Renata Pazera1, *Joanna Szczepańska2
Resorption as a sequela of dental trauma – diagnosis and management
Resorpcja jako powikłanie pourazowe – diagnostyka, leczenie
1Doctoral studies, Dentistry of Developing Dentition Department, Medical University of Łódź
Head of Department: Professor Joanna Szczepańska, MD, PhD
2Dentistry of Developing Dentition Department, Medical University of Łódź
Head of Department: Professor Joanna Szczepańska, MD, PhD
Mechaniczne uszkodzenie powierzchni tkanek przyzębia w trakcie m.in. intruzji lub zwichnięcia całkowitego staje się potencjalnym obszarem wystąpienia resorpcji. Celem pracy było przedstawienie na podstawie piśmiennictwa resorpcji patologicznej występującej w zębach stałych u dzieci, ze szczególnym uwzględnieniem diagnostyki, mechanizmu powstania oraz metod leczniczych. Zwrócono uwagę na jej związek przyczynowo-skutkowy po wystąpieniu urazu.
Często przyczyną zgłaszania się do gabinetu stomatologicznego w wieku rozwojowym jest uraz zębów stałych. Resorpcja jest jednym z możliwych poważnych powikłań, która może doprowadzić do utraty zęba. Na podstawie piśmiennictwa przytoczono metody zmniejszające ryzyko jej wystąpienia oraz skutki późnego wykrycia zmiany. Podkreślono istotę wizyt kontrolnych i wyszczególniono niepokojące zmiany kliniczno-radiologiczne mogące świadczyć o istnieniu resorpcji. Przedstawiono schematy leczenia endodontycznego oraz postępowanie w przypadku ankylozy.
Podsumowując, resorpcja jako powikłanie po urazie stanowi nieraz ryzyko utraty zęba pomimo prawidłowego zaopatrzenia zęba. Działanie czynnika uszkadzającego wraz z czynnikiem podtrzymującym, jakim jest m.in. infekcja, uniemożliwia samoistną regenerację tkanek przyzębia i skutkuje rozwojem resorpcji, nawet po długim czasie od wystąpienia urazu. Uświadomienie rodziców o istocie wizyt kontrolnych jest ważne dla możliwości wykrycia powikłań w odpowiednim czasie.
The area of mechanical damage rendered to the periodontal tissues upon intrusion or tooth avulsion becomes a potential site of resorption. The purpose of this study is to present the phenomenon of pathological resorption occurring in permanent teeth in children, with a particular emphasis on the course of diagnosis, the mechanism of occurrence, and the treatment options. Special attention has been paid to the cause-and-effect relationship between resorption and dental trauma.
Patients in developing age commonly seek the dentist’s help following dental trauma. Resorption is among the possible serious sequelae, potentially leading to loss of the tooth. Based on literature review, methods that reduce the risk of its occurrence, and the effects of a delayed diagnosis have been listed. The importance of follow-up appointments has been stressed, and the clinical and radiologic findings have been specified. Endodontic therapy protocols have also been presented, along with the indicated course of treatment for ankylosed teeth.
To recapitulate, resorption due to trauma frequently poses a risk of tooth loss in spite of adequate tooth treatment immediately following the trauma. The combined effect of the damaging factor and a stimulating factor such as an infection, may render the self-regeneration of the periodontal tissues impossible, and result in the development of resorption, even a long time after the trauma. The parents’ awareness concerning the importance of follow-up dental appointments is vital for a timely diagnosis of potential complications.
Resorption is a process leading to loss of the tissue of a tooth or the alveolar bone. In normal conditions it affects the roots of the primary teeth. Root resorption in permanent teeth is a pathological process. It is classified by its aetiology, advancement, and location. Dental trauma is among the initiating factors of external resorption, as it severs the periodontal ligament. Its progress depends on the presence of a stimulating factor such as an infection. Statistically, it is most common following tooth avulsion or intrusion (1, 2).
Adequate treatment of the traumatized tooth does not complete the therapy. The patient needs to be informed of the importance of the follow-up appointments. Early diagnosis of sequelae, including resorption, allows to arrest the pathological process, and facilitates longer survival of the tooth within the oral cavity. Management of resorption frequently fails, hence the significance of following strictly the current guidelines, including those by the International Association of Dental Traumatology, to reduce the risk of its occurrence (2, 3).
