruption.

Horizontal impaction. The third molar is in a horizontal position with respect to the body of
the mandible, and the crown may or may not be in contact with the distal surface of the
second molar crown or roots. In this type of impaction, the third molar may lie at any level
within the bone from the crest of the ridge to the inferior border of the mandible.

In addition to these types of impaction in which there is variation of angulation in the sagittal plane,
the impacted third molars may also be deflected either buccally or lingually in any case of the
foregoing circumstances. Cases also have been recorded of complicated impactions in which the
third molar is inverted, the crown pointing toward the inferior border of the mandible, or in which the
third molar has been situated completely within the ramus of the mandible.
In the case of impaction of any tooth, but particularly of the mandibular third molar, it is important to determine
whether the tooth is completely or only partially impacted. By definition, a completely impacted tooth is one which lies
completely within the bone and has no communication with the oral cavity. A partially impacted tooth is not completely
encased in bone but lies partially in soft tissue. Although there may be no obvious communication of the tooth with the
oral cavity, one may exist (e.g. through a periodontal pocket on the distal of the second molar) and create an ideal
situation for infection and even dental caries of the impacted tooth crown. A completely embedded or impacted tooth
cannot become infected or carious.

Classification of Impacted Maxillary Third Molars

A. Pell-Gregory Classification

Class A. The occlusal plane of the impacted tooth is at the same level as the occlusal
plane of the 2nd molar.
The lowest portion of impacted 3rd molar is on a level with or above
the occlusal plane of the 2nd molar.

Class B. The occlusal plane of the impacted tooth is between the occlusal plane &
the cervical margin of the 2nd molar.
The lowest portion of impacted 3rd molar is above the occlusal plane but
below the cervical line of the of 2nd molar.

Class C. The impacted tooth is above the cervical margin of the 2nd molar.
The lowest portion of impacted 3rd molar is above the cervical line of the
2nd molar.

* There is are no Classes 1 - 3 (as in the mandibular classification).

B. Archer and Kruger Classification
Impacted maxillary cuspids also assume a variety of positions ranging from horizontal to
vertical.

The vertically impacted cuspid is usually situated between the roots of the lateral incisor and
first premolar and is prevented from eruption simply by lack of space.
In horizontally impacted cuspids the crown usually points in an anterior direction and may
impinge on the roots of any of the incisors or premolars. The horizontal tooth may lie either
labial or lingual to the associated teeth.
Classification of Maxillary Impacted Cuspids

Class I - impacted cuspids located in the palate – horizontal, vertical, semi-vertical

Class II – impacted cuspids located in the labial or buccal surface of the maxilla

Class III – impacted cuspids located in both the palatine and maxillary bones;

Class IV – impacted cuspids located in the alveolar process vertically between incisor and first
premolar

Class V – impacted cuspids located in an edentulous maxilla

Clinical Significance of Impacted Teeth:

▪ The treatment of an impacted tooth depends to a great extent upon the type of tooth
involved and the individual circumstances. In some cases, such as the impacted cuspid,
it is possible by a suitable orthodontic appliance to bring the tooth into normal occlusion.

▪ The majority of impacted teeth; however, must be surgically removed. Because of their
location, impacted teeth frequently cause resorption of the roots of adjacent teeth.

▪ They may also cause periodic pain and even trismus, particularly when infection occurs
around partially impacted teeth.

▪ Referred pain from impacted teeth has also been described.

▪ A dentigerous cyst may develop around the coronal portion of an impacted tooth and
may cause displacement of the tooth and destruction of bone.

In the study of Dachi and Howell, 37% of impacted mandibular third molars and 15% of impacted
maxillary third molars exhibited an area of radiolucency about the crown. About 10% of these
radiolucencies were of such a size that they could be considered dentigerous cysts.

▪ Occasionally, impacted teeth allowed to remain in situ may undergo resorption. The
reason that some teeth are resorbed whereas others are not is unknown.

The process usually begins on the crown of the tooth and results in destruction of the enamel and dentin,
a well as of the cementum, with subsequent replacement by bone. Radiographically, early resorption
resembles a carious lesion of the crown and has often been mistakenly called caries of an impacted
tooth. Obviously, caries is impossible in a tooth that is completely impacted.

Prepared By:
DR. F. M. TAN
 1
DEVELOPMENTAL DISTURBANCES OF THE TEETH
I. ALTERATIONS IN SHAPE AND I. ALTERATIONS IN SHAPE AND
FORM OF THE CROWN FORM OF THE ROOT
▪ Gemination ▪ Concrescence
▪ Fusion ▪ Enamel Pearl
▪ Taurodontism ▪ Dilaceration
▪ Talon’s Cusp ▪ Flexion
▪ Dens Evaginatus ▪ Ankylosis
▪ Dens Invaginatus
▪ Peg-shaped Lateral
▪ Hutchinson’s Incisor
▪ Mulberry Molar
Gemination - Schizodontism
An anomaly which arise from an attempt of a single tooth germ to divide, resulting to incomplete formation of
two teeth. Gemination is also, the fusion of two teeth from a single enamel organ.
Commonly appear as two completely or incompletely separated crowns that have a single root and root canal
– partial cleavage
It is seen in deciduous as well as permanent dentition, and in some reported cases, appears to exhibit a
hereditary tendency. Commonly affects maxillary anteriors, and affected tooth presents a notch in the incisal
edge; there is normal number of teeth.

It is not always possible to differentiate between gemination and a case in which there has been fusion
between a normal tooth and a supernumerary tooth.

Complete cleavage, or twinning, occasionally occurs, resulting in two teeth from one tooth germ; “double
crowns” or “double roots” -
Although trauma has been suggested as a possible cause, the cause of gemination is unknown. These teeth
may be cosmetically unacceptable and may cause crowding.
 2
Fusion - Syndontism
Fusion arise through union of two normally separated tooth germs; joining of two developing tooth germs,
resulting in a single large tooth structure

Depending upon the stage of development of the teeth at the time of the union, fusion may be either
complete or incomplete. Fusion process may involve the entire length of the teeth – complete fusion, or
it may involve the roots only, in which case cementum and dentin are shared. Root canals may also be
separate or shared.

It has been thought that some physical force or pressure produces contact of the developing teeth and their
subsequent fusion.

If this contact occurs early, at least before calcification begins, the two teeth may be completely united to form
a single large tooth. If the contact of teeth occurs later, when a portion of the tooth crown has completed its
formation, there may be union of the roots only.

The tooth may have separate or fused root canals, and the condition is common in the deciduous as well as in
the permanent dentition. In addition to affecting two normal teeth, fusion may also occur between a normal
tooth and a supernumerary tooth such as the mesiodens or the distomolar

Fusion may result to clinical problems related to appearance, spacing, and periodontal conditions.

Taurodontism

The term ‘taurodontism’ was originated by Sir Arthur Keith in 1913 to describe a peculiar
dental anomaly in which the body of the tooth is enlarged at the expense of the roots. The
term means ‘bull-like’ teeth because this abnormality resembles teeth in bulls and other
ungulates, or cud- chewing animals.

In taurodontism, teeth have elongated crowns or apically displaced furcations, resulting in

pulp chambers that have increased apical-occlusal height.

Studies show that taurodontism is caused by failure of Hertwig’s epithelial sheath to

invaginate at the proper horizontal level.
 3
Taurodontism may affect either the deciduous or permanent dentition, although permanent
tooth involvement is more common.

It commonly affects molars, may be unilateral or bilateral or quadrant involvement. The teeth
themselves have no remarkable or unusual morphologic clinical characteristics.

Subclassifications to describe them appear to be of academic interest only. Taurodont teeth are classified into
hypotaurodont, mesotaurodont, and hypertaurodont, with hypertaurodontism being the extreme, and
hypotaurodontism being the mildest form.

Radiographic Features. The unusual nature of this condition is best visualized on the
radiograph.

▪ involved teeth frequently tend to be rectangular in shape rather than taper toward the
roots;
▪ the pulp chamber is extremely large with a much greater apico-occlusal height than
normal;
▪ the pulp lacks the usual constriction at the cervical of the tooth and the roots are
exceedingly short;
▪ the bifurcation or trifurcation may be only a few millimeters above the apices of the
roots - this radiographic picture is quite striking and characteristic.

