DENTAL TRAUMA

ppt / sas

Maxillary Incisors

most frequently injured teeth in the primary dentition

2-4 years → Peak age for injuries to the primary teeth

Crown Fractures → are the most common injuries to the primary teeth

Questions to ask in history taking

When did the trauma occur?

How did the trauma occur?

Were there any other injuries?

What initial treatment was given?

Have there been any other dental injuries in the past?

Are current immunizations up to date?

Battle sign or bruising of the mastoid region

is associated with base-skull fracture

NON-ACCIDENTAL TRAUMA

Up to 50% of abused children suffer head/neck injuries, Immediately suspect abuse if:

• Injuries are in various stages of healing

• Labial frena are inexplicably torn

• History provided is inconsistent with clinical presentation.

ANATOMICAL RISK

Vector: Maxillary incisors are the most frequently injured teeth.

Vulnerability: Protruding incisors (Class II malocclusion) increase trauma risk by 2-3x

PRIMARY VECTORS

Automobile accidents

Pacifier use

Indirect trauma

Automobile accidents

(unrestrained impacts)

Major cause of dental injuries

Pacifier use

(deflects force, causing displacement rather than fracture).

Indirect trauma

(blows to the chin).

PRIMARY INCISOR

Spongy Bone. The alveolar bone in young children is highly resilient and spongy, absorbing impact by allowing the tooth to move rather than crack.

Lower Crown-to-Root Ratio. A proportionally shorter root provides less leverage resistance against impact forces.

Primary teeth luxate (displace) far more often than they fracture when compared to permanent teeth.

Children with protruding incisors(class II malocclussions) are 2-3x more likely to suffer dental trauma

PERMANENT INCISOR

Dense alveolar bone and a higher crown-to-root ratio firmly anchor the tooth, making coronal fracture the path of least resistance during impact.

Prioritizing Critical Interventions

Triage:

• dental history (standard)

• CNS red flags (medical referral)

• tetanus alert

dental history (standard)

Assess the fundamental metrics of the injury:

• When: Determine exact time elapsed. Dictates viability of interventions (e.g., repositioning before coagulum forms)

• Where: Environmental context hints at wound contamination

• How: Mechanism of injury dictates structural damage severity.

CNS red flags (medical referral)

Rule out cervical spine and traumatic brain injuries. Immediately refer to physician if the patient exhibits:

• Loss of consciousness or amnesia

• Vomiting or nausea

• Disorientation or altered mental state

• Neck stiffness (c-spine risk)

Monitor closely for 24 hours (wake every 2-3 hours)

tetanus alert

Critically assess vaccination status specifically for:

• Dirty wounds (soil-embedded intrusions)

• Avulsions or deep lacerations

Children require 5 injections by age 4-6, plus boosters. Consult physician if status is unknown or incomplete.

Systematic Examination

Facial Skeleton: Palpate for discontinuities.

TMJ: Check for swelling, crepitus, or clicking.

Mastoid Region: Look for Battle Sign (bruising behind the ear indicates a base-skull _fracture).

Soft Tissue Lacerations: Clear all foreign debris from lips/ cheeks immediately to prevent disfiguring fibrosis.

Occlusion: Check for disturbances caused by palatally luxated incisors.

Crown Integrity: Transilluminate crowns to detect subtle cracks or color shifts.

Routine pulp vitality testing

is NOT reliable in the primary dentition due to patient age and reporting capability. Instead, rely on percussion:

2 reasons to percuss:

• Sensitivity in response to percussion gives information about the extent of damage to the apical tissues

• The sound in response to percussion is also an important indicator of the likelihood of ankylosis

Radiographic Baseline & Soft Tissue Protocol

Image all traumatized teeth to assess root development, fractures, and the critical relationship to the developing permanent tooth bud.

Soft Tissue Technique:

• Use 1/4 standard exposure time with film placed behind the lip/cheek to detect embedded tooth fragments in lacerations.

Follow-Up Imaging Timeline:

Baseline /Injury day

• 3 Weeks: Periapical radiolucencies (necrosis) become detectable

• 6-7 Weeks: Inflammatory root resorption ankylosis or becomes visible.

• Standard Recall: 1 month postoperative; wait 6 months if asymptomatic

All traumatized teeth should be radiographed to assess:

Stage of root development

Injuries to root and developing structures

Ellis & Davey Fracture Classification I

Simple fracture involving little to no dentin. Presents smooth sharp edges. Restore primarily for esthetics or smooth to prevent soft tissue irritation.