Management of internal resorption and external inflammatory resorption consists in endodontic therapy and temporary filling with calcium hydroxide. Chemo-mechanical preparation of the canal and introduction of an alkaline intracanal medicament improves the topical condition. The preferred method of canal obturation is the use of a liquid gutta-percha to seal sinus tracts, and prevent tension of the thinned and weakened root walls. The point where the sinus tract meets the periodontal ligament is treated with e.g. Mineral Trioxide Aggregate (MTA). Replacement resorption is not treated endodontically. An ankylosed tooth does not erupt, and in patients with developing dentition the growth of the alveolar ridge is arrested, resulting with an infra-position of the tooth. In such clinical conditions, the course of treatment is aimed at preserving a good quality alveolar ridge for further implantation and prosthetic treatment upon the completion of the patient’s growth. In such circumstances, coronectomy may be adopted as the treatment of choice (3, 4).
In this work on the basis of the literature was shown the mechanism of resorption, ways of avoid, diagnostic methods and treatment.
Ental trauma in children
Dental appointments due to teeth trauma in children have been on the rise. Among all injuries requiring treatment, dental traumas account for 5%. The analysis of all the of traumas treated at the Dentistry of Developing Dentition Department of the Medical University of Łódź in 2000-2003 revealed the most common reason for seeking dental help to be crown fractures involving a substantial part of the dentine without pulpal exposure, followed by subluxations (55 and 13% respectively of the total number of patients affected with dental traumas). Dental avulsion necessitating a replantation was found in 2.9% of the patients, and crown-root fracture in 2.5% of the treated children. Tooth avulsion is among the injuries with poor prognosis, leading to damaged pulp and periodontal tissues, i.e. the alveolar bone, the periodontal ligament, the root cementum, and the gingiva. The potential sequelae include pulpal necrosis, resorption, or ankylosis. Such complications, with lower prevalence, may also follow the intrusion of permanent teeth (5-7).
Sequelae of dental trauma
Adequate management of dental trauma, as early as immediately on the site of the accident, may have a major impact on the favourable outcome. Where there is enamel-dentine fracture involved, the management consists in crown reconstruction, typically with a composite material. Nonetheless, even such cases may entail complications, particularly when tissue breakage is substantial and the patient is young, i.e. the width of the dentinal tubules is large, and the mineralization degree of the intertubular dentine is low. Even prompt tooth reconstruction does not ensure treatment success. The most prevalent complications include chipped off reconstruction, pulpal necrosis with its sequelae (such as tooth discolouration, fissure, resorption, and ankylosis), tooth mobility, or tooth loss. Hence the importance of follow-up appointments, aimed at tooth assessment following the trauma, including such aspects as root development, and the condition of the pulp and of the tissues surrounding the root. Complications may follow the trauma as late as several years afterwards. The prevalence of resorption due to avulsion is estimated to range from 57.7-80%, and of resorption due to intrusion from 38-66%, these two entities being the injuries associated with the poorest prognosis (8-11).
The factors potentially reducing of the risk of resorption/its aggravation:
– early diagnosis and adequate management,
– replantation of the tooth within 20-30 minutes after the trauma increases favourable prognosis up to 85-97%,
– in the case of avulsion without an attempt at replanting the tooth on the site of the accident, storage of the tooth in a proper medium such as saliva, fresh cold milk, saline, HBSS (a balanced solution of potassium and sodium salts that preserves periodontal ligament’s viability up to 24 hrs, available as Sava-A-Tooth kit), ViaSpan solution used for organ storage in transplantology, that allows to limit cellular death within the periodontal ligament and the pulp,
– in the case of replantation of a tooth with an open apex (extra-oral dry time under 60 minutes, or in physiologic media), prior to replanting, soaking the tooth in a solution of doxycycline/minocycline 0.05 mg/ml for 5 minutes; additionally, prior 30-minute soak in HBSS is recommended to inhibit any bacterial infection and prevent complications,
– in the case of replantation of a tooth with an open apex (extra-oral dry time less than 60 minutes, or in wet, yet non-physiologic media), a 5-minute soak in citric acid, followed by a 20-minute soak in 2% sodium fluoride/2.5% zinc fluoride is recommended to prevent resorption,
– coverage of root surfaces with minocycline prior to replantation increases the chances for revascularization up to 91% (currently being tested),
– application of a flexible splint for 7-10 days or for 4 weeks, depending on the apex shape, with the use of materials designed for temporary bridges, orthodontic wire, glass fiber to prevent ankylosis and resorption,
– application of an antibiotic and steroid paste as an intracanal medicament following replantation and pulpal necrosis to inhibit the inflammation,
– following replantation, systemic administration of tetracycline in the dosage of 25 mg/kg of body weight/day; in children under 12 years of age, tetracycline is counter-indicated, owing to the risk of discolouration of the permanent teeth, with Phenoxymethyl Penicillin (Pen V) available as a possible alternative (an antibiotic from ß-lactam group, i.e. natural penicillins), e.g. Ospen, at a dosage appropriate for the child’s age and body weight, to facilitate the healing of the periodontal ligament, the pulp, and the soft tissues.