Treatment. No special treatment is necessary for this anomaly.

 4
Talon’s Cusp
Talon’s cusp, an anomalous structure resembling an eagle’s talon, projects lingually from the
cingulum areas of a maxillary or mandibular permanent incisor. It is a supplemental cusp
arising from the cervico-lingual ridge or overdeveloped cingulum. It is composed of normal
enamel and dentin and contains a horn of pulp tissue. It forms due to overstimulation of inner
dental epithelium.

This anomaly poses problems for the patient in terms of esthetics, caries control, and occlusal
accommodation. Prophylactically restoring the groove to prevent caries is recommended, and
if there is occlusal interference, it should be removed but exposure of the pulp horn,
necessitates endodontic therapy.

Dens Evaginatus - Leong’s Premolar

Dens evaginatus is a common developmental condition that appears clinically as an accessory
cusp, anomalous tubercle, or a globule of enamel on the occlusal surface between the buccal
and lingual cusps of premolars, unilaterally or bilaterally.

The pathogenesis of the lesion is thought to be the proliferation and evagination of an area of
the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ
during early tooth development.

Clinically, this ‘extra’ cusp may contribute to incomplete eruption, displacement of teeth
and/or pulp exposure with subsequent infection following occlusal wear or fracture.

Because of occlusal abrasion, the tubercle wears relatively fast, causing early exposure of an
accessory pulp horn that extends into the tubercle resulting in periapical pathology in young,
caries-free teeth, often before completion of root development and apical closure, making
root canal fillings more difficult.
 5
Judicious grinding of the opposing tooth or the accessory tubercle to stimulate secondary
dentin formation may prevent the periapical sequelae associated with this defect. Sealants,
pulp capping, and partial pulpotomy have been suggested as measures to allow complete root
development.

Dens Invaginatus - Dens in Dente

The ‘dens in dente’ is a developmental variation which is thought to arise as a result of an
invagination in the surface of tooth crown – an exaggeration or accentuation of the lingual pit
before calcification has occurred.

The permanent maxillary lateral incisors are the teeth most frequently involved, and in the
majority of cases the ‘dens in dente’ appears to represent simply an accentuation in the
development of the lingual pit

Radiographically, it is recognized as a pear-shaped invagination of enamel and dentin with a

narrow constriction at the opening on the surface of the tooth and closely approximating the
pulp in its depth. Food debris may become packed in this area with resultant caries and
infection of the pulp, occasionally even before the tooth has completely erupted. The more
severe forms of ‘dens in dente’ may exhibit an invagination that extends nearly to the apex of
the root, and these present a bizarre radiographic picture.

Because the defect cannot be kept free of plaque and bacteria, dens invaginatus predisposes
the tooth to early decay and subsequent pulpitis. Prophylactic filling of the pit is
recommended to avoid this complication.
 6

Hutchinson teeth is a sign of congenital syphilis, which occurs when a pregnant mother transmits
syphilis to her child in utero or at birth. The condition is noticeable when a child's permanent teeth
come in. The incisors and molars take on a triangular or peglike appearance.
 7
ALTERATIONS IN SHAPE AND FORM OF THE ROOT

Concrescence - a form of fusion in which adjacent, already formed teeth are joined by
cementum.

Concrescence of teeth is actually a form of fusion which occurs after root formation has been
completed. In this condition, teeth are united by cementum only. It is thought to arise as a
result of traumatic injury or crowding of teeth with resorption of the interdental bone so that
the two roots are in approximate contact and become fused by the deposition of cementum
between them. Concrescence may occur before or after the teeth have erupted, and although
it usually involves only two teeth, there is at least one case on record of union of three teeth
by cementum.

The diagnosis can frequently be established by radiographic examination. Since with fused
teeth the extraction of one may result in the extraction of the other, it is desirable that the
dentist be forewarned of the condition and advices the patient.

Concrescence is most commonly seen in association with the maxillary second and third
molars.

Enamel Pearls

Droplets of ectopic enamel, or so-called enamel pearls, may occasionally be found on the roots
of teeth. They occur most commonly in the bifurcation or trifurcation of teeth but may appear
on single-rooted premolar teeth as well. Maxillary molars are more commonly affected than
mandibular molars.
 8
These deposits are occasionally supported by dentin and rarely may have a pulp horn
extending into them. This developmental disturbance of enamel formation may be detected
on radiographic examination. It generally is of little significance except when located in an area
of periodontal disease. In such cases, it may contribute to the extension of a periodontal
pocket, because a periodontal ligament attachment would not be expected and hygiene would
be more difficult.

Dilaceration

The term ‘dilaceration’ refers to an angulation, or a sharp bend or curve, in the root or crown
of a formed tooth. The condition is thought to be due to trauma during the period in which the
tooth is forming, with the result that the position of the calcified portion of the tooth is
changed and the remainder of the tooth is formed at an angle. The curve or bend may occur
anywhere along the length of the tooth, sometimes at the cervical portion, at other times
midway along the root or even just at the apex of the root, depending upon the amount of
root formed when the injury occurred.

Injury to a permanent tooth, resulting in dilaceration, often follows traumatic injury to the
deciduous predecessor in which that tooth is driven apically into the jaw.

Since dilacerated teeth frequently present difficult problems at the time of extraction if the
operator is unaware of the condition, the need for preoperative radiographs before any
surgical procedures are carried out is self-evident.
 9
Flexion

A deviation or bend of a tooth that is restricted to the root portion of a tooth.

Ankylosis

Tooth ankylosis is the pathological fusion between alveolar bone and the cementum of teeth,
which is a rare phenomenon in the deciduous dentition and even more uncommon in
permanent teeth.

Prepared By:
DR. F. M. TAN
Stages in the Development of Normal Enamel

1. Secretion of the organic matrix

2. Mineralization of the matrix
3. Maturation of the enamel
Enamel Hypoplasia –
- the hardness of enamel is normal, but the
quantity/amount of enamel is defective;
- quantitatively defective enamel

Enamel Hypocalcification
- normal amounts of enamel are produced, but
are hypomineralized;
- the quality of enamel is defective, the enamel
is softer than normal
 Conditions that Affect the Extent of
Enamel Defect

1. Intensity of etiologic factor, both local or

systemic factors

2. Duration of the factor’s presence

3. Time when the factor occurred during crown

development
Causes of Enamel Hypoplasia or Enamel Hypocalcification

1. Local Factors
- Local trauma or abscess formation can adversely affect the
ameloblasts overlying a developing crown
- the resulting hypoplastic or hypocalcified permanent tooth is
sometimes known as Turner’s tooth.

2. Systemic Factors
- must occur after birth and before the age of 6 years to have an
effect on developing permanent teeth

3. Other causes:
- nutritional defects such as rickets, congenital syphilis, birth
trauma (neonatal line in primary teeth), fluoride, and
idiopathic factors.
Ingestion of drinking water containing fluoride at levels greater
than 1 part per million during the time crowns are being
formed may result in enamel hypoplasia or hypocalcification,
also known as fluorosis.
Endemic fluorosis is known to occur in areas where the
drinking water contains excessive naturally occurring fluoride.
Mild to moderate fluorosis ranges clinically from white enamel
spots to mottled brown-and-white discolorations.
Severe fluorosis appears as pitted, irregular, and discolored
enamel.
Although fluoride-induced enamel hypoplasia or
hypocalcification is caries resistant, it may be cosmetically
objectionable, making esthetic dental restorations desirable.
 Amelogenesis Imperfecta
(Other names: Hereditary enamel hypoplasia,
Hereditary brown enamel, Hereditary brown opalescent teeth)

- A group of rare, inherited disorders characterized by

abnormal enamel formation not associated with other
abnormalities of the body.

1. Hypoplastic Amelogenesis Imperfecta

2. Hypocalcified Amelogenesis Imperfecta
3. Hypomaturation Amelogenesis Imperfecta
Hypoplastic Amelogenesis Imperfecta

- there is inadequate deposition of enamel matrix;

- enamel is not formed to full thickness because

ameloblasts fail to lay down sufficient matrix.

