Vocabulary: Traumatic dental injuries

Luxation injuries

Fracture injuries

Injuries to gingiva or oral mucosa

Sequelae of dental trauma

Treatment and test definitions

Wound healing definitions

Definitions of tooth development and eruption disturbances of permanent teeth related to injury to primary predecessors

Luxation injuries


An injury to the tooth-supporting structures without increased mobility or displacement of the tooth, but with pain to percussion.


An injury to the tooth supporting structures with increased mobility, but without displacement of the tooth. In acute trauma, bleeding from the gingival sulcus confirms the diagnosis.


Partial displacement of the tooth out of its alveolar socket.

An injury to the tooth characterized by partial or total separation of the periodontal ligament resulting in loosening and displacement of the tooth. The alveolar socket bone is intact in an extrusion injury as opposed to a lateral luxation injury. Apart from axial displacement, the tooth will usually have an element of protusion or retrusion. In severe extrusion injuries the retrusion/protrusion element can be very pronounced. In some cases it can be more pronounced than the extrusive element.


Displacement of the tooth other than axially. Displacement accompanied by comminution or fracture of either the labial or the palatal/lingual alveolar bone.

Lateral luxation injuries, similar to extrusion injuries, are characterized by partial or total separation of the periodontal ligament. However, lateral luxations are complicated by a fracture of either the labial or the palatal alveolar bone and a compression zone in the cervical and sometimes the apical area. If both sides of the alveolar socket have been fractured, the injury should be classified as an alveolar fracture (alveolar fractures rarely affect only a single tooth). In most cases of lateral luxation the apex of the tooth has been forced into the bone by the displacement, and the tooth is frequently non-mobile.


Displacement of the tooth into the alveolar bone. This injury is accompanied by a comminution or fracture of the alveolar socket.


Complete displacement of the tooth out of its socket.

Fracture injuries


An incomplete fracture (crack) of the enamel without loss of tooth structure.


A fracture confined to the enamel with loss of tooth structure.


A fracture confined to enamel and dentin with loss of tooth structure, but not involving the pulp.


A fracture involving enamel and dentin with loss of tooth structure, and exposing the pulp.


A fracture involving enamel, dentin and cementum with loss of tooth structure, but not involving the pulp.


A fracture involving enamel, dentin, and cementum with loss of tooth structure, and involving the pulp.


A fracture involving cementum, dentin, and the pulp. Root fractures can be further classified by whether the coronal fragment is displaced (see luxation injuries).


A fracture of the alveolar process; may or may not involve the alveolar socket.

Teeth with alveolar fractures are characterized by mobility of the alveolar process; several teeth typically will move as a unit when mobility is checked.

Injuries to gingiva or oral mucosa


A shallow or deep wound in the mucosa resulting from a tear, usually produced by a sharp object.


A bruise usually produced by impact with a blunt object and not accompanied by a break in the mucosa, usually resulting in submucosal hemorrhage. This injury may be associated with an underlying bone fracture.


A superficial wound produced by rubbing or scraping of the mucosa, leaving a raw, bleeding surface.

Sequelae of dental trauma


Necrosis of the pulp tissue; can be coagulation/ischemic necrosis (uninfected) or infection-related (liquefaction) necrosis.


In traumatic dental injuries where the neurovascular supply to the pulp has been totally severed, mechanisms for revascularization and re-innervation are present. The probability of successful revascularization is determined primarily by the size of the apical foramen (stage of root development), the length of the pulp space and whether bacteria infect the revascularization site. In teeth where revascularization fails, the pulp tissue will undergo sterile necrosis. Although this avascular pulp usually becomes infected, in rare cases it may remain sterile indefinitely.

Diagnostic indicators for pulp necrosis:

  • Periapical radiolucency
  • Grey (blue or red) discoloration of the tooth crown
  • Infection-related external root resorption
  • No response to pulp sensitivity test
  • Tenderness to percussion and palpation in the vestibule develops after an asymptomatic period
  • Presence of a fistula (sinus tract)
  • Unchanged thickness of dentinal walls (arrested development) in cases where the neurovascular supply has been severed by the trauma and revascularisation has been attempted.

