A NOTE ON SPACE MAINTENANCE IN THE PRIMARY DENTITION

SPACE MAINTENANCE IN THE PRIMARY DENTITION

Space maintenance can be defined as the provision of an appliance (active or passive) which is concerned only with the control of space loss without taking into consideration measures to supervise the development of dentition.

Space maintainers are appliances used to maintain space or regain minor amounts of space lost, so as to guide the unerupted tooth into a proper position in the arch.

IDEAL REQUIREMENTS

• It should maintain the entire mesio-distal space created by a lost tooth.
• It must restore the function as far as possible & prevent over-eruption of opposing teeth.
• It should be simple in construction.
• It should be strong enough to withstand the functional forces.
• It should not exert excessive stress on adjoining teeth.
• It must permit maintenance of oral hygiene.
• It must not restrict normal growth & development and natural adjustments which take place during the transition from deciduous to permanent dentition.
• It should not come in the way of other functions.

A Note on Bone Swellings in Jaw Bones

Bone Swellings

Bone swellings are lesions that characteristically present as asymptomatic hard lumps, covered by normal epithelium. Developmental disorders, benign and malignant tumors are included in this group of lesions.

•        Torus mandibularis
•        Torus palatinus
•        Multiple exostoses
•        Osteoma
•        Osteosarcoma
•         Chondrosarcoma
•         Burkitt lymphoma
•         Multiple myeloma
•         Paget disease
•       Odontogenic tumors

Torus Mandibularis

Definition and etiology Torus mandibularis is a developmental malformation of unknown etiology.

Clinical features It presents as an asymptomatic bony swelling, covered by normal mucosa. The lesion displays slow growth during the second and third decades of life. Characteristically, the lesions appear bilaterally on the lingual surface of the mandible, usually in the area adjacent to the bicuspids. The diagnosis is based on clinical criteria.

Torus mandibularis

Treatment Unnecessary unless full denture construction is required.

Torus Palatinus

Torus palatinus at the midline of the hard palate

Definition and etiology Torus palatinus is a developmental malformation of unknown etiology.

Clinical features It presents as a slow-growing, nodular, lobular or spindled, asymptomatic bony swelling covered by normal mucosa. Characteristically, the lesion appears along the midline of the hard palate.It occurs more often in women, and usually appears during the third decade of life. The diagnosis is based on the clinical findings.

Treatment Unnecessary unless full denture construction is required.

Multiple Exostoses

Multiple exostoses may occur on the buccal surface of the maxilla, and rarely on the mandible. Clinically, the lesions appear as multiple asymptomatic bony swellings. The diagnosis is based on the clinical findings.

Multiple exostoses on the maxilla.

Treatment Unnecessary unless full denture preparation is required.

Osteoma

Definition Osteoma is a benign neoplasm that consists of mature compact or cancellous bone.

Etiology Unknown.

Clinical features

It presents as an asymptomatic, slow-growing bony swelling of the jaws. The size ranges from a few millimeters to several centimeters. Multiple jaw osteomas are a common feature of Gardner syndrome.

Gardner syndrome: osteoma of the mandible.

Laboratory tests Histopathological examination, radiography.

Differential diagnosis Exostoses, osteosarcoma.

Treatment Surgical excision.

Osteosarcoma

Definition Osteosarcoma is the most common primary malignant neoplasm of bone.

Etiology Unknown.

Clinical features

The jaws are affected in 6–7% of cases, and usually during the third decade of life. Both jaws are affected equally and it is more common in men. Clinically, the lesion presents as a rapidly growing hard swelling that progressively produces facial deformity. Pain, paresthesia, tooth loosening, and nasal obstruction may also occur.

Osteosarcoma of the upper jaw, presenting as a hard swelling.

Laboratory tests Histopathological examination, radiography, CT scans.

Differential diagnosis Chondrosarcoma, Ewing sarcoma, metastatic tumors, odontogenic tumors and cysts, giant-cell tumor.

Treatment Surgical excision and supplementary radiotherapy and chemotherapy.

Chondrosarcoma

Chondrosarcoma  is more common in men than in women, between 30 and 60 years of age. Clinically, it appears as a painless hard swelling that progressively enlarges, causing extensive bone destruction with pain and loosening of the teeth.

Burkitt Lymphoma

Definition Burkitt lymphoma is a high-grade malignant B-lymphocyte lymphoma.

Etiology Epstein–Barr virus is closely associated.