- pinpoint to pin-headsized pits are scattered across

the surface, buccal surfaces of are affected more
severely, and pits may be arranged in rows or columns

- the enamel between the pits is of normal thickness,

hardness and color; staining of the pits may occur
Hypoplastic Amelogenesis Imperfecta
 Hypocalcified Amelogenesis Imperfecta
- enamel matrix is laid down appropriately but no
significant mineralization occurred;

- the teeth are appropriately shaped on eruption, but the

enamel is very soft and friable, fractures easily and
easily lost;

- upon eruption, the enamel is yellow-brown or orange,

but it often becomes stained brown to black

- exhibits rapid calculus apposition

- occlusal surface become irregular after a period

of function;
- loss of proximal contact – “picket fence appearance”
Hypocalcified Amelogenesis Imperfecta
 Hypomaturation Amelogenesis Imperfecta

- there is a defect in the maturation of the enamel’s

crystal structure; rarest type of enamel defect

- defects occur during both the apposition and

histodifferentiation stages;

- affected teeth are normal in shape; exhibit a mottled,

opaque white-brown to yellow discoloration

- patchy areas of reduced enamel thickness leading to

loss of interproximal contacts

- enamel is softer and tends to wear away and break;

severe attrition.
Hypomaturation Amelogenesis Imperfecta
 Environmental Enamel Hypoplasia

Causes:

• Nutritional deficiencies
- Vitamins A, C, D, calcium and phosphorus

• Severe infections such as rubella, syphillis, and high fever

• Radiation

• Fluorosis

• Tetracycline
Localized Enamel Hypoplasia - Turner’s Tooth

- a type of enamel hypoplasia due to extension of

periapical infection or mechanical trauma from
deciduous predecessor
- local hypoplastic or hypomineralized defect in
crown of a permanent tooth
 Radiographic Features of Turner’s Tooth
• loss of enamel around the cervical region of the tooth,
• an open apex with no other abnormalities,
• calcified tissue that resembles pulp stones in the pulp chamber
• an elongated pulp chamber with bifurcation at the middle third
of the root.
Developmental Defects of Dentin

- Dentinogenesis Imperfecta

- Dentin Dysplasia
 Dentinogenesis Imperfecta
A rare genetic disorder of tooth development resulting to
teeth discoloration, most often a blue-gray or yellow-
brown color and translucence and can affect both
primary and permanent dentition.

Teeth are weaker than normal, making them prone to

rapid wear, breakage, and loss. Enamel frequently
separates easily from underlying defective dentin.

Radiographically presents: bulbous crowns, cervical

constriction – crowns are tulip or bell shaped, thin roots,
and early obliteration of root canals and pulp chambers.
Dentinogenesis Imperfecta
 Dentinogenesis Imperfecta

Type I - occurs in people with osteogenesis imperfecta

- primary teeth are more severely affected than primary teeth

- radiographically:
- partial or total obliteration of pulp chambers and root canals
- roots may be short and blunted
- cementum, PDL and bone appear normal

Type II – not associated with osteogenesis imperfecta; dentin defects

only , no bone disease

- most frequently referred to as Hereditary Opalescent Dentin

Type III – Brandywine type
– a rare condition seen in racial isolate of Maryland

- exhibits multiple pulp exposures and periapical lesions in deciduous

dentition

- large size of the pulp chamber is not due to resorption, but due to
insufficient and defective dentin formation
In type III, the dentin appears
thin and the pulp chambers
and root canals extremely
large, giving the appearance
of thin dentin shells, hence the
previous designation of shell
teeth.
 Dentin Dysplasia – Rootless Teeth
A rare hereditary disease that affects dentin, and is
subdivided into types I and II.

Type 1 – Radicular Type

- both dentitions are of normal color
- premature tooth loss may occur because of short
roots or periapical lesions such as granulomas,
cysts, chronic abscesses

- radiographically, pulps are almost obliterated

 Dentin Dysplasia – Rootless Teeth

Type II – Coronal Type

- the color of the primary dentition is opalescent and
the permanent dentition is normal;

- coronal pulps are usually large (thistle tube

appearance) and are filled with globules of abnormal
dentin.

- radiographically: roots of deciduous teeth are

extremely short and pulps are almost obliterated;
permanent teeth have abnormally large pulp
chambers in coronal portion of the tooth
Dentin Dysplasia – Rootless Teeth
 Regional Odontodysplasia

- also known as: Odontogenic Dysplasia,

Odontogenesis Imperfecta, Ghost Teeth

- one or several teeth in a localized area are affected;

more in maxillary area; tooth shape is altered

- delayed eruption or failure of eruption of affected tooth

- radiogrphically: marked reduction in radiodensity- teeth
assume “ghost appearance”
- enamel and dentin appear very thin
- pulp chamber s exceedingly large
-
Regional Odontodysplasia
Hard Tooth Tissue Reduction

1. Attrition
2. Abrasion
3. Erosion
4. Abfraction
 Attrition
- physiologic wearing of teeth.

Clinical Manisfestations of Attrition:

- clinically appear as small polished area on a cusp tip; slight

flattening of an incisal edge

- matching wear on occlusal sufaces

- shiny facets on amalgam contacts

- possible fracture of cusps or restorations

 Classification of Attrition
A. According to anatomical involvement:
1. Incisal attrition

2. Occlusal attrition

3. Proximal attrition

B. According to degree of anatomical involvement:

1. First degree attrition

2. Second degree attrition

3. Third degree attrition

4. Fourth degree attrition

 Abrasion
- physiologic wearing of teeth caused by a
mechanical process.

Etiology:

1. Toothbrush Abrasion
- found along the root side of the CEJ with
gingival recession

2. Habit or occupation
Clinical Features:
▪ Commonly located at the cervical areas of teeth
▪ Lesions are more wide than deep
▪ Common in premolars and cuspids

Clinical Significance:
Dentinal tubules are exposed and cause irritation
of the odontoblastic processes.
 Erosion
- loss of tooth structure from a non-bacterial chemical process.

Risk Factors:
• Citrus fruits intake - more than twice daily

• Soft drinks consumed - 4 to 6 glasses or more a week

• Sports drinks intake - weekly or more often

• Apple vinegar intake - weekly or more often
• Eating disorder
• Vomiting - weekly or more often
• Symptoms or history of gastro-esophageal reflex diseases
• Unstimulated saliva flow rate
• Excessive attrition
• Bruxism habit
Sources of acids in the oral cavity:

• intrinsic source
- gastroesophageal reflux, vomiting

• extrinsic sources
- acidic beverages, citrus fruits
Clinical Features:

• Scooped-out depression on the enamel surface.

• Broad concavity is shallow, smooth, and highly polished.

• Cupping of occlusal surfaces or incisal grooving with dentin exposure

• Increased incisal translucency

•Wear on non-occluding surfaces.

• “Raised” amalgam restorations with clean non-tarnished appearance.

• Loss of surface characteristics in young children.

• Hypersensitivity

• Pulp exposure in deciduous teeth

 Abfraction
- a theoretical concept explaining a loss of tooth
structure not caused by tooth decay
(non-carious cervical lesions).

- caused by forces placed on the teeth during biting,

eating, chewing and grinding;

- the enamel, especially at the cementoenamel junction

(CEJ), undergoes large amounts of stress,
causing micro fractures and tooth tissue loss.
Traumatic Injuries
of the Teeth
 Types of Traumatic
Injuries to the Teeth

1. Concussion

2. Luxation

3. Fracture
 1. Concussion

• An injury to a tooth and its

attachment apparatus without
displacement from its position
in the alveolus.
Clinical Features of Concussion

• No abnormal loosening of the tooth.

• No radiographic changes are

observed.

• Tooth is tender to percussion.

 Clinical Management of
Concussion

• Pulp testing and frequent monitoring of

pulp vitality is done for months to
two years.

• Soft diet for two weeks.

• This type of injury usually
requires no therapy and
usually resolves without
complication.
 2. Luxation

• An injury in which the tooth is

moved from its position in
the socket.
 Luxation
• There is a partial or complete
dislocation of the tooth
from the socket either to
labial, buccal, or lingual
directions.
• It is caused by a trauma that
affects the pulp, blood vessels,
cementum, and surrounding
bone.
 Clinical Features of Luxation

• Tooth is tender to percussion.