Most of the teeth with pulp necrosis are infected with bacteria. After 3-4 weeks these teeth will show radiographic indications of pulp necrosis with the development of an apical radiolucency. In rare cases a sterile necrosis occurs and no apical radiolucency develops.

Discoloration of the tooth is caused by remnants of biologically decomposed pulp tissue and blood clot. Discoloration of the tooth crown is a sign of internal damage, but not necessarily irreparable damage. The discoloration is a sign of defective transport mechanisms in the pulp rather than necrosis; a phenomenon frequently seen in primary teeth.

Pulp necrosis is a likely diagnosis if the tooth shows grey/blue or red crown discoloration in combination with an apical radiolucency.

The biologic mechanisms that lead to infection-related external resorption are related to pulp necrosis. The presence of infection-related resorption is, therefore, a clear sign of an infected pulp necrosis.

Development of a fistula (sinus tract) in the oral mucosa or gingiva, or subsequent pain/tenderness in a tooth which has been asymptomatic the first weeks after trauma is a sign of pulp necrosis.

Pulp sensitivity testing is a helpful dignostic tool in determining the presence of pulp necrosis. However, an immediate negative response should not be considered pathognomonic for pulp necrosis as initial severance of the neurovascular supply can be re-established in many cases. If reinnervation has not occurred in 3 months and there is no response to sensitivity tests, the revascularisation process has most likely failed. No response after 3 months should be considered a sign of pulp necrosis.

Unchanged thickness of dentinal walls (arrested root development) may indicate that the pulp of a young tooth has not survived. A neighboring tooth can serve as a comparison. Increased thickness of the dentinal walls (pulp canal obliteration) is always seen after revascularisation and is a sign that the pulp has survived.


A condition where hard tissue is deposited along the wall of the root canal and fills most of the pulp canal.


In traumatic dental injuries where the neurovascular supply to the pulp has been severed, mechanisms for revascularization and reinnervation are present. When revascularization is successful, these teeth will show an accelerated deposition of hard tissue along the pulp canal walls. Within one year most teeth show a partial or totally obliterated pulp canal. However, even in these teeth a small diameter pulp canal still exists. These restricted pulp canals have been found, often after some years, to have a small risk of developing infection-related pulp necrosis. The exact cause of this pathologic change is unknown, but new trauma and extensive crown preparation appear to be probable risks. PCO is a common sequela in all types of luxation injuries that include displacement.



Surface resorption (repair-related external resorption) represents the result of removal of injured periodontal ligament tissue next to the root surface by macrophages and osteoclasts. It results in a saucer-shaped cavity on the root surface mostly involving cementum. Surface resorption is the first part of a healing process. The resorption cavity will subsequently be fully or partially repaired by new cementum with insertion of new Sharpey’s fibers.

If the initial cavity is deep enough to come in contact with dentinal tubules that communicate with an infected pulp, there is a risk of developing an infection-related resorption (see definition). Although surface resorption may occur after all types of luxation injuries, it is frequently found after lateral luxations. It may affect all parts of the root. In root fractures, surface resorption is common near the fracture site.

Surface resorption sites are often to small to be detectable radiographically. However, surface resorption sites, large enough to be diagnosed radiographically, can somestime be seen already 2 months after the injury

Surface resorption represents a diagnostic problem, as it must be distinguished from infection-related resorption.


"An ankylosed tooth" is a tooth partially or totally anchored to the alveolar socket by a bridge or bridges of bone extending from the root dentin to the socket wall.


Ankylosis is a progressive resorptive process seen in traumas where the tooth has received extensive damage to the innermost layer of the periodontal ligament and sometimes also the cementum.