Clinical features

The malignancy is prevalent in central Africa (the endemic form), and usually affects children 2–12 years of age. Cases have also been observed in other countries (the nonendemic form), and recently in patients with AIDS. The jaws are the most common site of lymphoma (60–70%). Clinically, it presents as a rapidly growing hard swelling that causes bone destruction, tooth loss, and facial deformity.Pain, paresthesia and large ulcerating or nonulcerating masses may also be seen.

Burkitt lymphoma, facial deformity.

Burkitt lymphoma, gingival mass

Burkitt lymphoma on the gingiva in a young patient with AIDS

Laboratory tests Histopathological examination, radiography.

Differential diagnosis Central giant-cell granuloma, ossifying fibroma, other non-Hodgkin lymphomas, and odontogenic tumors.

Treatment Chemotherapy, radiotherapy.

Multiple Myeloma

Definition Multiplemyeloma is a relatively rare malignant plasma-cell disorder.

Etiology Unknown.

Clinical features The malignancy is more common in men over 50 years of age, and the jaws are affected in about 30% of cases. Clinically, it presents with bone swelling, tooth mobility, pain, and paresthesia. A painless soft swelling, usually on the alveolar mucosa and gingiva, may develop as part of the overall disease spectrum.

Multiple myeloma, swelling on the gingiva

Laboratory tests Bone-marrow biopsy, radiography, serum and urine protein electrophoresis.

Differential diagnosis Plasmacytoma, non-Hodgkin lymphoma, Ewing sarcoma, leukemia, Langerhans cell histiocytosis.

Treatment Chemotherapy, radiotherapy.

Paget Disease

Definition Paget disease, or osteitis deformans, is a chronic, relatively common disorder characterized by uncoordinated bone resorption and deposition.

Etiology Unknown.

Clinical features Clinically, the signs and symptoms develop gradually and are characterized by bone pain, headache, deafness, visual disorders, dizziness, and progressive bone enlargement. Progressive expansion of the maxilla and the mandible lead to symmetrical thickening of the alveolar ridges.

Paget disease, enlarged maxilla

Edentulous patients may complain that their dentures do not fit due to alveolar enlargement.

Paget disease, alveolar enlargement

Delayed wound healing, bleeding, and osteomyelitis after tooth extraction may occur. The maxilla is more frequently affected than the mandible. Malesare more often affected than females. Two major forms of the disease are recognized: (a) the monostotic, and (b) the polyostotic. The clinical diagnosis should be confirmed by a histopathological and radiographic examination. Elevations of serum alkaline phosphatase and urinary hydroxyproline levels are common findings.

Differential diagnosis Fibrous dysplasia, osteosarcoma, multiple exostoses, fibro-osseous lesions.

Treatment Most cases require no treatment. Calcitonin and bisphosphonates may slow the pathological process.

Odontogenic Tumors

Definition Odontogenic tumors are a group of lesions that originate from odontogenic epithelium and ectomesenchyme.

Etiology Unknown. Some are neoplasms and others hamartomas.

Classification On the basis of the tissue of origin, three major varieties are recognized: (a) tumors of odontogenic epithelium, (b) tumors of odontogenic ectomesenchyme, and (c) mixedod ontogenic tumors.

Clinical features Most odontogenic tumors are usually asymptomatic for long time and are discovered only during a routine radiographic examination. However, with time they may form a usually painless slow-growing swelling or expansion of the mandible or the maxilla.

Odontogenic myxoma, expansion of the retromolar area

Extraosseous calcifying epithelial odontogenic tumor presenting as a gingival mass

The clinical signs and symptoms are not diagnostic and the final diagnosis should be made by radiographic and histopathological examinations.

Differential diagnosis Different varieties of odontogenic tumors, odontogenic cysts, osteosarcomas, chondrosarcomas, multiplemyeloma.

Treatment Surgical excision.

A NOTE ON CLASSIFICATION, CLINICAL FEATURES, PATHOGENESIS OF PERIODONTAL POCKET

The periodontal pocket, defined as a pathologically deepened gingival sulcus, is one of the most important clinical features of periodontal disease. All different types of periodontitis share histopathologic features such as tissue changes in the periodontal pocket, mechanisms of tissue destruction, and healing mechanisms. They differ, however, in their etiology, natural history, progression, and response to therapy.

CLASSIFICATION

Deepening of the gingival sulcus may occur by coronal movement of the gingival margin, apical displacement of the gingival attachment, or a combination of the two processes.