• Soft tissues may be lacerated.

• Periodontal membrane may be torn and

bone may be fractured
Clinical Features of Luxation

• Hemorrhage due to ruptured blood

vessels.

• Necrosis of the pulp may develop and

tooth becomes discolored.

• Ecchymosis of the gingiva

Classification of Luxation
a. Subluxation

b. Extrusive luxation

c. Lateral luxation

d. Intrusive luxation

e. Avulsion
 a. Subluxation

• Injury to the supporting structure

of the tooth with abnormal
loosening, but without displacement
of the tooth.
 b. Extrusive Luxation

• The injury is characterized

by partial displacement of
the tooth from its socket.
• Extruded teeth appear elongated.

• Hemorrhage from the periodontal

ligament.
 c. Lateral Luxation

• Characterized by eccentric
displacement of the tooth
from its socket.
• The tooth is usually
displaced to the
lingual side, with
fracture of the wall
of the alveolar
socket.
 d. Intrusive Luxation

• Displacement of the tooth into

the alveolar bone.
 e. Avulsion

• Complete displacement of the

tooth out of its socket.
Anatomy of Tooth Avulsion
• Avulsed teeth must be
re-implanted within
thirty minutes of injury
to maximize treatment
success.
• The goal of tooth re-implantation
is complete redevelopment of the
periodontal ligament.
• Avulsed primary teeth
are not reimplanted due
to possible injury to the
developing permanent tooth.
 3. Fracture

• A split or break in the tooth.

 Types of Fracture
a. Pathological - spontaneous fracture

- fracture which occur in teeth

which has been weakened so
that ordinary masticatory
forces could break it.
b. Traumatic fracture

- fracture or injury to the

teeth caused by external
force.
Classification of
Fracture
1. According to Extent of Fracture
a. Partial fracture
– the split separates a portion of
the tooth

b. Complete fracture
– a through and through separation
of the tooth
2. According to Location of Fracture

a. Crown fracture
– occurs in coronal region of tooth

b. Root fracture
– occurs either in cervical,
midroot or apical third of tooth
Crown fracture
3. According to Type

a. Horizontal fracture

b. Vertical fracture
– generally requires tooth
extraction
Classification of Crown
Fractures
• Type 1 - or "chip fracture“
- involves the enamel only

• Type 2
- a fracture through enamel and dentin

• Type 3
- involves the enamel, dentin, and pulp
• Type 4
- fractures involve the root.
Crown fracture Root fracture
Vertical fracture Horizontal fracture
Crown fracture
The End
Luxation
Classification of Luxation
a. Subluxation

b. Extrusive luxation

c. Lateral luxation

d. Intrusive luxation

e. Avulsion
Crown fracture
Crown fracture Root fracture
 ABNORMALITIES OF DENTAL PULP

1. Pulp Calcification
2. Resorption
a. Internal Resorption
b. External Resorption

1. Pulp Calcification
- A rather common phenomenon that occurs with increasing age for no apparent reason;
there appears to be no relation to inflammation, trauma, or systemic disease.
- Pulp calcification may be of microscopic size or may be large enough to be detected
radiographically.

The two chief morphologic forms of pulp calcifications are:

1. Discrete Pulp Stones - denticles, pulp nodules

- Pulp stones have been classified as either true or false stones, depending upon their microscopic
structure.
a. True denticles are made up of localized masses of calcified tissue that resemble dentin
because of their tubular structure, resembling secondary dentin since the tubules are
irregular and few in number.
- They are considerably more common in the pulp chamber than in the root canal.

- True denticles may be subdivided further according to whether or not they are attached to
the wall of the pulp chamber. Denticles lying entirely within the pulp tissue and not attached
to the dentinal walls are called ‘free denticles’, while those that are continuous with dentinal
walls are referred to as ‘attached denticles’.

b. False denticles are composed of localized masses of calcified material, and do not exhibit
dentinal tubules. Instead, the nodule appears to be made up of concentric layers or
lamellae deposited around a central nidus.
- The false denticle also may be classified as free or attached. As the concentric deposition of
calcified material continues, it approximates and finally is in apposition with the dentinal wall.
- False denticles commonly occur in the pulp chamber, and generally larger than true denticles.
They may fill nearly the entire pulp chamber, while true denticles are seldom larger than a
fraction of a millimeter in diameter.
2. Diffuse Calcification - frequently termed ‘calcific degeneration’
- commonly seen in the root canals of teeth and resembles the calcification seen in other tissues of
the body following degeneration.
- the diffuse or linear deposits are typically found in the root canals and generally are parallel to
the blood vessels.

Etiology. The etiology of the various types of pulp calcification is unknown. Although the incidence
appears to increase with the age of the persons, there is no definite association with pulpal irritation or
inflammation such as that arising from caries or trauma.

Clinical Significance.
Pulp calcification is a purely coincidental finding without clinical significance. Difficulty may be
encountered in extirpating the pulp during root canal therapy if calcifications are present.
2. Resorption of Teeth
Resorption of teeth occurs in many circumstances other than the normal process associated with the
shedding of deciduous teeth. The roots of permanent teeth may undergo resorption in response to a
variety of stimuli; moreover, it is recognized that root resorption in permanent teeth occurs to a slight
degree even under apparently normal conditions.

Resorption- common type of dental injury or irritation that causes a loss of a part or parts of a tooth.

a. Internal Resorption
- chronic perforating hyperplasia of pulp,
- internal granuloma,
- odontoclastoma,
- pink tooth

Resorption inside the tooth from a pulpal tissue reaction. Resorption of the dentin of the pulpal
walls may be seen as part of an inflammatory response to pulpal injury, or it may be seen in cases
in which no apparent trigger can be identified (idiopathic).

Etiology:
The resorption occurs as a result of activation of osteoclasts or dentinoclasts on internal surfaces
of the root or crown. Resorption lacunae containing these cells and chronic inflammatory cells are
seen. Reversal lines may also be found in adjacent hard tissue, indicating attempts at repair. In
time, the root or crown is perforated by the process, making the tooth useless.

Clinical Features
The first evidence of the lesion may be the appearance of a pink-hued area on the crown of the
tooth, which represents the hyperplastic, vascular pulp tissue filling the resorbed area and showing
through the remaining overlying tooth substance.
Tooth appear pink because of the proximity of the pulp tissue to the tooth surface.

In the event that the resorption begins in the root, there are no significant clinical findings.
Affected tooth remains asymptomatic until root fracture or communication with periodontal
pockets occur
Radiographic Features of Internal Resorption
The involved tooth exhibits a round or ovoid radiolucent area in the central portion of the tooth,
associated with the pulp Complete perforation is common finding if the tooth is left untreated.

Treatment
Treatment of choice is root canal therapy before perforation. Once communication between pulp
and periodontal ligament occurs, the prognosis for saving the tooth is very poor. Occasionally, the
process may spontaneously stop for no apparent reason.
b. External Resorption
Resorption of a tooth may begin either on the external surface, arising as a result of a tissue
reaction in the periodontal or pericoronal tissue. A periapical granuloma arising as a result of pulpal
infection or trauma occasionally causes subsequent resorption of the root apex if the inflammatory
lesion persists for a sufficient period of time.

Etiology
Chronic inflammatory lesions, cysts, benign tumors, malignant neoplasms.
May also occur as a result of trauma, reimplantation/transplantation, impaction
Trauma that causes injury or necrosis of the periodontal ligament may initiate resorption of tooth
root such as in malocclusion or excessive orthodontic forces

Prepared By: DR. F. M. TAN

 ENDODONTICS
Colleagues for
Excellence
Fall 2013

Endodontic Diagnosis

Published for the Dental Professional Community by the

American Association of Endodontists
www.aae.org/colleagues

Cover artwork: Rusty Jones, MediVisuals, Inc.