Competitive healing events occur between bone formation and regeneration of new periodontal ligament tissue. From the socket wall, bone will be formed by bone marrow derived cells. From the intact PDL, new cementum and Sharpey’s fibers will be formed.

If the injury site is between 1-4 mm2 in size, a transient ankylosis can result in which the initial ankylosis subsequently is resorbed and replaced with new cementum and PDL. This process may be hampered if the tooth is rigidly splinted. In contrast, if the tooth is splinted with a flexible splint or not splinted, small movements of the tooth during the healing period may lead to a break-up of the initially formed, small ankylotic sites.

In injuries producing damaged areas larger than 4 mm2, healing with new periodontal ligament is unlikely. In these areas ankylosis with progressive resorption of root dentin and its replacement of with osseous tissue occurs. In effect, the tooth root becomes an integral part of the bone remodelling system.

Ankylosis is a very serious complication that inevitably leads to tooth loss. In children and adolescents 8-16 years old, tooth loss occurs rapidly and is expected within 1-5 years. In contrast, in adults the tooth may remain functional for many years.


In cases of minor ankylosis that develop subsequent to trauma, a function related resorption of the bony bridges may occur after some months. Clinically, this is represented by a return of normal mobility, In some cases the restoration of a functioning PDL is evident radiographically. Transient external ankylosis appears to occur when the initial ankylosis site is less than 4 mm2.

The process of resorption at the initial ankylosis site appears to be influenced by the type of fixation (splinting) used and possibly the splinting time. No splinting or flexible splinting allows small movements of the tooth which seem to promote the process of bony bridge resorption, whereas long-term rigid splinting appears to maintain the ankylosis site.


Resorption involving the root and the adjacent alveolar bone.


Infection-related resorption is a progressive resorption that leads to tooth loss, unless endodontic therapy is initiated to eliminate the etiological agents (bacteria and necrotic tissue) responsible for the resorption process.

Infection-related resorption may occur after an initial surface resorption has penetrated through the cementum, exposing dentinal tubules in a tooth with infected pulp necrosis.

The osteoclastic process and the associated inflammation at the resorption site are fueled by toxins created by bacteria located in the pulp and/or dentinal tubules. The toxins travel by diffusion through the exposed dentinal tubules to the resorption site where they trigger osteoclastic activity and lead to resorption of the root surface and the adjacent socket bone. This will proceed as long as infection-related resorption can be arrested if the infected pulp is removed and endodontic therapy performed. When the infection-related resorption is arrested, a healing process will be initiated in which new cementum, bone and periodontal ligament will be formed. If infection-related resorption affects a large surface area, healing with normal periodontal ligament may not occur. Instead ankylosis may occur (see ankylosis).


This event takes place when the revascularization front meets an area of infected tissue located coronally (infected necrotic pulp tissue and/or infected dentinal tubules).


An event that takes place when a revascularization front meets an area of ischemic (sterile) pulp tissue. This event may be seen in the apical area or at a root fracture site.


A condition seen when pulp metaplasia has occurred. When bone tissue is formed inside the pulp canal, a progressive replacement of dentin, cementum and sometimes enamel with bone may occur.


An invasive resorption process, which usually starts in the cervical area and later spreads in a coronal and/or apical direction. A possible etiology is that the cementoblast layer, for a still unknown reason, does not protect the root from osteoclastic activity. Cervical invasive resorption can sometime be caused by a dental trauma.


Loss of crestal bone around a traumatized tooth.


When an area of periodontal ligament (PDL) tissue and alveolar socket bone are injured, resorption occurs as part of a repair process. Sometimes this causes permanent loss of tooth supporting bone and gingival attachment. Alternately, the bone loss may be transient as the periodontium may recover by forming new alveolar bone tissue and PDL over a period of 2-3 months.


In teeth where revascularisation takes place in a narrow root canal, the initial phase of a series of events can be the apical breakdown radiographically of the lamina dura by the revascularization front. When this process moves in a coronal direction, the apical lamina dura is gradually reformed. Although rare, it especially affects extruded and laterally luxated teeth with complete root formation.