Illustration of pocket formation indicating expansion in two directions (arrows) from the normal gingival sulcus (left) to the periodontal pocket (right)

Different types of periodontal pockets. A, Gingival pocket. There is no destruction of the supporting periodontal tissues. B, Suprabony pocket. The base of the pocket is coronal to the level of the underlying bone. Bone loss is horizontal. C, Intrabony pocket. The base of the pocket is apical to the level of the adjacent bone. Bone loss is vertical.

Pockets can be classified as follows:

Gingival pocket (pseudo pocket):

This type of pocket is formed by gingival enlargement without destruction of the underlying periodontal tissues. The sulcus is deepened because of the increased bulk of the gingiva

Periodontal pocket:

This type of pocket occurs with destruction of the supporting periodontal tissues. Progressive pocket deepening leads to destruction of the supporting periodontal tissues and loosening and exfoliation of the teeth.

Two types of periodontal pockets exist:

Suprabony (supracrestal or supraalveolar), in which the bottom of the pocket is coronal to the underlying alveolar bone.

Intrabony (infrabony, subcrestal or intraalveolar), in which the bottom of the pocket is apical to the level of the adjacent alveolar bone. In this second type, the lateral pocket wall lies between the tooth surface and the alveolar bone.

Pockets can involve one, two, or more tooth surfaces and can be of different depths and types on different surfaces of the same tooth and on approximating surfaces of the same interdental space . Pockets can also be spiral (i.e., originating on one tooth surface and twisting around the tooth to involve one or more additional surfaces). These types of pockets are most common in furcation areas.

Classification of pockets according to involved tooth surfaces. A, Simple pocket. B, Compound pocket. C, Complex pocket

CLINICAL FEATURES

Clinical signs such as bluish-red, thickened marginal gingiva;

A bluish-red vertical zone from the gingival margin to the alveolar mucosa;

Gingival bleeding, suppuration,or both;

Tooth mobility;

And diastema formation and symptoms such as localized pain or pain "deep in the bone" are suggestive of the presence of periodontal pockets.

The only reliable method of locating periodontal pockets and determining their extent is careful probing of the gingival margin along each tooth surface.

A, Extrusion of the central incisor and diastema associated with the periodontal pocket. B, The entire length of the periodontal probe inserted to the base of the periodontal pocket in the central incisor

Correlation of Clinical and Histopathologic Features of the Periodontal Pocket
Clinical Features	Histopathologic Features
1. The gingival wall of the periodontal pocket presents various degrees of bluish-red discoloration; flaccidity; a smooth, shiny surface; and pitting on pressure.	1. The discoloration is caused by circulatory stagnation; the flaccidity, by destruction of the gingival fibers and surrounding tissues; the smooth, shiny surface, by the atrophy of the epithelium and edema; the pitting on pressure, by edema and degeneration.
2. Less frequently, the gingival wall may be pink and firm.	2. In such cases, fibrotic changes predominate over exudation and degeneration, particularly in relation to the outer surface of the pocket wall. However, despite the external appearance of health, the inner wall of the pocket invariably presents some degeneration and is often ulcerated.
3. Bleeding is elicited by gently probing the soft tissue wall of the pocket.	3. Ease of bleeding results from increased vascularity, thinning and degeneration of the epithelium, and the proximity of the engorged vessels to the inner surface.
4. When explored with a probe, the inner aspect of the periodontal pocket is generally painful.	4. Pain on tactile stimulation is due to ulceration of the inner aspect of the pocket wall.
5. In many cases, pus may be expressed by applying digital pressure.	5. Pus occurs in pockets with suppurative inflammation of the inner wall.

On the basis of depth alone, however, it is sometimes difficult to differentiate between a deep normal sulcus and a shallow periodontal pocket. In such borderline cases, pathologic changes in the gingival distinguish the two conditions.

PATHOGENESIS

The initial lesion in the development ofperiodontitis is the inflammation of the gingiva in response to a bacterial challenge. Changes involved in the transition from the normal gingival sulcus to the pathologic periodontal pocket are associated with different proportions of bacterial cells in dental plaque. Healthy gingiva is associated with few microorganisms, mostly coccoid cells and straight rods. Diseased gingiva is associated with increased numbers of spirochetes and motile rods. However, the microbiota of diseased sites cannot be used as a predictor of future attachment or bone loss because their presence alone is not sufficient for disease to start or progress.