 ENDODONTICS: Colleagues for Excellence

istorically, there have been a variety of diagnostic classification systems advocated for determining endodontic disease (1).
H Unfortunately, the majority of them have been based upon histopathological findings rather than clinical findings, often
leading to confusion, misleading terminology, and incorrect diagnoses (2). A key purpose of establishing a proper pulpal
and periapical diagnosis is to determine what clinical treatment is needed (3, 4). For example, if an incorrect assessment is
made, then improper management may result. This could include performing endodontic treatment when it is not needed
or providing no treatment or some other therapy when root canal treatment is truly indicated. Another important purpose
of establishing a universal classification system is to allow for communication between educators, clinicians, students and
researchers. A simple and practical system which uses terms related to clinical findings is essential and will help clinicians
understand the progressive nature of pulpal and periapical disease, directing them to the most appropriate treatment
approach for each condition.
In 2008, the American Association of Endodontists held a consensus conference to standardize diagnostic terms used
in endodontics (1). The goals were to propose universal recommendations regarding endodontic diagnoses; develop a
standardized definition of key diagnostic terms that will be generally accepted by endodontists, educators, test construction
experts, third parties, generalists and other specialists, and students; resolve concerns about testing and interpretation of
results; and determine the radiographic criteria, objective test results, and clinical criteria needed to validate the diagnostic
terms established at the conference. Both the AAE and the American Board of Endodontics have accepted these terms and
recommend their usage across all dental disciplines and health care professions (5, 6, 7). Each of the following diagnostic
terms will be defined with typical respective clinical and radiographic characteristics along with representative case
examples when appropriate. However, clinicians must recognize that diseases of the pulp and periapical tissues are dynamic
and progressive and as such, signs and symptoms will vary depending on the stage of the disease and the patient status.
Coupled with this are the limitations associated with current pulp testing modalities as well as clinical and radiographic
examination techniques. In order to render proper treatment, a complete endodontic diagnosis must include both a pulpal
and a periapical diagnosis for each tooth evaluated.

Examination and Diagnostic Procedures

Endodontic diagnosis is similar to a jigsaw puzzle—diagnosis cannot be made from a single isolated piece of information
(4). The clinician must systematically gather all of the necessary information to make a “probable” diagnosis. When taking
the medical and dental history, the clinician should already be formulating in his or her mind a preliminary but logical
diagnosis, especially if there is a chief complaint. The clinical and radiographic examinations in combination with a thorough
periodontal evaluation and clinical testing (pulp and periapical tests) are then used to confirm the preliminary diagnosis
(4). In some cases, the clinical and radiographic examinations are inconclusive or give conflicting results and as a result,
definitive pulp and periapical diagnoses cannot be made. It is also important to recognize that treatment should not be
rendered without a diagnosis and in these situations, the patient may have to wait and be reassessed at a later date or be
referred to an endodontist.

Diagnostic Terminology Examination procedures required to make an endodontic diagnosis (8)

Approved by the American
Association of Endodontists and the Medical/dental history Past/recent treatment, drugs
American Board of Endodontics (5-7) Chief complaint (if any)
How long, symptoms, duration of pain, location, onset, stimuli, relief,
referred, medications
Pulpal Diagnoses (9-14) Facial symmetry, sinus tract, soft tissue, periodontal status (probing,
Clinical exam
mobility), caries, restorations (defective, newly placed?)
Normal Pulp is a clinical diagnostic category
in which the pulp is symptom-free and Clinical testing:
pulp tests Cold, electric pulp test, heat
normally responsive to pulp testing. Although
the pulp may not be histologically normal, a periapical tests Percussion, palpation, Tooth Slooth (biting)
“clinically” normal pulp results in a mild or Radiographic analysis New periapicals (at least 2), bitewing, cone beam-computed tomography
transient response to thermal cold testing, Additional tests Transillumination, selective anesthesia, test cavity
lasting no more than one to two seconds after
the stimulus is removed. One cannot arrive at
a probable diagnosis without comparing the tooth in question with adjacent and contralateral teeth. It is best to test the
adjacent teeth and contralateral teeth first so that the patient is familiar with the experience of a normal response to cold.

2
 ENDODONTICS: Colleagues for Excellence

Reversible Pulpitis is based upon subjective and objective findings indicating that the inflammation should resolve and the
pulp return to normal following appropriate management of the etiology. Discomfort is experienced when a stimulus such
as cold or sweet is applied and goes away within a couple of seconds following the removal of the stimulus. Typical etiologies
may include exposed dentin (dentinal sensitivity), caries or deep restorations. There are no significant radiographic changes
in the periapical region of the suspect tooth and the pain experienced is not spontaneous. Following the management of
the etiology (e.g. caries removal plus restoration; covering the exposed dentin), the tooth requires further evaluation to
determine whether the “reversible pulpitis” has returned to a normal status. Although dentinal sensitivity per se is not an
inflammatory process, all of the symptoms of this entity mimic those of a reversible pulpitis.
Symptomatic Irreversible Pulpitis is based on subjective and objective findings that the vital inflamed pulp is incapable of
healing and that root canal treatment is indicated. Characteristics may include sharp pain upon thermal stimulus, lingering
pain (often 30 seconds or longer after stimulus removal), spontaneity (unprovoked pain) and referred pain. Sometimes
the pain may be accentuated by postural changes such as lying down or bending over and over-the-counter analgesics are
typically ineffective. Common etiologies may include deep caries, extensive restorations, or fractures exposing the pulpal
tissues. Teeth with symptomatic irreversible pulpitis may be difficult to diagnose because the inflammation has not yet
reached the periapical tissues, thus resulting in no pain or discomfort to percussion. In such cases, dental history and thermal
testing are the primary tools for assessing pulpal status.
Asymptomatic Irreversible Pulpitis is a clinical diagnosis based on subjective and objective findings indicating that the
vital inflamed pulp is incapable of healing and that root canal treatment is indicated. These cases have no clinical symptoms
and usually respond normally to thermal testing but may have had trauma or deep caries that would likely result in exposure
following removal.
Pulp Necrosis is a clinical diagnostic category indicating death of the dental pulp, necessitating root canal treatment.
The pulp is non-responsive to pulp testing and is asymptomatic. Pulp necrosis by itself does not cause apical periodontitis
(pain to percussion or radiographic evidence of osseous breakdown) unless the canal is infected. Some teeth may be non-
responsive to pulp testing because of calcification, recent history of trauma, or simply the tooth is just not responding. As
stated previously, this is why all testing must be of a comparative nature (e.g. patient may not respond to thermal testing on
any teeth).
Previously Treated is a clinical diagnostic category indicating that the tooth has been endodontically treated and the
canals are obturated with various filling materials other than intracanal medicaments. The tooth typically does not respond
to thermal or electric pulp testing.
Previously Initiated Therapy is a clinical diagnostic category indicating that the tooth has been previously treated by
partial endodontic therapy such as pulpotomy or pulpectomy. Depending on the level of therapy, the tooth may or may not
respond to pulp testing modalities.

Apical Diagnoses (9-14)

Normal Apical Tissues are not sensitive to percussion or palpation testing and radiographically, the lamina dura
surrounding the root is intact and the periodontal ligament space is uniform. As with pulp testing, comparative testing for
percussion and palpation should always begin with normal teeth as a baseline for the patient.
Symptomatic Apical Periodontitis represents inflammation, usually of the apical periodontium, producing clinical
symptoms involving a painful response to biting and/or percussion or palpation. This may or may not be accompanied by
radiographic changes (i.e. depending upon the stage of the disease, there may be normal width of the periodontal ligament
or there may be a periapical radiolucency). Severe pain to percussion and/or palpation is highly indicative of a degenerating
pulp and root canal treatment is needed.
Asymptomatic Apical Periodontitis is inflammation and destruction of the apical periodontium that is of pulpal origin. It
appears as an apical radiolucency and does not present clinical symptoms (no pain on percussion or palpation).
Chronic Apical Abscess is an inflammatory reaction to pulpal infection and necrosis characterized by gradual onset, little
or no discomfort and an intermittent discharge of pus through an associated sinus tract. Radiographically, there are typically
signs of osseous destruction such as a radiolucency. To identify the source of a draining sinus tract when present, a gutta-
percha cone is carefully placed through the stoma or opening until it stops and a radiograph is taken.
Acute Apical Abscess is an inflammatory reaction to pulpal infection and necrosis characterized by rapid onset,
spontaneous pain, extreme tenderness of the tooth to pressure, pus formation and swelling of associated tissues. There may
be no radiographic signs of destruction and the patient often experiences malaise, fever and lymphadenopathy.

