| Abstract|| |
Miniscrew implant (MSI) has been reported to be an excellent, supportive orthodontic anchorage tool. The placement of MSI is not free from complication and foremost of which is penetration of MSI into the vital tooth structures. This case report is probably the first to report a newer underreported complication. Interestingly, a small bit of gingival tissue was found deep inside the dentin of the tooth, surviving and proliferating in the MSI-damaged zone. This case report is probably the first to give direct histological evidence in humans that a MSI can cause implantation phenomenon which has the potential to give rise to numerous pathologies including pulpal, periodontal, and cystic transformation. Through this report, it is emphasized that clinicians should have a structured, formal MSI placement training to avoid such instances and also underlines the need to develop protocols to be followed in the instance of an inadvertent MSI penetration.
Keywords: Dental pulp, gingival tissue proliferation, implantation cyst, miniscrew, trauma
|How to cite this article:|
Rooban T, Krishnaswamy NR, Ahmed VK. Gingival tissue proliferation into the tooth following iatrogenic miniscrew insertion: A newer underreported complication. Indian J Dent Res 2017;28:198-202
|How to cite this URL:|
Rooban T, Krishnaswamy NR, Ahmed VK. Gingival tissue proliferation into the tooth following iatrogenic miniscrew insertion: A newer underreported complication. Indian J Dent Res [serial online] 2017 [cited 2021 May 18];28:198-202. Available from: https://www.ijdr.in/text.asp?2017/28/2/198/207792
| Introduction|| |
Temporary anchorage devices such as miniscrew implant (MSI) have gained prominence as a reliable source of anchorage. Better patient compliance, relatively low cost, and ease of placement and removal have been cited as the added advantages of the MSI.,,,, However, the technology comes with certain drawback that includes the possibilities of damage to vital tooth structures. In the available pertinent literature, there are evidences of periapical pathologies that have been attributed to the placement of MSI., Previous studies have delineated the effect of the MSI on periodontal structures, cementum, and even pulp.,,,,,,,,, However, such studies have concentrated on the type and quantum of healing of hard and soft tissues associated with the teeth. In addition, literature reported in oral and maxillofacial surgery, where fixation screws are used to fix fracture reduction plates, have been shown to cause root damage of varying intensities.
All such studies have not identified the possibilities of surface epithelial ingrowth (EIg) or epithelial implantation (EIp) along the site of damage though the possibility of such EIg has been postulated and shown along the MSI-tissue interface.
When a surface epithelium is forced into the underlying tissues, including hard tissues, there is a possibility of the displaced tissue to survive, proliferate, and give rise to a pathological entity called implantation cysts., There are isolated case reports in literature, where oral implantation cysts have been associated with previous trauma or surgery., However, the possibility of self-drilling MSI driving the epithelium into the underlying tissues has not been postulated till date. The current article highlights a case of inadvertent root damage caused by MSI which resulted in the phenomenon. The possibility of such a clinical scenario and its consequences has been discussed in the current article. The precautions and strategies to prevent such an occurrence have been suggested.
| Case Report|| |
A 22-year-old otherwise healthy female voluntarily participated in an ongoing trial, which evaluated the rate of healing of the damaged root surface after prolonged MSI contact (Dentos, Daegu, Korea). This trial was an extension of a previously published study from the institution. This study was approved by the institutional review board, and written informed consent was obtained from the patient. Patients warranting extraction of first premolars were included in the study. No exceptions were made in the treatment protocols to suit the study requirements. As per the schedule, MSIs were placed and left in prolonged contact with the root surface of the first premolar for a period of either 4 or 6 or 8 weeks as per randomization. After this period, MSIs were removed, and root was allowed to heal for 4 weeks, after which tooth was extracted atraumatically.