Extension of the junctional epithelium along the root requires the presence of healthy epithelial cells. Marked degeneration or necrosis of the junctional epithelium retards rather than accelerates pocket formation. Degenerative changes seen in the junctional epithelium at the base of periodontal pockets are usually less severe than those in the epithelium of the lateral pocket wall. Because migration of the junctional epithelium requires healthy, viable cells, it is reasonable to assume that the degenerative changes seen in this area occur after the junctional epithelium reaches its position on the cementum.

The transformation of a gingival sulcus into a periodontal pocket creates an area where plaque removal becomes impossible, and the following feedback mechanism is established:

The rationale for pocket reduction is based on the need to eliminate areas of plaque accumulation.

A NOTE ON DENTAL CALCULUS

Dental calculus

For the periodontal diseases:

•     The primary etiologic factor is: Is the dental plaque.
•       The associated factor: is the dental calculus, it helps in new formation of the plaque.
•       The modifying factor: is a systemic disease, it aggravates the disease when the plaque is presents.

 Calculus:

•    Is a mineralized dental plaque that occurs in the tooth surfaces & dental prosthesis, it has many forms:
•    Bridging over the gingival margin.
•     Follow the festooning shape of the dentition.
•     Lobular form.
•     In case of malalignment :àprotected area for the plaque à calculus

 Classification:

             Supragingival                  &               subgingival calculus..

         Generally: both can occur together or one may appear alone.

Subgingival calculus: 

•      Gingival fluid origin.
•       Below the crest of the gingival margin.
•       Hard, dark& flint like.
•       Greenish black or dark brown in color.
•       Firmly attached to the tooth, can’t be seen and detected by explorer No.621 probe.
•       Extent nearly to the base of the pocket in chronic periodntitis, but doesn’t reach the Junctional epithelium.

 Supragingival calculus:    

•     Saliva origin.
•    Coronal to the gingival margin. Can be composed of supra &sub gingival calculus.
•    Hard, clay like consistency, White, white yellowish in color& its color may be affected by the tobacco or food stain.
•     Easy to be seen in the oral cavity, may be generalized or localized.
•     Easy to be removed &usually recurrent especially in the: Lower incisors. 

• Most common location :near to the orifices of the S. glands’ ducts

Parotid gland’s duct ”stenson”----->opposite to buccal surface of maxillary molars.

Submandibular “bartholine” & sublingual “wharton” ducts ----->Lingual surface of lower incisors.

it’s shape : either covers the occlusal surfaces or  bridge like structure over interdental papilla.

                                                Calculus contents:

Inorganic contents:70-90%		Organic contents
2/3 of the calculus inorganic component is in crystalline form ;there are  4 types of crystals . The crystals are: hydroxyappatite ,58% à magnesium white locate,21%  àmost in post octacalcium phosphate,12% Brushite, 9% àmost in mandibular anteriors. Detected more frequently in supragingival calculus. Constitute the bulk. Generally 2 or more crystals are detected in the calculus. Incidence of 4 crystals à varies with age of calculus.		Mixture of  : Protein-poly saccharide complex + desquamated host cells (leukocytes & host cells) + microorganisms. Carbohydrates (1.9-9.1%): Glucose , glactose   ,mannose ,arabinose ,rhamnose glucoric acid ,glactouric acid glucoseamine & glactose amine. à all are present in saliva except : Rhaminose  &  arabinose . Salivary proteins (5.9-8.2%): Most are amino acids. lipids 0.2%:nutral fat ,fatty acids ,cholesterol ester, phospholipids & cholesterol.
*Contents:	The differences     Supra gingival calculus	Between: Sub gingival calculus
hydroxyappatite: Ca Ph : Mg white: brushite: ratio of Ca/Ph: sodium contents: salivary proteins:	Equal.   More. Less. More. Low.   Increase with the depth of PD pocket. Yes	Equal Less. More Less. Higher. No.

Calculocementum:

Is the calculus has morphological appearance similar to cementum. This is because the calculus is interdigitates the cementum & no differences between them.

Mode of attachment of the calculus to the tooth surface:

• Close adaptation under surface depression.
• In sub gingival calculus.
• By organic pellicle (very weak)
• Penetration of the bacteria to the cementum.
• Mechanical interlocking to the surface irregularities: resorption lacuna or caries, in the cementum by sharpies fibers.                          

Calculus formation:

Calculus is the dental plaque that undergoes mineralization.