Continued on p. 4
3
 ENDODONTICS: Colleagues for Excellence

Condensing Osteitis is a diffuse radiopaque lesion representing a localized bony reaction to a low-grade inflammatory
stimulus usually seen at the apex of the tooth.

Diagnostic Case Examples

Fig. 1. Mandibularright first molar had been hypersensitive to cold and sweets over the
past few months but the symptoms have subsided. Now there is no response to thermal
testing and there is tenderness to biting and pain to percussion. Radiographically,
there are diffuse radiopacities around the root apices. Diagnosis: Pulp necrosis;
symptomatic apical periodontitis with condensing osteitis. Non-surgical endodontic
treatment is indicated followed by a build-up and crown. Over time the condensing
osteitis should regress partially or totally (15).

Fig. 1.

Fig. 2. Following the placement of a full gold crown on the maxillary right second
molar, the patient complained of sensitivity to both hot and cold liquids; now the
discomfort is spontaneous. Upon application of Endo-Ice® on this tooth, the patient
experienced pain and upon removal of the stimulus, the discomfort lingered for 12
seconds. Responses to both percussion and palpation were normal; radiographically,
there was no evidence of osseous changes. Diagnosis: Symptomatic irreversible
pulpitis; normal apical tissues. Non-surgical endodontic treatment is indicated;
access is to be repaired with a permanent restoration. Note that the maxillary second
premolar has severe distal caries; following evaluation, the tooth was diagnosed with
symptomatic irreversible pulpitis (hypersensitive to cold, lingering eight seconds);
symptomatic apical periodontitis (pain to percussion). Fig. 2.

Fig. 3. Maxillary left first molar has occlusal-mesial caries and the patient has been
complaining of sensitivity to sweets and to cold liquids. There is no discomfort to
biting or percussion. The tooth is hyper-responsive to Endo-Ice® with no lingering
pain. Diagnosis: reversible pulpitis; normal apical tissues. Treatment would
be excavation of the caries followed by placement of a permanent restoration.
If the pulp is exposed, treatment would be non-surgical endodontic treatment
followed by a permanent restoration such as a crown.

Fig. 3.

Fig. 4. Mandibularright lateral incisor has an apical radiolucency that was discovered during a
routine examination. There was a history of trauma more than 10 years ago and the tooth was
slightly discolored. The tooth did not respond to Endo-Ice® or to the EPT; the adjacent teeth
responded normally to pulp testing. There was no tenderness to percussion or palpation in
the region. Diagnosis: pulp necrosis; asymptomatic apical periodontitis. Treatment is non-
surgical endodontic treatment followed by bleaching and permanent restoration.

4 Fig. 4.
 ENDODONTICS: Colleagues for Excellence

Mandibular left first molar demonstrates a relatively large apical radiolucency

Fig. 5.
encompassing both the mesial and distal roots along with furcation involvement.
Periodontal probing depths were all within normal limits. The tooth did not respond
to thermal (cold) testing and both percussion and palpation elicited normal responses.
There was a draining sinus tract on the mid-facial of the attached gingiva which was
traced with a gutta-percha cone. There was recurrent caries around the distal margin
of the crown. Diagnosis: pulp necrosis; chronic apical abscess. Treatment is crown
removal, non-surgical endodontic treatment and placement of a new crown.

Fig. 5.
Maxillary left first molar was endodontically treated more than 10 years ago.
Fig. 6.
The patient is complaining of pain to biting over the past three months. There appear
to be apical radiolucencies around all three roots. The tooth was tender to both
percussion and to the Tooth Slooth®. Diagnosis: previously treated; symptomatic
apical periodontitis. Treatment is nonsurgical endodontic retreatment followed by
permanent restoration of the access cavity.

Fig. 6.

Fig. 7. Maxillary left lateral incisor exhibits an apical radiolucency. There is no history of pain and
the tooth is asymptomatic. There is no response to Endo-Ice® or to the EPT, whereas the adjacent
teeth respond normally to both tests. There is no tenderness to percussion or palpation. Diagnosis:
pulp necrosis; asymptomatic apical periodontitis. Treatment is nonsurgical endodontic treatment
and placement of a permanent restoration.

Fig. 7.
References

1. Glickman GN. AAE consensus conference on diagnostic terminology: background and perspectives. J Endod 2009;35:1619.
2. Seltzer S, Bender IB, Ziontz M. The dynamics of pulp inflammation: correlations between diagnostic data and actual histologic findings in the pulp. Oral
Surg Oral Med Oral Pathol 1963;16:846-71;969-77.
3. Berman LH, Hartwell GR. Diagnosis. In: Cohen S, Hargreaves KM, eds. Pathways of the Pulp, 11th ed. St. Louis, MO: Mosby/Elsevier; 2011:2-39.
4. Schweitzer JL. The endodontic diagnostic puzzle. Gen Dent 2009; Nov/Dec. 560-7.
5. AAE Consensus Conference Recommended Diagnostic Terminology. J Endod 2009;35:1634.
6. American Association of Endodontists. Glossary of Endodontic Terms. 8th ed. 2012.
7. Glickman GN, Bakland LK, Fouad AF, Hargreaves KM, Schwartz SA. Diagnostic terminology: report of an online survey. J Endod 2009;35:1625.
8. Abbott PV, Yu C. A clinical classification of the status of the pulp and the root canal system. Aust Dent J 2007;52 (Endod Suppl):S17-31.
9. Jafarzadeh H, Abbott PV. Review of pulp sensibility tests. Part 1: general information and thermal tests. Int Endod J 2010;43:738-62.
10. Jafarzadeh H, Abbott PV. Review of pulp sensibility tests. Part II: electric pulp tests and test cavities. Int Endod J 2010;43:945-58.
11. Newton CW, Hoen MM, Goodis HE, Johnson BR, McClanahan SB. Identify and determine the metrics, hierarchy, and predictive value of all the
parameters and/or methods used during endodontic diagnosis. J Endod 2009;35:1635.
12. Levin LG, Law AS, Holland GR, Abbot PV, Roda RS. Identify and define all diagnostic terms for pulpal health and disease states. J Endod 2009;35:1645.
13. Gutmann JL, Baumgartner JC, Gluskin AH, Hartwell GR, Walton RE. Identify and define all diagnostic terms for periapical/periradicular health and
disease states. J Endod 2009;35:1658.
14. Rosenberg PA, Schindler WG, Krell KV, Hicks ML, Davis SB. Identify the endodontic treatment modalities. J Endod 2009;35:1675.
15. Green TL, Walton RE, Clark JM, Maixner D. Histologic examination of condensing osteitis in cadaver specimens. J Endod 2013; 39:977-9.

5
 ENDODONTICS: Colleagues for Excellence

The AAE wishes to thank Drs. Gerald N. Glickman and Jordan L. Schweitzer for authoring this issue of the newsletter,
as well the following article reviewers: Drs. Peter J. Babick, Gary R. Hartwell, Terryl A. Propper and Martin J. Rogers.

Exclusive Online Bonus Materials: Endodontic Diagnosis

This issue of the Colleagues newsletter is available online at
www.aae.org/colleagues with the following exclusive bonus
materials:
• Full-Text Article: Glickman GN. AAE consensus
conference on diagnostic terminology: background and
perspectives. J Endod 2009;35:1619.
• Full-Text Article: AAE Consensus Conference
Recommended Diagnostic Terminology. J Endod
2009;35:1634.
• American Association of Endodontists Glossary of
Endodontic Terms

Earn CE Online With Colleagues

With an annual subscription to the AAE Live Learning Center,
you can earn CE credit online for the ENDODONTICS:
Colleagues for Excellence newsletter series and much more. Visit
www.aae.org/livelearningcenter today.

The information in this newsletter is designed to aid dentists. Practitioners must use their best professional
judgment, taking into account the needs of each individual patient when making diagnosis/treatment plans.
The AAE neither expressly nor implicitly warrants against any negative results associated with the application
of this information. If you would like more information, consult your endodontic colleague or contact the AAE.
Did you enjoy this issue of Colleagues? Are there topics you would like to cover in the future? We want to hear
from you! Send your comments and questions to the American Association of Endodontists at the address
below, and visit the Colleagues online archive at www.aae.org/colleagues for back issues of the newsletter.