– radiographic control of the affected site after 2-3 weeks from the replantation to assess the periodontal ligament and the bone; in the case of inflammation, the endodontic therapy should be extended up to 6-24 months, with the medicament replaced every 3 months,
– adequate oral hygiene following the trauma to limit bacterial growth within the oral cavity and the gingival socket, particularly important where there is damage rendered to the tooth’s suspension apparatus, to prevent an infection of the periodontal ligament, including external inflammatory resorption,
– soft food to relieve the tooth’s functional load, thus facilitating improved healing of the pulp, the periodontal ligament, and the bone (1, 2, 10, 12-15).
The mechanism of resorption occurrence and progress
In normal circumstances, resorption affects only primary (deciduous) teeth before they are naturally replaced by permanent teeth. Both primary and permanent teeth may be affected by pathological resorption. The aetiology of this process is complex, and remains the subject of numerous studies. External resorption is initiated by mechanical or chemical damage to root surfaces. The protective layer of precementum and cementoblasts is then compromised, resulting in the exposure of the cellular cementum. For self-regeneration to occur, no infection or pressure in this area may take place (healing time is approximately 2-3 weeks when the damage is not extensive). This is referred to in literature as repair-related surface resorption.
The progress of resorption depends on the presence of clastic cells unable to adhere and act on an uncompromised root surface. Osteoclasts and odontoclasts demineralize the root surface. Ultimately, they also destroy the organic layer. The mechanism of action for odontoclasts and their origin remain unclear, even though their numerous similarities to osteoclasts have been identified, the presence of RANK (Receptor Activator of Nuclear Factor κβ) on their surface among them, instrumental in regulating the osteoclast and odontoclast activity. The activation takes place when RANKL (receptor activator of nuclear factor κβ ligand) is bound (1, 2, 4, 16, 17). There are many factors regulating the activity of clastic cells (tab. 1).
Tab. 1. The factors regulating the activity of clastic cells
|Kind of factor ||Action |
|M-CSF (monocyte macrophage colony stimulating factor)||inhibit cell activity by blocking RANK|
|TGF-β (transforming growth factor-β)||stimulates OPG production|
|TGF-β (transforming growth factor-β)||increase the activity of cells by upregulating RANKL|
|interferon gamma||inhibits the process of osteoclastogenesis|
|CSF-1 (colony stymulating factor)||contribute to the formation of osteoclast precursor cells|
The activated clastic cells acidify the environment through their presence in the cellular membranes of proton pumps. The dissolution of the apatites of dental tissue is facilitated by the decreased pH and the release of hydrolytic enzymes, and chloride and hydrogen ions. Moreover, MMP-9 and cathepsin k secreted by the clastic cells damage the organic portion of the dental tissue. The continuous activity of the damaging factor results in more profound destruction of the tissues (1, 11, 16).
Types of resorption
Depending on the place of its initiation, resorption is classified as internal or external. Two types of external resorption may be listed, namely inflammatory and replacement resorption. The first type results in loss of the dental tissue and its weakening, the second obliterates the canal. According to its location, external location is classified as type A located in the crown, type B located in the root canal, type C which ultimately leads to perforation of the root canal wall, and type D where the pulp chamber is perforated. External resorption is classified into surface resorption, replacement resorption, and ankylosis. On the root surface it may involve the cervical area, the central area, or the periapical area (1, 3, 11, 17).
According to Andreasen, the consequences of teeth damage due to trauma may include various forms of external resorption, i.e. surface (repair-related) resorption, resorption related to infection (inflammatory), or to ankylosis (replacement resorption, bone fusion), as well as transient destruction of the bone in the periapical area/the marginal region.