Ellis & Davey Fracture Classification II

Extensive fracture involving considerable dentin, but the pulp is intact. Requires covering exposed dentin to prevent pulpal irritation.

Ellis & Davey Fracture Classification III

Extensive fracture exposing the dental pulp. Appears as a red dot or bleeding point. Requires immediate endodontic intervention or extraction.

Ellis & Davey Fracture Classification IV

Complete loss of the clinical crown.

Cervical/Partial Pulpotomy

management for class III crown fracture with vital pulp + thin root dentin (open apex) to preserve vitality

Complete Pulpectomy (fill with resorbable paste).

management for class III crown fracture with Necrotic or Neglected Pulp

Immediate Extraction

management for class III crown fracture with Massive Resorption / Follicle at Risk to protect permanent bud.

Remove loose fragment. Perform pulpotomy on main stable fragment.

management for crown-root fracture (split tooth) with Shallow Splitting (Supracrestal)

Extract both fragments. Unrestorable

management for crown-root fracture (split tooth) with Deep Splitting (Creates Periodontal Pocket)

2 ways to determine fracture depth in crown-root fracture / split tooth

Shallow Splitting (Supracrestal)

Deep Splitting (Creates Periodontal Pocket)

MECHANICS OF CHIN BLOWS

Sudden, forced closure of the mandible causes indirect trauma. Watch for:

• Posterior crown fractures

• Condylar, symphysis, or mental mandibular fractures

ROOT FRACTURE DYNAMICS

The coronal fragment is typically pushed lingually. If the mobile coronal fragment interferes with occlus

THE APICAL FRAGMENT RULE

NEVER attempt to surgically dig out or retrieve a retained apical root fragment. Surgical intervention risks catastrophic damage to the succedaneous permanent tooth bud. The fragment must be left alone to undergo physiologic resorption.

concussion

Clinical Presentation:

• NOT mobile. NOT displaced. Tender to biting and percussion.

PDL Status:

• PDL absorbs impact and is inflamed (leaves the tooth tender to biting pressure and percussion)

Radiographic Findings:

• Normal. No changes.

Management:

• No tx. Monitor pulpal condition. Soft diet. Meticulous hygiene.

subluxation

Clinical Presentation:

• LOOSENED, but NOT displaced. Bleeding from gingival crevice.

PDL Status:

• PDL damaged but attachment remains largely intact.

Radiographic Findings:

• Widened periodontal ligament space.

Management:

• Monitor. Soft diet. Chlorhexidine application.

intrusion

Tooth is DRIVEN INTO ITS SOCKET Compressed PDL and crushed alveolar socket

management:

• If the root of the primary tooth is pushed against the crown of the permanent incisor, it may severely damage the developing tooth bud. Immediate removal of the primary tooth to relieve the pressure and minimize damage

• Intruded incisors that do not pose a risk the permanent teeth can be left to spontaneously reerupt.

extrusion

Clinical Presentation:

• ELONGATED from socket. Increased mobility. Central dislocation.

PDL Status:

• PDL is severely torn. High risk of ischemia.

Radiographic Findings:

• Increased periapical radiolucency / apical gap.

Management:

• Reposition and splint, or extract based on severity and apex closure.

lateral luxation

clinical presentation:

• Displaced labially, lingually, or laterally. PDL is torn. Alveolar bone is contused or fractured.

management:

• Mild: Allow spontaneous repositioning.

• Severe: Reposition and splint (7-14 days), initiate endodontic therapy, or extract if labial bone is heavily fractured.

lingual luxation

clinical presentation:

• Crown moves palatally (often interfering with occlusion); apex is pushed labially. Labial bone plate is fractured.

management:

• Reposition immediately before coagulum forms.

• Utilize intentional open bite (composite buttons on molars) to clear occlusion.

• Extract if severely displaced.

labial root displacement

80% of cases are safe

clinical signs:

• Palatal crown inclination.

• Hard swelling palpated in the labial vestibule.

Radiograph:

• Tooth appears foreshortened and highly opaque.

management:

• safe to preserve

• Allow spontaneous re-eruption (typically begins within 2 to 6 months). Monitor for rotation.

palatal root displacement

dangerous

clinical signs:

• Root is pressed directly against the developing permanent tooth bud.