©
2013, American Association of Endodontists
211 E. Chicago Ave., Suite 1100
Chicago, IL 60611-2691 www.facebook.com/endodontists
Phone: 800/872-3636 (U.S., Canada, Mexico) or 312/266-7255 @aaenews / @savingyourteeth
Fax: 866/451-9020 (U.S., Canada, Mexico) or 312/266-9867 www.youtube.com/rootcanalspecialists

Email: info@aae.org Website: www.aae.org

DISEASES OF THE PULP
The dental pulp:

- a vascular connective tissue

encased within rigid dentin
walls

- there is no collateral
circulation

- direct application of
medications is impossible

- contain free nerve endings

only

- lack of proprioceptors in the

pulp
 Causes of Pulpitis
1. Physical
a. Mechanical - exposure during operative procedure leading to
pulp exposure; trauma; clenching/ grinding
b. Thermal - heat generated during tooth preparations
c. Electrical - galvanic current from dissimilar metallic filling

2. Chemical – exposure to acid and other chemical irritants

3. Bacterial - dental caries

 PULPAL DIAGNOSES

1. Normal Pulp

2. Reversible Pulpitis

3. Symptomatic Irreversible Pulpitis

4. Asymptomatic Irreversible Pulpitis

5. Pulp Necrosis
I. Reversible Pulpitis - Focal Reversible Pulpitis
- acute mild inflammation of the pulp, the first stage when the pulp gets inflamed

- the pulp is vital and can actively respond to any irritant or stimuli;

- clinically, discomfort is experienced when a stimulus such as cold or sweet is applied and
goes away within a couple of seconds following the removal of the stimulus;

- the pain experienced is not spontaneous, sharp pain of short duration, and pain does
not continue after the cause is removed

- pain or sensitivity is caused by cold water or food, cold air, sweet or sour foodstuffs;

- pulp is inflamed but still retain reparative capabilities to return to normal health after
appropriate clinical management;

- no significant radiographic changes in the periapical region of affected tooth

I Causes Reversible Pulpitis:
- cavities that have not reached the pulp;
- exposed dentin- due to erosion, enamel fracture
- thermal shock;

Management of Reversible Pulpitis:

- prevention; regular dental checkup;

- early restoration once cavity has developed;
- use of cavity varnish or cement base

The pulp is still considered to be vital,

once the irritant is eliminated,
the pulp will recover to its normal,
healthy state.
 II. Irreversible Pulpitis - Symptomatic Irreversible Pulpitis

A clinical diagnosis based on subjective and objective findings that the vital, inflamed pulp
is incapable of healing and that root canal treatment is indicated.

- characterized by sharp pain upon thermal stimulus, lingering pain ( 30 secs or longer after
removal of stimulus); spontaneous or unprovoked pain and referred pain;

- episodes of pain are triggered by: sudden temperature change (cold), sweet or acid
foodstuffs, or pressure from food impaction;

- sometimes the pain may be accentuated by postural changes such as lying down or
bending over; change of position intensifies the pain;

- pain is generally severe, boring, gnawing, throbbing - as if pressure is constantly present

in the tooth; patient is kept awake at night due to continuous, intolerable pain;

- over-the-counter analgesics are typically ineffective;

II. Irreversible Pulpitis - Symptomatic Irreversible Pulpitis

- common etiologies may include deep caries, extensive restorations, or fractures exposing
the pulpal tissues;

- teeth with symptomatic irreversible pulpitis may be difficult to diagnose because the
inflammation has not yet reached the periapical tissues, thus resulting in no pain or
discomfort to percussion - in such cases, dental history and thermal testing are the
primary tools for assessing pulpal status.
II. Irreversible Pulpitis - Symptomatic Irreversible Pulpitis
 II. Irreversible Pulpitis - Asymptomatic Irreversible Pulpitis

- presence of a deep cavity extending to the pulp or a decay under a filling

II. Irreversible Pulpitis - Asymptomatic Irreversible Pulpitis

A clinical diagnosis based on subjective and objective findings indicating that the vital,
inflamed pulp is incapable of healing and that root canal treatment is indicated.

- there are no clinical symptoms and usually respond normally to thermal testing but may
have had trauma or deep caries that would likely result in exposure following removal;

- an inflammatory reaction that results from: long-term, low-grade injury to the pulp and
quiescence of an acute process;

- the irritant is of low virulence & therefore the response is milder;

- generally seen only in teeth of children and young adults

II. Irreversible Pulpitis - Hyperplastic Pulpitis ,
Proliferative Pulpitis, Pulp Polyp
A productive pulpal inflammation to extensive carious exposure of any young pulpal tissue.

Pulp tissue reacts in a hyperplastic manner, producing a red mass of reparative granulation
tissue. A fleshy, reddish mass (polyp) fills most of the pulp chamber or extends beyond
the tooth structure. Generally seen only in teeth of children and young adults.

Causes of pulp polyp:

- Dental caries in young tooth with significant loss of tooth structure.

- Fractured tooth, causing trauma to the pulpal tissues.

- Mechanical irritation from chewing and bacterial infection.

II. Irreversible Pulpitis - Hyperplastic Pulpitis
- asymptomatic, polyp less responsive when compared to normal pulp tissue.
polyps cover the entire cavity by enlarging itself;

- masticatory stress can cause tenderness; localized bleeding may occur, polyp bleeds
easily because of a rich network of blood vessels;

- radiographs show a large, open cavity with direct access to the pulp chamber
Treatment of pulp polyp:

- Removal of the polypoid tissue, followed by pulp extirpation.

- Formocresol dressing is placed after the entire pulp is removed.

 III. Pulp Necrosis

A clinical diagnosis indicating death of the dental pulp, indicating root canal treatment.

The pulp is non-responsive to pulp testing and is asymptomatic.

Pulp necrosis by itself does not cause apical periodontitis (pain to percussion or radiographic
evidence of osseous breakdown) unless the canal is infected.

Some teeth may be nonresponsive to pulp testing because of calcification, recent history of
trauma, or simply the tooth is just not responding.

Pulp necrosis may be due to untreated pulpitis, or traumatic injury that disrupts the blood to
the pulp.
III. Pulp Necrosis
Pulpal Diseases Apical Diagnosis
 1
ODONTOGENIC INFECTIONS

An odontogenic infection is an infection of the alveolus, jaws, or face that originates from a
tooth or from its supporting structures and is one of the most frequently encountered infections.

Infection arises either from dental caries or periodontal infections that have extended
beyond the alveolar bone and tends to spread along planes of least resistance from the
supporting structures of the affected tooth.

Causes of Odontogenic Infection

• dental pulp infection, as a result of caries - the leading cause of odontogenic infection.
• pulp necrosis - premature death of the cells in the pulp of the tooth
• the anaerobic bacteria inhabiting the periodontal tissues may provide an additional source of
odontogenic infection

General Factors Affecting Spread of Infection

• Host resistance
• Virulence of infecting organism

Local Factors Affecting Spread of Infections

• Anatomic location of the tooth
• Position of muscle and facial attachments
 2

- Once the odontogenic infection perforates the bone, then the local muscle attachments
control the specific position of its appearance in the soft tissue.

- The muscles of facial expression and mastication, along with others in the head and neck,
originate and insert into various parts of the skeleton and soft tissues. Depending on this
muscular insertion, the spread of infection can be diverted or blocked.

- The spread of odontogenic infection, is dependent upon the relationship of the teeth
apices to the muscle attachments as this will dictate which potential spaces will
become involved.

- If the odontogenic infection punctures the bone just above the muscle parts, the infection
spreads through the fascial space also.

In case the infection spreads through the fascial space, the chance for severe infections
with fast spread of the infection to other areas is possible.

- The infection spreads from the apex of the tooth to the bone depending on the overlying
bone thickness and the relationship of the bone (perforation site) with the muscle
attachments of the jaws.
 3

> In the maxilla, the thinner bone is located in the labial-buccal side, whereas the palatal cortex
is comparatively thicker. Hence, infection erodes labial-buccal side at first.
Once the odontogenic infection perforates the bone, then the local muscle attachments control
the specific position of its appearance in the soft tissue. Infection then attacks the labial bone,
producing a vestibular abscess. This is seen as a small pouch of fluid in the soft tissue covering
the affected tooth.