A self-drilling MSI was placed in the patient to establish a root contact and to assess repair of damaged surface after prolonged MSI contact as per the protocol mentioned in previously published literature. However, for this particular patient, the routine confirmatory Intraoral periapical (IOPA) radiograph revealed that the MSI has inadvertently penetrated through the mid-portion of the root instead of shearing the proximal root surface [Figure 1]a, in spite of taking best precautionary measures. Sticking to the standard operating procedure, MSI was immediately retrieved and reinserted into the proximal root surface. Subsequently, the repeated IOPA revealed proper positioning of the MSI as per the requirement of the study design [Figure 1]b. The MSI was left in situ for 4 weeks after which it was extracted uneventfully.
|Figure 1: (a) First attempt of miniscrew implant insertion failed to establish proximal root contact, resulted in miniscrew implant penetration into the mid-portion of the root. Note the inadvertent penetration, (b) second attempt of miniscrew implant insertion established a proper proximal root contact. Note the lateralization|
Click here to view
Slow decalcification of the tooth was performed using commercial decalcification agent, Osteomoll ® (Merck Millipore, Germany); tissue was processed and stained with Harris hematoxylin and eosin. The slides were subjected to microscopical examination.
Under low power microscopic view, the MSI contacted root revealed two distinct areas of damage. One damage was observed in the mid-portion of the root while the other damage was associated with the proximal surface of the root [Figure 2]a and [Figure 2]b. There was a clear, visible split in between these two areas of damage. In the deeper sections, none of the damages were observed. The damage along the proximal root surface exhibited a regular attempt to healing. Lining with surface cells, an attempt by the adjoining periodontal ligament cells to heal and seal the proximal damaged area was observed. However, the proximal damaged area was not completely filled, either by soft or hard tissue. On the contrary, the defect was fresh with no classic signs of epithelial cell lining.
|Figure 2: (a) Low power scanned version of the demineralized histopathological sections revealed two distinct areas of miniscrew implant penetration, (b) deeper sections revealed no visible miniscrew implant penetration – but remarkable changes in the pulp cavity were observed with proliferation and obstruction along the area|
Click here to view
The damage observed in the mid-portion of the root was clear cut with less debris and partially filled by a soft tissue. The soft-tissue proliferation exhibited fibrovascular connective tissue lined by epithelium. The epithelium was thin pseudostratified squamous surface type with numerous thin proliferating rete ridges in arcading fashion, architecturally resembling the classic gingival tissue. The underlying connective tissue was filled with vascular channels with red blood cells and diffusely placed chronic inflammatory cells. The proliferation was confined to the internal damage and which partially filled the defect. The split or the tract connecting these two damaged areas did not contain any connective tissue or epithelial elements but had debris in the tract [Figure 3]a,[Figure 3]b,[Figure 3]c.
|Figure 3: Demineralized sections (×10). (a) Two distinct areas of damage caused by the first and second attempt of miniscrew implant insertion were observed. First damaged area was observed in the mid-root portion which shows proliferation of epithelium and the connective tissue while the second damage caused by proximal insertion of miniscrew implant shows the periodontal healing alone, (b) damage in the mid-root damage areas reveals the proliferation of epithelium in gingival architecture with connective tissue and blood vessel, (c) the tract that connects both the defects caused by miniscrew implant penetrations|
Click here to view
The pulp tissue exhibited intense inflammatory reaction. Diffuse chronic infiltration was observed all along the pulp, even at the radicular end. The end exhibited damage and large vacuolization of the odontoblast along the dentin-pulp complex, proliferating and replacing the cellular pulp with fibrous elements and with one focus resembling questionable dentin-like debris [Figure 4]a,[Figure 4]b,[Figure 4]c,[Figure 4]d. The blood vessels were characteristically dilated. Consecutive serial histological sections failed to establish or associate the continuity of the surface epithelium into the defect. The deeper part of the mid-root portion damage showed shearing of the dentin at its terminal end suggesting the damage during the retrieval attempt. The damaged area showed organizing of the epithelial lining [Figure 4]d. Based on the above-mentioned information, one could infer that some dentinal debris has been pushed into the dental pulp. The damage has caused disruption of the odontoblastic layer even in remote apical region.