Calcification starts                      4-8 hrs   after plaque.

50 % become mineralized after   2 days.

60-90                                          12 days.

• Plaque can be daily removed at home by brushing but the calculus is
• not ,it is only removed clinically by the dentist .

• Calculus formation à the bacterial action will stopped (adv) but it will act as stagnation area for new plaque accumulationà (protection for plaque). 

• Early plaque contains small amount of inorganic material but it will increase as the plaque develops into calculus. 

• All plaque doesn’t necessarily undergo calcification.

• It reaches a plateau of maximal mineral by 2 days.

• Microorganisms are not always essential in calculus formation. 

• Plaque has ability to conc. The Ca at  2-20 times it’s level in saliva. 

• There is a suggestion that Ph is more critical than Ca in plaque mineralization.

• Early plaque of heavy former àmore Ca ,3 times Ph &less K than non calculus former.

A Note On Definition, Diagnosis, Treatment & Prognosis Of Dental Trauma

Enamel Infraction

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

Diagnosis: normal gross anatomic and radiographic appearance; craze lines apparent, especially with transillumination.

Treatment objectives: to maintain structural integrity and pulp vitality.

General prognosis: Complications are unusual.

Crown fracture–uncomplicated

Definition: an enamel fracture or an enamel-dentin fracture that does not involve the pulp.

Diagnosis: clinical and/or radiographic findings reveal a loss of tooth structure confined to the enamel or to both the enamel and dentin.

Treatment objectives: to maintain pulp vitality and restore normal esthetics and function. Injured lips, tongue, and gingiva should be examined for tooth fragments. When looking for fragments in soft tissue lacerations, radiographs are recommended. For small fractures, rough margins and edges can be smoothed. For larger fractures, the lost tooth-structure can be restored.

 General prognosis: The prognosis of uncomplicated crown fractures depends primarily upon the concomitant injury to the periodontal ligament and secondarily upon the extent of dentin exposed. Optimal treatment results follow timely assessment and care.

Crown fracture–complicated

Definition: an enamel-dentin fracture with pulp exposure.

Diagnosis: clinical and radiographic findings reveal a loss of tooth structure with pulp exposure.

Treatment objectives: to maintain pulp vitality and restore normal esthetics and function. Injured lips, tongue, and gingiva should be examined for tooth fragments. When looking for fragments in soft tissue lacerations, radiographs are recommended.

• Primary teeth: Decisions often are based on life expectancy of the traumatized primary tooth and vitality of the pulpal tissue. Pulpal treatment alternatives are pulpotomy, pulpectomy, and extraction.

• Permanent teeth: Pulpal treatment alternatives are direct pulp capping, partial pulpotomy, full pulpotomy, and pulpectomy (start of root canal therapy). There is increasing evidence to suggest that utilizing conservative vital pulp therapies for mature teeth with closed apices is as appropriate a management technique as when used for immature teeth with open apices.

General prognosis: The prognosis of crown fractures appears to depend primarily upon a concomitant injury to the periodontal ligament. The age of the pulp exposure, extent of dentin exposed, and stage of root development at the time of injury secondarily affect the tooth’s prognosis. Optimal treatment results follow timely assessment and care.

Crown/root fracture

Definition: an enamel, dentin, and cementum fracture with or without pulp exposure.

Diagnosis: Clinical findings usually reveal a mobile coronal fragment attached to the gingiva with or without a pulp exposure. Radiographic findings may reveal a radiolucent oblique line that comprises crown and root in a vertical direction in primary teeth and in a direction usually perpendicular to the central radiographic beam in permanent teeth. While radiographic demonstration often is difficult, root fractures can only be diagnosed radiographically.

Treatment objectives: to maintain pulp vitality and restore normal esthetics and function.

• Primary teeth: When the primary tooth cannot or should not be restored, the entire tooth should be removed unless retrieval of apical fragments may result in damage to the succedaneous tooth.

• Permanent teeth: The emergency treatment objective is to stabilize the coronal fragment. Definitive treatment alternatives are: to remove the coronal fragment followed by a supragingival restoration or necessary gingivectomy, osteotomy, or extrusion (surgical or orthodontic) to prepare for restoration. If the pulp is exposed, pulpal treatment alternatives are pulp capping, pulpotomy, and root canal treatment.

General prognosis: Although the treatment of crown-root fractures can be complex and laborious, most fractured permanent teeth can be saved. Fractures extending significantly below the gingival margin may not be restorable. 