The damage of the root surface without the exposure of the dentinal tubules or compromising the cementoblast layer allows for self-regeneration, i.e. spontaneous reconstruction of Sharpey’s fibres and the cementum, thus facilitating the repair of localized, slight sinus tracts. When an inflammatory factor contributes, the resorption process is enhanced, which is referred to as inflammatory resorption, occurring when at the same time the pulp is infected, and the damage to the root results in the exposure of the dentinal tubules. Endodontic therapy aimed at removing the source of bacteria is the most appropriate course of treatment. When there is no bacterial factor present, yet the root surface damage is extensive (> 4 mm2), the bone’s remodelling properties are enhanced. Consequently, the tooth fuses with the bone, and thus replacement resorption occurs. Injuries resulting in the compression of the periodontal ligament may cause transient changes in the marginal periodontium or the periapical tissues, which is referred to as transient apical breakdown (TAB). This type of resorption of the damaged periodontal tissue precedes spontaneous regeneration. In a clinical examination, granulomatous tissue in the gingival socket may be found. Radiographic images, in turn, show transient widening of the apical opening, or an atrophy of the bone/dental tissue. An increased blood supply to the pulp through the widened apical opening is thus facilitated in TAB, and its regenerative properties are enhanced (14).
The underlying causes of internal resorption include chronic inflammatory conditions of the pulp, treatment by amputation or direct coverage, and traumatic factors (iatrogenic, such as overheated pulp or ill-fitted filling). Additionally, the general factors stimulating this type of resorption include herpes zoster virus, parathyroid hyperactivity, hypertension, vitamin deficiency (particularly vitamin A deficiency). External resorption may be caused or facilitated by chronic inflammation of apical tissue, orthodontic treatment, dental trauma, replantation, whitening of non-viable teeth, pressure rendered by the adjacent teeth, periodontal diseases, radiotherapy, systemic diseases (such as Paget’s disease, Gaucher’s disease, Turner’s syndrome, Kabuki syndrome) (2, 3, 11, 18, 19).
The symptoms characteristic of resorption may be mentioned:
– discolouration of the dental crown when the sinus tract is located in the crown portion of the tooth. The highly vascularized connective tissue is visible through the thin layer of dental tissue, particularly in the cervical area,
– spontaneous pain and a purulent condition in the case of advanced perforating internal resorption, owing to the infected tissue from the dental cavity being transferred to the periodontal tissues,
– dental cavity visible in radiographs or in CBCT scans (cone beam computer tomography). A number of characteristic signs of internal resorption that differentiate it from external resorption have been described, including the regularity and the smoothness of the cavity borders, uniformly dense radiolucence of an oval or round shape smoothly extending into the chamber or canal wall, symmetrically located relative to canal lumen, x-ray angulation does not affect the location of the radiolucence,
– in the case of extensive damage to the periodontal ligament (over 20%), ankylosis occurs. The clinical findings include a metallic sound on percussion, lack of physiological tooth mobility, progressing reinclusion, the periodontal ligament space invisible in a radiograph. Frequently, the bone fuses with the labial, buccal or lingual surface of the root, which is not visible in a 2D radiograph. First resorption symptoms may occur 2 months after the trauma. Resorption may be suspected when, relative to its counterpart, a tooth is in 1/8-1/4 infra-occlusion. The area in question should then be re-examined every 3 months,
– shortening root length due to inflammatory external resorption in the periapical area,
– increasing tooth mobility when resorption is severe (2, 3, 14, 16, 20-23).
At the site of damage to the fibres of the periodontal ligament and the cementum, surface root resorption may occur that does not require medical intervention, and is frequently asymptomatic. This is in contrast to inflammatory resorption which is a progressive and aggressive process. The severity of this kind of resorption has been known to be related to the infected canal’s bacterial count (14, 24).
Proper treatment is initiated by removing the underlying cause, with pulpectomy being the initial stage of internal resorption management. Similarly, progressive inflammatory external resorption due to trauma also requires the application of endodontic therapy. The course of management depends on the condition’s severity. Radiolucence not meeting the periodontal ligament in a radiograph allows for conservative chemo-mechanical treatment of the canal, which is subsequently irrigated with 5.25% sodium hypochlorite until the lavage fluid comes out clear. Metaplastic inflammatory tissue may be effectively removed by heating the highly concentrated rinsing agent (5.25% NaOCl) up to a temperature of 60-70°C and additionally applying 3% H2O2. Calcium hydroxide medicament is then introduced into the canal for 3 weeks to reduce the acidic pH, inhibit the activity of osteoclasts and hydrolases, and enhance the activity of alkaline phosphatase. In the case of inflammatory external resorption, this period of provisional treatment is extended. Visibly arrested resorption and reduced inflammatory lesions within the bone allow for the definitive filling of the canal. The thermal method is preferable, due to the presence of sinus tracts and the weakened root structure (2, 17).