When a contusion of the marginal supporting bone occurs, resorption of avascular bone must take place before bone regeneration can occur. During this phase the clinical and radiographic appearance of transient marginal breakdown is similar to that seen in a permanent loss of marginal bone. However, in the case of transient marginal breakdown, the condition normalizes over several months when bone and periodontal ligament regenerate If regeneration fails, the marginal breakdown becomes permanent.


Term used to describe the condition in which normal pulp tissue has been replaced with other tissue types such as loose or dense fibrous connective tissue, bone, cementum or periodontal ligament.


A healing process in which lacerated, displaced or lost gingiva is regenerated with a normal sulcular attachment and new gingival collageneous fibers.


Ruptures of the periodontal ligament are typically seen after luxation injuries. They usually heal by a regenerative process where newly formed Sharpey’s fibers and fibroblasts splice the ruptured PDL. This process is far advanced as soon as 2 weeks after the injury.


Externally, a change in tooth color due to an accumulation of staining medias on the tooth surface or a developmental disturbance of enamel. Internally, a change in color due to absorption of pigmented particles into dentin and cementum.

Most discolorations are internal in traumatized teeth.

White discoloration may be seen in disturbances of enamel formation in permanent teeth where trauma to their primary predecessors influences enamel formation or enamel maturation.

Yellow discoloration of the tooth crown is a common finding after pulp canal obliteration. It also may be seen in the permanent dentition as a sequel to traumatic injures affecting the primary predecessors.

Grey discoloration is a common finding in trauma induced pulp necrosis and develops weeks or months after the injury. It is caused by the incorporation of pigments released from necrotic pulp tissue and degraded blood into the dentinal structure. In rare cases it may be reversible.

Red discoloration may appear almost instantaneously after a luxation injury. This discoloration is anticipated to occur when a minor luxation injury severs the veins in the apical foramen and the arteries continue to carry blood into the pulp. Subsequent decomposition of the blood gradually results in a bluish or bluish/ brown discoloration.

Treatment and test definitions


Covering of exposed dentinal tubules with a suitable filling material. (e.g. glass ionomer, composite or calcium hydroxide-containing cement) to prevent bacteria from entering the tubules and subsequently the pulp.


A covering over an exposed pulp to encourage the formation of new dentin to wall off the exposure. Commonly used materials are calcium hydroxide, calcium hydroxide-containing cement or mineral trioxide aggregate (MTA).


Partial pulpotomy is the surgical removal of the coronal portion (2 mm) of an exposed vital pulp as a means of preserving the vitality of the remaining pulp in the crown and root. The exposed pulp is then covered with a material that induces formation of a hard tissue barrier. Calcium hydroxide or MTA usually is used for this purpose. In some cases the amputation site is placed in the cervical region when the vascular supply to the most coronal portion of the pulp is compromised by inflammation or lack of vascularity.


The intentional removal of the crown, leaving the root portion of the tooth intact in order to preserve the alveolar bone structure. The root canal filling is removed and the canal allowed to fill with blood. The remaining root portion usually undergoes ankylosis, but may retain a normal periodontal ligament in some areas. In both events the remaining root portion appears to maintain not only the labial-lingual/palatal dimension of the alveolar process, but also partially allow the development of the vertical height of the alveolar process. Preservation of the ridge is crucial in treatment planning for children and adolescents. An intact alveolar process is a precondition for esthetic tooth replacement procedures.


An apical healing event in which an open apex is closed with newly formed hard tissue. Traditionally calcium hydroxide has been used to induce the barrier which usually consists of an irregular cementum-like tissue. In rare cases a new apex is formed (apexogenesis), a finding related to the presence of a viable Hertwig’s epithelial root sheath.


A term used in connection with implants. It describes the condition where new bone forms directly against the implant material and fuses to the surface of the alveolar socket. A similar healing event takes place in cases of tooth replantation where some or all of the PDL is damaged. In this situation the term is ankylosis or osseous replacement resorption.