|Figure 4: Demineralized sections stained with hematoxylin and eosin. (a) Pulpal region with debris of dentin (×4), (b) close-up view of the dentinal debris in the pulp (×10), (c) fibrous nature of the pulp, showing increased vascularity, and vacuolization of odontoblastic layer (×10), (d) splitting of dentinal tubules was observed around the cutting thread of miniscrew implant. The entire area of damage is associated multiple splits in the dentin. The organization of the epithelial lining along the periphery was observed (×10)|
Click here to view
| Discussion|| |
In spite of widespread usage of the MSI, many clinicians are reluctant to use MSI in their clinical practice. They were reportedly apprehensive about the possible inadvertent trauma to root and the adjoining structures., There are reports in the literature of such inadvertent damage of the root/dentin-pulp.,,,,,,,,,, The healing of damage to human tooth structures and pulpal tissues was increasingly reported., All these reports were either done by intentional MSI damage (of shorter duration) or isolated case reports (with wider time frame). The present case report is probably the first to report the possibility of an EIg or EIp phenomenon. The consecutive histological sections failed to demonstrate the “epithelial connections” from surface of the tooth (and thus probably to gingival surface). The absence of epithelium or other tissues in the tract connecting two damages, further rules out the epithelial migration from proximal surface damage to mid-portion root damage. Hence, this could be only viewed and deduced as EIp and not as an EIg phenomenon.
Half a decade ago, Henry attempted to use the gingival epithelium as a biological pulp capping material. Harvested gingival epithelium was inserted into the pulp through a carefully prepared Class V cavity of teeth in young dogs. Even before that, there have been reports of cysts with epithelial lining inside the tooth. In the results of their experiment, Henry observed epithelium organizing into islands, lining the abscess (infected), and in some instances, suggestive of cyst formation as early as 96 h of insertion of the gingival tissue. This study, though failed to meet its objective, gives a clue of survival of epithelium in the dental tissues and probably forms a cyst at a later stage. In a study, Petersson et al. demonstrated the EIg into the intentionally damaged teeth of dogs. The epithelium was either from surface or gingival pockets. The EIg was observed as early as 3 weeks to as late as 1-year period. However, this study failed to show organization of cyst in their samples. Probably, the associated inflammatory response following the damage would probably reduce the chance of survival of the EIg in deep tissue planes. If the epithelial tissue rapidly fills the damage area and retains the connection to its external surface parent tissues, the pushed epithelium survives and proliferates. In either case, the origin of epithelium is undoubtedly gingiva.
In the present case too, the self-drilling MSI has probably pushed the superficial epithelium, along with connective tissue into the root where they continued to survive, probably deriving nourishment from the inflammatory exudate during earlier phase and transudate in latter phase. The survived tissue components further multiplied and established angiogenesis. The presence of gingival architecture and abundant, vascular channels supports the possibility of this condition as EIp. If only surface epithelium is pushed into the root, they probably would not have survived successfully.
Alternatively, the surface epithelium along with the connective tissue, in the presence of inflammatory mediators (in response to trauma), probably has “crept” into the defect by growing along the edges into the root and this phenomenon is called EIg. If the condition had been an EIg, the continuity or the ingrowth would have been seen in at least one of the serial sections. In addition, the proliferation was seen only in the damaged area caused by first MSI penetration site and not in the second MSI penetration. Probably, the clinician used the same puncture site, which by the second time was devoid of epithelium. The second damage site was mostly superficial which showed only connective tissue elements. Based on the above features, we had empirically concluded that the condition is an EIp rather than an EIg. The difference is clinically obscure as both entities can lead to organization of the epithelial proliferation. This at a later stage could lead to cystogenesis if conditions were suitable.
In addition, the intense damage of dentin at the apical region, the presence of intense inflammation, increased fibrotic nature, damaged odontoblastic layer, and dentinal debris, one could infer the significant pulpal damage though the patient was clinically asymptomatic. Later, this condition could lead to periapical pathosis and probably an endodontic cyst, as reported in German dental literature and cited by Henry  though pertinent orthodontic and maxillofacial surgical literature have no reports of such “endodontic cysts” or EIg or EIp. To the best of our knowledge, this could be the first report of such EIp associated with MSI. With newer technical procedures to accelerate tooth movement using propel and other corticotomies could theoretically drive the gingival epithelium causing a EIg or EIp at a later stage.