Root fracture

Definition: a dentin and cementum fracture involving the pulp.

Diagnosis: Clinical findings reveal a mobile coronal fragment attached to the gingiva that may be displaced. Radiographic findings may reveal 1 or more radiolucent lines that separate the tooth fragments in horizontal fractures. Multiple radiographic exposures at different angulations may be required for diagnosis. A root fracture in a primary tooth may be obscured by a succedaneous tooth.

Treatment objectives:

• Primary teeth: Treatment alternatives    include extraction of coronal fragment without insisting on removing apical fragment or observation. It is not recommended to reposition and stabilize the coronal fragment.

• Permanent teeth: Reposition and stabilize the            coronal fragment in its anatomically correct position as soon  as possible to optimize healing of the periodontal ligament and neurovascular supply while maintaining esthetic and functional integrity.

General prognosis: Pulp necrosis in root-fractured teeth is attributed to displacement of the coronal fragment and mature root development. In permanent teeth, the location of the root fracture has not been shown to affect pulp survival after injury. Therefore, preservation of teeth with root fractures occurring in the tooth’s cervical third should be attempted. Young age, immature root formation, positive pulp sensitivity at time of injury, and approximating  the dislocation within 1 mm have been found to be advantageous to both pulpal healing and hard tissue repair of the fracture.

Concussion

Definition: injury to the tooth-supporting structures without abnormal loosening or displacement of the tooth.

Diagnosis: Because the periodontal ligament absorbs the injury and is inflamed, clinical findings reveal a tooth tender to pressure and percussion without mobility, displacement, or sulcular bleeding. Radiographic abnormalities are not expected.

Treatment objectives: to optimize healing of the periodontal ligament and maintain pulp vitality.

General prognosis: For primary teeth, unless associated infection exists, no pulpal therapy is indicated. Although there is a minimal risk for pulp necrosis, mature permanent teeth with closed apices may undergo pulpal necrosis due to associated injuries to the blood vessels at the apex and, therefore, must be followed carefully.

Subluxation

Definition: injury to tooth-supporting structures with abnormal loosening but without tooth displacement.

Diagnosis: Because the periodontal ligament attempts to absorb the injury, clinical findings reveal a mobile tooth without displacement that may or may not have sulcular bleeding. Radiographic abnormalities are not expected.

Treatment objectives: to optimize healing of the periodontal ligament and neurovascular supply.

• Primary teeth: The tooth should be followed for pathology.

• Permanent teeth: Stabilize the tooth and relieve any occlusal interferences. For comfort, a flexible splint can be used. Splint for no more than 2 weeks.

General prognosis: Prognosis is usually favorable. The primary tooth should return to normal within 2 weeks. Mature permanent teeth with closed apices may undergo pulpal necrosis due to associated injuries to the blood vessels at the apex and, therefore, must be followed carefully.

Lateral luxation

Definition: displacement of the tooth in a direction other than axially. The periodontal ligament is torn and contusion or fracture of the supporting alveolar bone occurs.

Diagnosis: Clinical findings reveal that a tooth is displaced laterally with the crown usually in a palatal or lingual direction and may be locked firmly into this new position. The tooth usually is not mobile or tender to touch. Radiographic findings reveal an increase in periodontal ligament space and displacement of apex toward or though the labial bone plate.

Treatment objectives:

• Primary teeth: to allow passive or spontaneous repositiong if there is no occlusal interference. When there is occlusal interference, the tooth can be gently repositioned or slightly reduced if the interference is minor. When the injury is severe or the tooth is nearing exfoliation, extraction is the treatment of choice.

• Permanent teeth: to reposition as soon as possible and then to stabilize the tooth in its anatomically correct position to optimize healing of the periodontal ligament and neurovascular supply while maintaining esthetic and functional integrity. Repositioning of the tooth is done with digital pressure and little force. A displaced tooth may need to be extruded to free itself from the apical lock in the cortical bone plate. Splinting an additional 2 to 4 weeks may be needed with breakdown of marginal bone.

General prognosis: Primary teeth requiring repositioning have an increased risk of developing pulp necrosis compared to teeth that are left to spontaneously reposition. In mature permanent teeth with closed apices, pulp necrosis and pulp canal obliteration are common healing complications while progressive root resorption is less likely to occur.

Intrusion

Definition: apical displacement of tooth into the alveolar bone. The tooth is driven into the socket, compressing the periodontal ligament and commonly causes a crushing fracture of the alveolar socket.