Radiograph:

• Tooth appears elongated.

management:

• immediate extraction

• Extract immediately to relieve pressure and minimize irreversible damage to the permanent successor.

avulsion

The tooth is COMPLETELY DISPLACED from the alveolus PDL is Severed Fractures of alveolar bone may occur

general rule: Avulsed primary incisors are NEVER replanted.

The Biomechanical Risk:

Complete displacement from the alveolus severs the PDL. Reinsertion forces the contaminated root or coagulum directly into the delicate follicle of the developing permanent successor, irreversibly irreversibly damaging it in up to 75% of cases.

Next Steps:

1. Account for the avulsed tooth immediately to rule out aspiration.

2. If a well-meaning parent has already replanted the tooth at home, advise them of the extreme risk. If retained, it requires splinting and immediate root canal treatment with resorbable paste to prevent rapid inflammatory resorption.

Pathologic Sequelae of Trauma to the Teeth

reversible pulpitis

infection of the periodontal ligament

coronal discoloration

pink / red discoloration

Observed shortly after the injury may represent intrapulpal hemorrhage

early presentation:

• Intrapulpal hemorrhage

• Rupture of blood vessels causes extravasation of RBCs into dentinal tubules.

late presentation:

• Internal resorption

• The coronal dentin is destroyed from within

• Apical root can be left to resorb spontaneously if the crown is lost.

yellow discoloration

Can be seen when the dentin is thick and the pulp chamber narrower than usual. This condition is termed as pulp canal obliteration

• pathology

  • Pulp Canal Obliteration (PCO)

  • Accelerated deposition of thick dentin narrows the pulp chamber.

• pathology

  • Pathologic, but requires NO treatment.

  • Monitor radiographically.

dark (gray / black)

RBC hemolysis, Often indicates pulp necrosis.

When the pulp becomes necrotic or when pulpal hemorrhage occurs, red blood cells lyse and release hemoglobin.

Hemoglobin and its derivatives such as hematin molecules that contain iron ions, invade the dentin tubules and stain the tooth dark.

management:

• this color alone does NOT mandate extraction. Over 70% of asymptomatic dark primary incisors exhibit no radiographic pathology.

• Extract or treat endodontically ONLY if swelling, fistula, mobility, or periapical radiolucency are present.

internal resorption

Odontoclasts attack dentin from within due to chronic inflammation. Can lead to root perforation.

external (atypical) resoprtion

aka: ankylosis

Gradual elimination of apical root dentin with preservation of the PDL. Mimics early natural exfoliation.

Results after irreversible injury to the PDL

Alveolar bone directly contacts and fuses with the root surface

rapidly progressing (inflammatory)

Related to necrotic pulp and inflamed PDL. Extremely rapid destruction. Requires immediate endodontic filling with resorbable paste.

replacement (ankylosis)

Irreversible PDL injury causes alveolar bone to fuse directly to the root surface.

Complications for the Permanent Dentition

arrested development

follicle deflection

enamel defects

space loss & ectopic eruption

arrested development

Loss of pulp vitality at an early age halts dentin apposition, apposition, leaving the primary tooth with thin, fragile root walls.

follicle deflection

An infected, expanded primary follicle can physically push and deflect the permanent central incisor away from its normal eruption path.

enamel defects

Permanent incisors succeeding infected primary teeth often present with enamel hypoplasia caused by the inflammatory cascade or over-instrumentation during primary endodontics.

space loss & ectopic eruption

Premature loss of primary incisors (especially before canine eruption) leads to arch crowding, delayed permanent eruption, and a İack of eruption guidance.

at-home care protocols

Diet Modification: Maintain a strictly soft diet for 7-14 days to stabilize luxated or repositioned teeth.

Topical Disinfection: Apply 0.2% chiorhexidine gluconate to the injured gingiva twice daily.

Application Technique: Use a cotton-tipped applicator to swab the crevices. Do not use as a rinse to prevent the toddler from swallowing the solution while effectively disinfecting the torn PDL.

monitoring & clinical alerts

Vigilance for Infection:

• Return to the clinic immediately if facial swelling, red mucosal tracking, or a "pimple" (fistula) appears on the gums.

• Watch closely for suddenly increased tooth mobility or expressions of chewing sensitivity.

Reassurance on Esthetics:

• Warn parents that the tooth may transition to a dark gray or black color over the coming weeks.

• Reassure them that color change without associated pain or swelling often requires monitoring only, not immediate surgical extraction.

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