Stabilization of loosened teeth, bone fractures or a combination of both with various splinting materials including sutures, acid-etch flexible resin splints, acid-etch-wire composite splints, acid-etch composite nylon line splints, acid-etch orthodontic wire splints, titanium trauma splints (TTS), arch bars, cap splints, or steel wire splints.


Stabilisation of a loosened tooth by a splinting device which allows mobility (within physiologic ranges) during the healing period (e.g., resin, orthodontic wire, TPS splints).


Stabilisation of a loosened tooth or root fractured tooth by a splinting device which allows no mobility during the healing period (e.g., capsplint, composite splint).


Repositioning of displaced tooth, alveolar fracture, root fracture or jaw fracture with finger or hand pressure.


Repositioning of displaced tooth, alveolar fracture, root fracture or jaw fracture with forceps or by surgical exposure of a fracture site.


Repositioning of displaced tooth, alveolar fracture, root fracture or jaw fracture with orthodontic appliances.


Repositioning a displaced tooth into a non-optimal position in the socket.


Repositioning a displaced tooth into its anatomically correct position in the alveolar socket.


The complete removal of the pulp.


The aim of pulp testing is to assess the circulatory or sensory status of a traumatized tooth. Several methods have been developed including thermal, electrometric and Laser Doppler Flowmetry (LDF) techniques.

The thermal and the electrometric test results are based upon the sensory competency of the pulp rather than the circulatory status. The vascular and sensory status of the teeth is, however, closely related. A positive sensibility test is an indirect but good indication of satisfactory vascularisation of the pulp. Without an adequate vascular supply, the sensory nerves of the pulp will soon cease to function and become necrotic.

An immediate negative response after trauma should not be considered pathognomonic for pulp necrosis as initial rupture of the neurovascular supply in many cases can be repaired. If reinnervation of the pulp has not occurred over a 3 month period, and sensibility tests still give negative results, the revascularization process has probably failed. A lack of response after 3 months should be considered a sign of pulp necrosis.

The LDF method is based directly on the circulation of blood in the pulp. Therefore, it can measure the vascular status directly. Comparisons between thermal, electrometric and LDF methods have shown that LDF is the most reliable test for circulatory status.

Wound healing definitions


A healing modality where tissue (e.g., pulp, periodontal ligament, alveolar bone, gingival or oral mucosa) is replaced with an identical tissue. The new tissue is identical to the original tissue in both anatomy and function.


A healing modality where damaged tissue (e.g., pulp, periodontal ligament, alveolar bone, gingiva or oral mucosa) is replaced with a fibrous connective (scar) tissue. The new tissue differs from the original tissue in both anatomy and function.


A basic wound healing concept introduced by Tom Hunt in 1978. The wound healing module consists of a front of macrophages degrading damaged tissue followed by newly formed blood vessels and fibroblasts. In the advancing zone neutrophilic leucocytes, which have emigrated from the invading blood vessels, are also seen.


A process of healing in which ischemic pulp tissue, which results from the rupture of the apical neurovascular supply, becomes gradually replaced with new tissue. This process can take place in two modalities:

  • Gradual replacement of the ischemic pulp tissue by migration of new tissue from the apical area (the most common). Under optimal conditions this will result in the replacement of the injured ischemic pulp tissue with new pulp tissue possessing some of the characteristics of normal pulp tissue, including the ability to form a new odontoblastic layer lining the root canal.
  • Immediate revascularization when optimal repositioning allows an end-to-end anastomosis in the apical area between ruptured blood vessels. This implies that the vascular supply is re-established after a few days and existing odontoblasts survive.

In some cases the pulp tissue specificity is lost when fibrous tissue replaces the original pulp or, in rare cases, a pulp metaplasia occurs where bone, periodontal ligament and cementum are formed inside the root canal.