Advanced resorption perforating the root wall or leading to the occurrence of a wide apical opening calls for additional MTA treatment of these areas. It is customary to begin the therapy with chemo-mechanical treatment of the canal, irrigating it with 5.25% sodium hypochlorite. Owing to the canal lumen connected with the periodontal ligament, radiographic assessment of the canal length is essential. After the perforation of the root wall or the widened apical opening has been filled with MTA, the remaining portion is filled applying thermal obturation or gutta-percha with AH Plus sealer (2, 13, 17, 25).
Where there are extensive cavities perforating the root, and treatment from the side of the dental chamber is not possible, endodontic surgery becomes necessary. This is initiated uncovering the perforated site by resecting a full-thickness mucogingival flap and accessing the affected site. As the next step, granulomatic tissue is removed applying curettage, irrigation, and ultrasound. Thorough removal of the tissue replacing the root structure is essential for the treatment’s success. The obtained cavity should be filled with e.g. MTA, a light-cured glass-ionomer material. The procedure is completed by filling the bone defect with a proper material and grafting the wound with the previously prepared flap (8, 26).
Endodontic therapy is not indicated for the treatment of ankylosis, as it can neither arrest nor cure it. This condition in children with developing dentition poses a serious problem, as it results in arrested tooth eruption and disrupted bone growth in its area, i.e. infra-occlusion. The course of management varies depending on the patient’s growth stage, with the child’s growth spurt serving as the point of referral. Accordingly, management plan may be classified into 4 distinct age groups, i.e. prior to the growth spurt, from the beginning to the maximum of the growth spurt, from the maximum to its completion, and after the completed growth. Thus, the course of management depends upon the patient’s developmental stage, i.e. indirectly the child’s age. In children under 10 years of age, who have not entered the growth spurt stage, such a tooth must be extracted within 2-3 years from the diagnosis, otherwise a severe infra-position of the tooth will ultimately result. An ankylosed tooth in a growing child must be closely monitored. Prompt removal is essential if it is infrapositioned, or a misalignment of the adjacent teeth is forming. If the patient has completed their growth, periodical follow-up examinations of the area are sufficient. Infra-occlusion affects primarily deciduous teeth, whereas in permanent teeth its prevalence is estimated at 0.01% (6, 24, 27).
The possible management protocols in the case of diagnosis of an infrapositioned tooth in a child who has not entered their growth spurt comprise e.g. the following:
– early tooth extraction followed by replacement with a prosthesis/orthodontic appliance combined with a prosthesis,
– orthodontic closure of the gap resulting from the extraction, possible when there occurs concomitant crowded dentition,
– intended reimplantation, possible when the ankylosis is detected early and thus not advanced,
– tooth extraction with the protection of the alveolar ridge margins, and bone augmentation,
– autogenous transplantation, most typically with the use of crowded immature premolars whose root has developed in no more than 3/4 of their definitive length,
– coronectomy with orthodontic preservation of the gap to conduct prosthetic/implantation treatment at an adequate age,
– osteotomy, possible in patients who have completed their growth (19, 21, 24, 28, 29).
Lack of appropriate course of treatment results with cosmetic and orthodontic deformities, such as crooked adjacent teeth, shortened dental arch, and disrupted bone growth (31).
More and more commonly, coronectomy is the treatment method of choice for ankylosis. The procedure is indicated when the tooth is in 1 mm infra-occlusion relative to its counterpart. It consists in removing the tooth’s crown while leaving in situ its root which is replaced with osseous tissue due to replacement resorption. The remaining root is resorbed within a year. No optimal age has been established for this procedure. The patient’s growth spurt should be considered, and the procedure performed in its course (19, 28, 29, 31). Coronectomy is a treatment option used to:
– treat replanted ankylosed permanent teeth,
– treat infra-occluded permanent teeth,
– treat conditions resulting from dental trauma where deep crown-root fracture has occurred,
– remove lower third molars, as root extraction could in this case potentially lead to permanent alveolar nerve damage (the nerve is located in the vicinity) (7, 12, 27, 31, 32).