The easier way to prevent EIg or EIp would be to avert “tissue rolling” while placing the MSI. In case, a rolling of tissue is felt while inserting MSI, copious irrigation, and cleaning of MSI with saline is essential before the next attempt. Alternatively, the best way would be to incise the region of MSI insertion and place it directly on the bone rather than on any soft tissue.
The current case highlights the mechanism of splitting of teeth by multiple MSI insertion through crack propagation and linking of the multiple damages. Literature has reports of teeth associated with unintentional MSI damage to split.,
The present case demonstrates that MSI is not free from complications, especially one that could compromise the vitality of teeth or even possibly cause a gingival tissue proliferation inside the teeth or even bone. Although the clinician was trained, calibrated, and supervised by experienced orthodontists, such unique instance has been encountered. The clinician, especially orthodontists, needs to undergo special education, training, and probably frequent clinical updating before they place MSI in their clinical practice. The following simple precautionary procedures would avoid or avert such instances.
Recently, there has been a report of an interesting episode associated with MSI. A well-experienced orthodontist placed a MSI between the apices of maxillary central incisors for correction of the mal-aligned incisors. During the course of treatment, right maxillary central incisors became sensitive and started losing its natural color. As the MSI was very close to its root apex, the MSI was removed. Within 2 weeks, the acute symptoms resolved. The authors claimed that the presence of the MSI in root apex would have probably hindered normal pulpal blood flow that caused a reversible, ischemic response in the pulp. However, this report is based on radiology, and the pulpal events are largely speculative. This case report reflects the following facts:
- Even experienced dental specialists have adverse episodes of MSI placement
- Failure rate of MSI was relatively high even in the hands of a well-trained, experienced specialty dentist
- This case report adds to our current report to highlight the need for training before the placement of MSI.
| Conclusion|| |
This case report presents a newer iatrogenic complication induced by unintentional trauma following MSI placement to tooth, leading to subsequent gingival proliferation, into the tooth. Such inadvertent instances may happen in clinical scenarios and often go unreported. Proper protocol and evidence of practice need to be evolved. Exclusive clinical training for MSI placement shall be made mandatory as part of curriculum.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Kanomi R. Mini-implant for orthodontic anchorage. J Clin Orthod 1997;31:763-7.
Bae SM, Park HS, Kyung HM, Kwon OW, Sung JH. Clinical application of micro-implant anchorage. J Clin Orthod 2002;36:298-302.
Deguchi T, Takano-Yamamoto T, Kanomi R, Hartsfield JK Jr., Roberts WE, Garetto LP. The use of small titanium screws for orthodontic anchorage. J Dent Res 2003;82:377-81.
Maino BG, Bednar J, Pagin P, Mura P. The spider screw for skeletal anchorage. J Clin Orthod 2003;37:90-7.
Carano A, Velo S, Incorvati C, Poggio P. Clinical applications of the Mini-Screw-Anchorage-System (M.A.S.) in the maxillary alveolar bone. Prog Orthod 2004;5:212-35.
Poggio PM, Incorvati C, Velo S, Carano A. “Safe zones”: A guide for miniscrew positioning in the maxillary and mandibular arch. Angle Orthod 2006;76:191-7.
Lim G, Kim KD, Park W, Jung BY, Pang NS. Endodontic and surgical treatment of root damage caused by orthodontic miniscrew placement. J Endod 2013;39:1073-7.
Hwang YC, Hwang HS. Surgical repair of root perforation caused by an orthodontic miniscrew implant. Am J Orthod Dentofacial Orthop 2011;139:407-11.
Asscherickx K, Vannet BV, Wehrbein H, Sabzevar MM. Root repair after injury from mini-screw. Clin Oral Implants Res 2005;16:575-8.
Maino BG, Weiland F, Attanasi A, Zachrisson BU, Buyukyilmaz T. Root damage and repair after contact with miniscrews. J Clin Orthod 2007;41:762-6.