A partial revascularization may occur if bacteria gain access to the coronal part of the ischemic pulp.

Definitions of tooth development and eruption disturbances of permanent teeth related to injury to the primary predecessors


These lesions appear as sharply demarcated, stained enamel opacities, most often located on the facial surface of the crown; their extent varies from small spots to large areas. These color changes are usually not associated with clinically detectable defects in the enamel surface. In this context, it should be mentioned that white enamel discolorations with a diameter of less than 0.5 mm are frequent in teeth without a history of trauma to their predecessors.


These lesions are a more severe manifestation of trauma sustained during the formative stage of the permanent tooth germ. The typical finding, which distinguishes these from white or yellow-brown discolorations of enamel, is a narrow horizontal groove which encircles the crown cervical to the discolored areas. In some cases, an external defect is found centrally in the coronally placed white or yellow-brown lesions.


Dilaceration malformations of the tooth crown are due to traumatic non-axial displacement of already formed hard tissue in relation to the developing soft tissues. Due to their close contact to the primary incisors, crown dilacerated teeth are usually maxillary or mandibular central incisors. Approximately half of these teeth become impacted, whereas the remaining half erupt normally or in facio- or linguo-version.


Odontoma-like malformations are rare sequelae to injuries in the primary dentition. Reported cases are confined primarily to maxillary incisors. The histology and radiology of these cases show a conglomerate of hard tissue, having the morphology of a complex odontoma or separate tooth elements. Experimental evidence supports the theory that these malformations occur during early phases of odontogenesis and affect the morphogenetic stages of ameloblastic development.


Root duplication is a rare occurrence seen following intrusive luxation of primary teeth. This complication is usually the result of an injury at the time when half or less than half of the crown is formed. The pathology of these cases indicates that a traumatic division of the cervical loop occurs at the time of injury, resulting in the formation of two separate roots. Radiographically, a mesial and distal root can be demonstrated, which extends from a partially formed crown.


Vestibular root angulation is a developmental disturbance which appears as a marked curvature confined to the root as a result of an injury sustained between ages 2 to 5 years. The malformed tooth is usually impacted and the crown palpable in the labial sulcus. The only teeth demonstrating this malformation are maxillary central incisors.


Lateral root angulation or dilaceration are changes that appear as a mesial or distal bending confined to the root of the tooth. The dilaceration appears to be the result of an acute displacement of the tooth germ. The root angulation is possibly created when the erupting tooth meets an obstacle such as scar tissue during eruption.


Partial or complete arrest of root formation is a rare complication. This disturbance reflects a primary tooth injury that displaces a developing successor in such a way that Hertwig’s epithelial root sheath has been partly or totally destroyed.


Sequestration of permanent tooth germs is exceedingly rare after injuries to the primary dentition. In these instances, swelling, suppuration and fistula formation are typical clinical features that sometimes lead to spontaneous sequestration of the involved tooth germ. Radiographic examination discloses osteolytic changes around the tooth germ, including disappearance of the outline of the dental crypt and expanded cortical alveolar bone.


Disturbances in permanent tooth eruption may occur after trauma to the primary dentition. It is suggested that this is related to abnormal changes in the connective tissue overlying the tooth germ. The eruption of succeeding permanent incisors is generally delayed for about 1 year after premature loss of primary incisors, whereas premature eruption of permanent successors is rare. Early loss of primary incisors (avulsion or extraction) leads to space loss only in rare instances. However, ectopic eruption of permanent successors can occur, possibly due to lack of eruption guidance otherwise provided by the primary teeth. These succedaneous teeth often erupt labially to their normal position. Impaction is very common among teeth with malformations confined to either the crown or the root. When the permanent tooth does erupt, it is often in facio- or linguo-version.

Dental Trauma Guide 2010 - produced in cooperation with the Resource Centre for Rare Oral Diseases and Department of Oral and Maxillo-Facial Surgery
at the University Hospital of Copenhagen - Last edited the 07-01-2014.