1. Local anaesthesia is administered.
2. Mucogingival flap is resected in the vicinity of the tooth and the adjacent teeth.
3. The crown portion of the tooth is resected at 1.5-2-3 mm below the margin of the alveolar bone, while the pulp is continuously cooled with saline solution to prevent it from overheating.
4. The healthy pulp is preserved, or the root canal is generously irrigated with saline solution to remove the infected tissue/the previously planted intracanal medicament, and to facilitate filling the canal with blood.
5. The preserved pulp or the blood-filled canal facilitate the desired root resorption.
6. The wound is gently treated. The mucosa does not cover the free space following the coronectomy, allowing for bone apposition in this place.
7. The resected tooth crown may be used as a temporary substitute (19, 21, 24, 28, 31-33).
– extraction of a tooth affected with ankylosis leading to an extensive tissue loss and a cosmetic deformity is avoided,
– the appropriate height of the alveolar ridge is maintained, thus allowing for effective implantation following the growth spurt. The presence of the unresorbed root fragment does not disrupt the osteointegration,
– it is an effective treatment alternative in patients with developing dentition, where neither orthodontic closure can be obtained, nor autotransplantion can be applied,
– it allows for implantation upon 6 months from the procedure, provided no counter-indications exist (such as the patient’s age) (12, 20, 30, 32).
– the root can migrate towards the oral cavity. To prevent it, the root surface is covered with a biocompatible material, i.e. hydroxyapatite,
– the resulting gap must be preserved until adequate reconstruction is possible,
– it is difficult to perform in young patients,
– numerous follow-up appointments with multiple radiographs are necessary,
– it is a novelty procedure, keeping up with research reports is necessary (21, 34).
Pathological resorption weakens the root structure. The destructive and the reconstructive processes overlap, yet resorption may lead to tooth loss when untreated. The degree of damage to the dental tissue is an important prognostic factor that has to be considered upon diagnosis and when commencing treatment. Hence, follow-up appointments are of particular importance in the case of patients who have suffered dental trauma. Early diagnosis and initiation of adequate treatment improve the prognosis for long-term survival of the tooth within the oral cavity.
1. Kowalczyk K, Wójcicka A, Iwanicka-Grzegorek E: Resorpcja zewnętrzna twardych tkanek zęba i kości wyrostka zębodołowego – patomechanizm powstawania. Nowa Stomatol 2011; 4: 170-174. 2. Fuss Z, Tsesis I, Lin S: Root resorption – diagnosis, classification and treatment choices based on stimulation factors. Dent Traumatol 2003; 19(4): 175-182. 3. Ciesielski P, Łaszkiewicz J: Wewnętrzna resorpcja zapalna – na podstawie piśmiennictwa i własnych obserwacji. Czas Stomatol 2008; 61(1): 40-47. 4. Jasiński P, Sobiech P, Korporowicz E: Resorpcja zewnętrzna korzenia spowodowana urazem – opis przypadku. Nowa Stomatol 2011; 4: 158-162. 5. Ghafoor R: Conservative management of progressive external inflammatory root resorption after traumatic tooth intrusion. J Conserv Dent 2013; 16(3): 265-268. 6. Malmgren B, Malmgren O: Rate of infraposition of reimplanted ankylosed incisors related to age and growth in children and adolescents. Dent Traumatol 2002; 18(1): 28-36. 7. Hilt A, Rybarczyk-Townsend E, Filipińska-Skąpska R et al.: Urazowe uszkodzenia zębów u pacjentów zgłaszających się do Zakładu Stomatologii Wieku Rozwojowego UM w Łodzi w latach 2000-2003. Nowa Stomatol 2006; 1: 15-18. 8. Kim Y, Lee CY, Kim E, Roh BD: Invasive cervical resorption: treatment challenges. Restor Dent Endod 2012; 37(4): 228-231. 9. Bücher K, Neumann C, Thiering E et al.: Complications and survival rates of teeth after dental trauma over a 5-year period. Clin Oral Invest 2013; 17: 1311-1318. 