Chen YH, Chang HH, Chen YJ, Lee D, Chiang HH, Yao CC. Root contact during insertion of miniscrews for orthodontic anchorage increases the failure rate: An animal study. Clin Oral Implants Res 2008;19:99-106.
Kadioglu O, Büyükyilmaz T, Zachrisson BU, Maino BG. Contact damage to root surfaces of premolars touching miniscrews during orthodontic treatment. Am J Orthod Dentofacial Orthop 2008;134:353-60.
Brisceno CE, Rossouw PE, Carrillo R, Spears R, Buschang PH. Healing of the roots and surrounding structures after intentional damage with miniscrew implants. Am J Orthod Dentofacial Orthop 2009;135:292-301.
Hembree M, Buschang PH, Carrillo R, Spears R, Rossouw PE. Effects of intentional damage of the roots and surrounding structures with miniscrew implants. Am J Orthod Dentofacial Orthop 2009;135:280.e1-9.
Ahmed VK, Rooban T, Krishnaswamy NR, Mani K, Kalladka G. Root damage and repair in patients with temporary skeletal anchorage devices. Am J Orthod Dentofacial Orthop 2012;141:547-55.
Renjen R, Maganzini AL, Rohrer MD, Prasad HS, Kraut RA. Root and pulp response after intentional injury from miniscrew placement. Am J Orthod Dentofacial Orthop 2009;136:708-14.
Kim H, Kim TW. Histologic evaluation of root-surface healing after root contact or approximation during placement of mini-implants. Am J Orthod Dentofacial Orthop 2011;139:752-60.
Ito K, Matsuoka K, Matsuzaka K, Morinaga K, Inoue T. Hypoxic condition promotes differentiation and mineralization of dental pulp cells in vivo
. Int Endod J 2015;48:115-23.
Borah GL, Ashmead D. The fate of teeth transfixed by osteosynthesis screws. Plast Reconstr Surg 1996;97:726-9.
Sutton JB. A clinical lecture on some unusual tumours: Delivered at Middlesex Hospital. Br Med J 1895;1:461-4.
Ozan F, Polat HB, Ay S, Goze F. Epidermoid cyst of the buccal mucosa: A case report. J Contemp Dent Pract 2007;8:90-6.
Noffke CE. Implantation-type epidermoid cyst of the mandible. Dentomaxillofac Radiol 1999;28:383-5.
Abrams MB, Andrews JE, Laskin DM. Epidermoid (implantation) cyst after temporomandibular joint surgery. J Oral Surg 1977;35:587-9.
Hyde JD, King GJ, Greenlee GM, Spiekerman C, Huang GJ. Survey of orthodontists' attitudes and experiences regarding miniscrew implants. J Clin Orthod 2010;44:481-6.
Ahmed VK, Krishnaswamy NR, Thavarajah R. Miniscrew implant fracture and effects of such retained tip on dentin-pulp complex: A histological report. Dent Traumatol 2016;32:161-5.
Henry M. A Histological Study of Gingival Implants into the Dental Pulp and Connective Tissue of Dogs. (Doctoral Dissertation), School of Dentistry, Indiana University; 1967.
Petersson K, Hasselgren G, Tronstad L. Endodontic treatment of experimental root perforations in dog teeth. Endod Dent Traumatol 1985;1:22-8.
Farinazzo Vitral RW, Santiago RC, Oliveira GS, Fraga MR, da Silva Campos MJ. Mini-implants: When orthodontists are caught in their own web. J Clin Case Rep 2012;2:130.
Qin YJ, Zhang GD, Zhang Y, Ping YF, Zhao CY. Natural reversal of tooth discoloration and pulpal response to testing following removal of a miniscrew implant for orthodontic anchorage: A case report. Int Endod J 2016;49:402-9.
Valai Kasim Shakeel Ahmed
Department of Orthodontics and Dentofacial Orthopedics, Ragas Dental College and Hospital, 2/102, East Coast Road, Uthandi, Chennai - 600 119, Tamil Nadu
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2], [Figure 3], [Figure 4]