Diagnosis: Clinical findings reveal that the tooth appears to be shortened or, in severe cases, it may appear missing. The tooth’s apex usually is displaced labially toward or through the labial bone plate in primary teeth and driven into the alveolar process in permanent teeth. The tooth is not mobile or tender to touch. Radiographic findings reveal that the tooth appears displaced apically and the periodontal ligament space is not continuous. Determination of the relationship of an intruded primary tooth with the follicle of the succedaneous tooth is mandatory. If the apex is displaced labially, the apical tip can be seen radiographically with the tooth appearing shorter than its contralateral. If the apex is displaced palatally towards the permanent tooth germ, the apical tip cannot be seen radiographically and the tooth appears elongated. An extraoral lateral radiograph also can be used to detect displacement of the apex toward or though the labial bone plate. An intruded young permanent tooth may mimic an erupting tooth.

Treatment objectives:

• Primary teeth: to allow spontaneous reeruption except when displaced into the developing successor. Extraction is indicated when the apex is displaced toward the permanent tooth germ.

• Permanent teeth: to reposition passively (allowing re-eruption to its preinjury position), actively (repositioning with traction), or surgically and then to stabilize the tooth with a splint for up to 4 weeks in its anatomically correct position to optimize healing of the periodontal ligament and neurovascular supply while maintaining esthetic and functional integrity. For immature teeth with more eruptive potential (root ½ to ²/³ formed), the objective is to allow for spontaneous eruption. In mature teeth, the goal is to reposition the tooth with orthodontic or surgical  extrusion and initiate endodontic treatment within the first 3 weeks of the traumatic incidence.

General prognosis: In primary teeth, 90% of intruded teeth will re-erupt spontaneously (either partially or completely) in 2 to 6 months. Even in cases of complete intrusion and displacement of primary teeth through the labial bone plate, a retrospective study showed the reeruption and survival of most teeth for more than 36 months. Ankylosis may occur, however, if the periodontal ligament of the affected tooth was severely damaged, thereby delaying or altering the eruption of the permanent successor. In mature permanent teeth with closed apices, there is considerable risk for pulp necrosis, pulp canal obliteration, and progressive root resorption. Immature permanent teeth that are allowed to reposition spontaneously demonstrate the lowest risk for healing complications. Extent of intrusion (7 mm or greater) and adjacent intruded teeth have a negative influence on healing.

Extrusion

Definition: partial displacement of the tooth axially from the socket; partial avulsion. The periodontal ligament usually is torn.

Diagnosis: Clinical findings reveal that the tooth appears elongated and is mobile. Radiographic findings reveal an increased periodontal ligament space apically.

Treatment objectives:

 •Primary teeth: to allow tooth to reposition spontaneously or reposition and allow for healing for minor extrusion (<3 mm) in an immature developing tooth. Indications for an extraction include severe extrusion or mobility, the tooth is nearing exfoliation, the child’s inability to cope with the emergency situation, or the tooth is fully formed.      

• Permanent teeth: to reposition as soon as possible and then to stabilize the tooth in its anatomically correct position to optimize healing of the periodontal ligament and neurovascular supply while maintaining esthetic and functional integrity. Repositioning may be accomplished with slow and steady apical pressure to gradually displace coagulum formed between root apex and floor of the socket. Splint  for up to 2 weeks.

General prognosis: There is a lack of clinical studies evaluating repositioning of extruded primary teeth.6 In permanent mature teeth with closed apices, there is considerable risk for pulp necrosis and pulp canal obliteration. These teeth must be followed carefully.

Avulsion

Definition: complete displacement of tooth out of socket. The periodontal ligament is severed and fracture of the alveolus may occur.

Diagnosis: Clinical and radiographic findings reveal that the tooth is not present in the socket or the tooth already has been replanted. Radiographic assessment will verify that  the tooth is not intruded when the tooth was not found.

Treatment objectives:

•Primary teeth: to prevent further injury to the developing successor. Avulsed primary teeth should not be replanted because of the potential for subsequent damage to developing permanent tooth germs.     