10. Tsilingaridis G, Malmgren B, Andreasen JO, Malmgren O: Intrusive luxation of 60 permanent incisors: a retrospective study of treatment and outcome. Dent Traumatol 2012; 28: 416-422. 11. Darcey J, Qualtrough A: Resorption: part 1. Pathology, classification and aetiology. Br Dent J 2013; 214(9): 439-451. 12. Cohenca N, Stabholz A: Decoronation – a conservative method to treat ankylosed teeth for preservation of alveolar ridge prior to permanent prosthetic reconstruction: literature review and case presentation. Dent Traumatol 2007; 23(2): 87-94. 13. Oktem ZB, Cetinbaş T, Ozer L, Sönmez H: Treatment of aggressive external root resorption with calcium hydroxide medicaments: a case report. Dent Traumatol 2009; 25(5): 527-531. 14. Fortuniak A, Szczepańska J: Późna replantacja zęba siecznego stałego – opis przypadku. Poradnik Stomatol 2008; 3(77): 69-72. 15. Marczuk-Kolada G, Łuczaj-Cepowicz E, Sołtysiuk I et al.: Leczenie wybitych siekaczy górnych stałych – opis dwóch przypadków. Nowa Stomatol 2005; 2: 70-74. 16. Majewska-Beśka S, Szczepańska J: Genetic and molecular mechanisms of root resorption – a literature based study. Dent Med Probl 2012; 49(3): 329-335. 17. Nilsson E, Bonte E, Bayet F, Lasfargues JJ: Management of Internal Root Resorption on Permanent Teeth. Int J Dent 2013; 2013: 929486. 18. Talebzadeh B, Rahimi S, Abdollahi AA et al.: Varicella Zoster Virus and Internal Root Resorption: A Case Report. J Endod 2015; 41(8): 1375-1381. 19. Jurczak A, Kołodziej I, Kościelniak D, Słowik J: Resorpcja zewnętrzna zamienna korzenia zęba jako późne powikłanie pourazowe u pacjentów w wieku rozwojowym. Implantoprot 2009; 4(37): 41-43. 20. Díaz JA, Sandoval HP, Pineda PI, Junod PA: Conservative treatment of an ankylosed tooth after delayed replantation: a case report. Dent Traumatol 2007; 23(5): 313-317. 21. Sapir S, Shapira J: Decoronation for the management of an ankylosed young permanent tooth. Dent Traumatol 2008; 24(1): 131-135. 22. Berkan C, Ceren FU, Hakan K: Multiple idiopathic external and internal resorption: Case report with cone-beam computed tomography findings. Imaging Sci Dent 2014; 44: 315-320. 23. Consolaro A, Furquim LZ: Extreme root resorption associated with induced tooth movement: a protocol for clinical management. Dental Press J Orthod 2014; 19(5): 19-26. 24. Sigurdsson A: Decoronation as an approach to treat ankylosis in growing children. Pediatr Dent 2009; 31(2): 123-128. 25. Mohammadi Z, Yazdizadeh M, Shalavi S: Non-Surgical Repair of Internal Resorption with MTA: A Case Report. Iran Endod J 2012; 7(4): 211-214. 26. Gandi P, Disha S: Treatment of maxillary central incisor with external root resorption using mineral trioxide aggregate: 18 months follow-up. BMJ Case Rep 2013; 2013: bcr2013200241. 27. Chalmers E, Goodall C, Gardner A: Coronectomy for infraoccluded lower first permanent molars: a report of two cases. J Orthod 2012; 39(2): 117-121. 28. Malmgren B: Ridge preservation/decoronation. J Endod 2013; 39(3): 67-72. 29. Peretz B: Cantilevered pontic for anterior decoronated tooth. Dental Abstracts 2013; 58(5): 250-251. 30. Sapir S, Kalter A, Sapir MR: Decoronation of an ankylosed permanent incisor: alveolar ridge preservation and rehabilitation by an implant supported porcelain crown. Dent Traumatol 2009; 25(3): 346-349. 31. Ahmed C, Wafaeel W, Bouchra T: Coronectomy of third molar: a reducedrisk technique for inferior alveolar nerve damage. Dent Update 2011; 38(4): 267-268. 32. Buczek O, Zadurska M, Osmólska-Bogucka A: Ankylosis in adolescence – treatment options with special focus on decoronation – review of literature. J Stoma 2014; 67(3): 346-359. 33. Pogrel MA, Lee JS, Muff DF: Coronectomy: a technique to protect the inferior alveolar nerve. J Oral Maxillofac Surg 2004; 62: 1447-1452. 34. Dominiak M, Papiór P, Hadzik J: Koronektomia jako alternatywa wobec zabiegu ekstrakcji zęba trzeciego trzonowego w żuchwie – opis przypadku. TPS 2014; 11: 65-69.