Spread of Infection

Infections spread along the path of least resistance. Anatomical structures in the body will limit
and direct the spread of infection in a known pattern. These structures include fascial layers,
ligaments, tendons, muscles and bony architecture.

Odontogenic infection is usually self-limiting and spatially confined, infection occasionally

spreads due to a highly virulent organism leading to serious or potentially lethal conditions.

Stages of Infection
I. Cellulitis
II. Abscess
III. Sinus Tract/Fistula
 4

CELLULITIS

Cellulitis is a diffuse inflammation of soft tissues which is not circumscribed or confined to one
area, it tends to spread through tissue spaces and along fascial planes (“spreading infection”).
It results from a diffuse spreading of purulent exudate along the fascial planes that separate the
muscle bundles.

Clinical Features:

- may first appear as a red, swollen area that feels hot and tender to the touch, and the
redness and swelling often spread rapidly
- patient is usually moderately ill and has elevated temperature and leukocytosis;
- a painful swelling of the soft tissue of the mouth and face; swelling is due to inflammatory
edema
- involved tissue is firm;
- if the superficial tissue spaces are involved, the skin is inflamed, has an orange peel
appearance or sometime purplish;
- if inflammatory spread of infection occurs along deeper tissue spaces, the overlying skin
may be of normal color;
- regional lymphadenitis is usually present

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. If early treatment is instituted, a resolution usually occurs
without drainage through a break in the skin.
 5

ABSCESS is a pus-filled cavity of pus accumulation in tissues with well-defined border and
fluctuant to palpation.
- it is a “localized infection”
 6

FISTULA or SINUS TRACT is a drainage pathway or abnormal communication between two

epithelium-lined surfaces due to destruction of the intervening tissue; Abscess ruptures to
produce a draining sinus tract.

A tunneling wound or sinus tract is a narrow opening or passageway extending from a

wound underneath the skin in any direction through soft tissue and results in dead space with
potential for abscess formation.
 7

PROGRESSION OF INFECTION:
If untreated or unresolved, mild infection and inflammation will progress into cellulitis, which is
usually caused by aerobic bacteria. If it progresses further without resolution and/or
treatment, an abscess, which is a pus-filled cavity, (typically caused by anaerobic organisms)
forms. Pus is a collection of necrotic debris (usually of white blood cells and microorganism
byproducts). Chronic or long-standing abscesses, will usually lead to formation of a continually
draining sinus tract, which is the body’s way of relieving pressure of infection.

Drainage by perforation of a bony plate occurs along lines of least resistance, so that,
perforation of a thin cortex occurs before that of a thick cortex. The attachment of muscles may
determine the route that an infection will take, channeling the infection into certain tissue
spaces.

DEEP SPACE INFECTIONS:

- Ludwig’s Angina
- Cavernous Sinus Thrombosis

LUDWIG’S ANGINA - named after the German physician Wilhelm Friedrich von Ludwig

It is an acute, potentially life threatening, toxic cellulitis, beginning usually in the submandibular
space and secondarily involving the sublingual and submental spaces as well. The disease is
not usually considered to be true Ludwig’s angina unless all submandibular spaces are involved.
It is most commonly a disease of dental origin.

The chief source of infection is involvement of a mandibular molar, either periapical or

periodontal.
 8
Clinical Features of Ludwig’s Angina:

- The patient with Ludwig’s angina manifests a rapidly developing board-like swelling of the
floor of the mouth and consequent elevation of the tongue.

- The swelling is firm, painful and diffuse, showing no evidence of localization and paucity of
pus.

- There is difficulty in eating and swallowing as well as in breathing.

- Patients usually have a high fever, rapid pulse and fast respiration and a moderate leuko-
cytosis is also found.

- As the disease continues, the swelling involves the neck, and edema of the glottis may
occur. This carries the serious risk of death by suffocation.

- Next, the infection may spread to the parapharyngeal spaces, to the carotid sheath or to the
pterygopalatine fossa. Cavernous sinus thrombosis with subsequent meningitis may be
sequela to this type of spread of the infection.
 9

CAVERNOUS SINUS THROMBOSIS - Thrombophlebitis

Cavernous sinuses are bilateral venous channels for the content of middle cranial fossa, particularly the
pituitary gland. Areas drained by cavernous sinus include the orbit, paranasal sinuses, anterior mouth, and
middle portion of the face.

Cavernous sinus thrombosis is a serious condition consisting in the formation of a thrombus

in the cavernous sinus or its communicating branches.
Infections of the head, face, and intraoral structures above the maxilla are particularly prone to
produce this disease.
There are many routes by which the infection may reach the cavernous sinus. The facial and
angular veins carry infection from the face and lip, while dental infection is carried by way of the
pterygoid plexus.

Infection spreading by the facial or external route is very rapid with a short fulminating course
because of the large, open system of veins leading directly to the cavernous sinus.

The blood clot typically forms when an infection that starts in your face or head moves into your
cavernous sinuses.
Your body creates a blood clot to try to stop the infection from spreading. However, the clot can
restrict the flow of blood from your brain, potentially damaging your brain, eyes, or nerves.
In cavernous sinus thrombosis, a blood clot develops in the sinuses behind your eyes or at the
bottom of your skull after an infection. The clot is meant to prevent the infection from spreading,
but it often blocks the blood flow out of your brain.

Clinical Features of Cavernous Sinus Thrombosis:

- The patient is extremely ill and manifests the characteristic features of exophthalmos with
edema of the eyelids as well as chemosis.
Chemosis is a sign of eye irritation. The outer surface of the eye (conjunctiva) may look like a big blister. It can also look like it has fluid in it.
When severe, the tissue swells so much that you can't close your eyes properly. Chemosis is often related to allergies or an eye infection.

- Paralysis of the external ocular muscles is reported, along with impairment of vision and
sometimes photophobia and lacrimation.

- There are also headaches, nausea and vomiting, pain, chills and fever.
 10
Treatment and Prognosis. A combination of intravenous antibiotics, anticoagulants, and
surgery is the optimal treatment for cavernous sinus thrombosis. The primary site of infection
may require early drainage, especially when acute sinusitis is the cause of infection.

OSTEOMYELITIS

Osteomyelitis is defined as inflammation of the bone. It involves adjacent cortical plates and
often periosteal tissues.
The incidence of osteomyelitis is much higher in the mandible because of the dense, poorly
vascularized cortical plates.
It is much less common in the maxilla due to the excellent blood supply from multiple blood
supply. In addition, the maxillary bone is much less dense than the mandible.

The most common cause of suppurative osteomyelitis is an odontogenic infection.

Depending on the signs and symptoms, osteomyelitis can be classified as acute, subacute,
and chronic forms.

Acute Suppurative Osteomyelitis

- radiographic changes do not appear immediately because it may take about 2 weeks for the
trabecular pattern of bone to change and areas of radiolucency to start to appear;

Chronic Suppurative Osteomyelitis

- results from acute osteomyelitis that is not treated effectively;
- the infection may be a manifestation of lowered patient resistance; such as in
immunosuppressed patients, poorly controlled diabetes mellitus, or malnutrition.
- clinically, the disease is dominated by pain and the development of intraoral and/or
extraoral sinuses.
- induration of soft tissues overlying the infected segments of the jawbones is marked;
- distension of the periosteum with pus or inflammatory exudate, which may cause trismus
and difficulty in swallowing.
- regional lymph nodes are usually tender and enlarged

- radiographically, there is loss of detail of the trabecular pattern of the osseous architecture,
giving the bone a mottled or moth-eaten appearance;
- the ischemic or necrotic islands of bone tend to sequestrate, appearing more radiopaque
than the surrounding bone; these form a sequestrum of necrotic bone
 11

In younger persons, subperiosteal new bone formation appears adjacent to the diseased area.
This new bone, known as involucrum, tends to be structureless or granular in appearance
radiographically and may surround the necrotic sequestrum and pus lying with‐ in the bone.

Prepared By:
Dr. F. M. Tan