• Permanent teeth: to replant as soon as possible and then to stabilize the replanted tooth in its anatomically correct  location to optimize healing of the periodontal ligament  and neurovascular supply while maintaining esthetic and functional integrity except when replanting is contra-indicated by:

1.  The child’s stage of dental development (risk for ankylosis where considerable alveolar growth has to take place);

2.   Compromising medical condition; or

3.   Compromised integrity of the avulsed tooth or supporting tissues.

 Flexible splinting for 2 weeks is indicated. Tetanus  prophylaxis and antibiotic coverage should be considered. Treatment strategies are directed at avoiding inflammation that may occur as a result of the tooth’s attachment damage and/or pulpal infection.

General prognosis: Prognosis in the permanent dentition is primarily dependent upon formation of root development and extraoral dry time. The tooth has the best prognosis if replanted immediately. If the tooth cannot be replanted within 5 minutes, it should be stored in a medium that will help maintain vitality of the periodontal ligament fibers. The best (ie, physiologic) transportation media for avulsed teeth include (in order of preference) Viaspan, Hank’s Balanced Salt Solution (tissue culture medium), and cold milk. Next best would be a non-physiologic medium such as saliva (buccal vestibule), physiologic saline,  or water. Although water is detrimental to cell viability due to its low osmolality and long term storage (ie, more than 20 minutes) in water has an adverse effect on periodontal ligament healing, it is a better choice than dry storage. Limited tooth storage in a cell-compatible medium prior to replantation has produced similar healing results as compared with immediately-replanted teeth.

The risk of ankylosis increases significantly with an extraoral dry time of 20 minutes An extraoral dry time of 60 minutes is considered the point where survival of the root periodontal cells is unlikely. In permanent avulsed teeth, there is considerable risk for pulp necrosis, root resorption, and ankylosis.

Additional considerations: Recent evidence suggests that success of replantation is dependent upon many factors, some of which the clinician can manipulate in a manner that favors more successful outcomes. Decision trees for acute management of avulsed permanent incisors have been developed with up-to-date information in an easy to use  flowchart format.

Revascularization: An immature (ie, open apex) tooth has  the potential to establish revascularization when there is a minimum of a 1.0 mm apical opening. Complete pulpal revascularization has been shown to occur at a rate of 18% among immature teeth. It appears that antibiotic treatment reduces contamination of the root surface and/or pulp space, thereby creating a biological environment that aids revascularization. On the other hand, a mature tooth (ie, closed apex or apical opening <1 mm) has little or no chance of revascularization. Researchers have demonstrated that immature teeth soaked in doxycycline solution have a greater rate of pulp revascularization.

Periodontal ligament (PDL) management – transitional therapy: When a tooth has been out of the oral cavity and in a dry environment for greater than 60 minutes, the PDL has no chance of survival. If such a tooth is replanted, it is likely to undergo osseous replacement resorption and, over time, the tooth will become ankylosed and ultimately will be lost. Because pediatric dentists need to consider the growth and development of the child patient, the goal for a tooth that has been avulsed for greater than 60 minutes with dry storage is to delay the osseous replacement and, hence, ankylotic process as long as possible. To slow down this process, the remaining PDL should be removed because otherwise it becomes a stimulus for inflammation that accelerates infection-related resorption. The remaining PDL can be removed by several methods: gentle scaling and root planning, soft pumice prophylaxis, gauze, or soaking the tooth in 3% citric acid for 3 minutes. This should be followed by a sodium fluoride treatment for 20 minutes. The rationale for this fluoride soak is based upon evidence that this procedure will delay, but not prevent, ankylosis; fluoroapatite is more resistant to ankylosis than hydroxy-apatite. When teeth are soaked in fluoride before replantation, it has been shown to reduce significantly the risk of resorption after a follow-up of 5 years. Despite these recommendations, teeth that have been out of the  oral cavity for greater than 60 minutes with dry storage  have a poor prognosis and will not survive long term.

Possible contraindications to replantation: There are possible contraindications to tooth replantation. Examples are  immunocompromised health, severe congenital cardiac anomalies, severe uncontrolled seizure disorder, severe mental disability, severe uncontrolled diabetes, and lack of alveolar integrity.

Current research: Antiresorptive-regenerative therapies may have potential for enhancing the prognosis of avulsed teeth.

Treatment strategies are directed at avoiding or minimizing inflammation, increasing revascularization, and producing hard barriers in teeth with open apices. New treatment strategies also are directed at specific clinical challenges that include decoronation as an approach to treat ankylosis in growing children and transplantation of premolars as an approach for replacing avulsed teeth. Dental practitioners should follow current literature and consider carefully evidence-based recommendations that may enhance periodontal healing and revascularization of avulsed permanent teeth.