Tissue response in hemisectioned primary mandibular second molars

Authors

  • Jenny Öhman Department of Oral Medicine and Pathology, Institute of Odontology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Department of Clinical Pathology, Sahlgrenska University Hospital, Gothenburg, Sweden
  • Vini Rughwani Institute of Odontology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
  • Julia Naoumova Specialist Clinic of Orthodontics, University Dental Care, Public Dental Service, Region Västra Götaland, Gothenburg, Sweden; Department of Orthodontics, Institute of Odontology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

DOI:

https://doi.org/10.2340/aos.v85.46272

Keywords:

Congenitally missing premolars, hemisection, prolonged pulp exposure, reparative dentinogenesis, histopathological features

Abstract

Objective: Congenital absence of mandibular second premolars occur in 2.91–3.22% of individuals, with nearly half of cases being bilateral. Interceptive hemisection of primary second molars promotes mesial drift but exposes the pulp for an extended period. This study investigates histopathological responses of pulp and associated mineralized tissues.

Material and methods: Children aged 7–12 in Skaraborg region, Sweden, were screened for over-retained primary mandibular second molars as part of a single-center, blinded, prospective split-mouth randomized controlled clinical trial comparing hemisection with extraction. Mesial roots of 21 hemisected teeth were collected for histopathological analysis of inflammatory infiltrate, pulpal necrosis, fibrosis, and hard tissue formation.

Results: Mean interval between distal and mesial root extraction was 11.54 ± 4.3 months. Histopathological analysis revealed no pulpal inflammation in 14% of specimens, acute/subacute inflammation in 38%, chronic inflammation in 48%, and necrosis in 24%. Reparative tertiary dentin with capping occurred in 48% and without capping in 33%. Necrotic mineralized tissue appeared in one specimen. Three patients reported symptoms during follow-up.

Conclusion: Prolonged pulp exposure following hemisection induced tertiary dentinogenesis, maintaining pulp vitality for up to 17 months. Despite histological evidence of inflammation or necrosis, most cases remained asymptomatic, indicating remarkable regenerative capacity of primary pulp–dentin complex.

Downloads

Download data is not yet available.

References

Polder BJ, Van’t Hof MA, Van der Linden FP, Kuijpers-Jagtman AM. A meta-analysis of the prevalence of dental agenesis of permanent teeth. Community Dent Oral Epidemiol. 2004;32(3):217–26. DOI: https://doi.org/10.1111/j.1600-0528.2004.00158.x

Sletten DW, Smith BM, Southard KA, Casko JS, Southard TE. Retained deciduous mandibular molars in adults: a radiographic study of long-term changes. Am J Orthod Dentofacial Orthop. 2003;124(6):625–30. DOI: https://doi.org/10.1016/j.ajodo.2003.07.002

Valencia R, Saadia M, Grinberg G. Controlled slicing in the management of congenitally missing second premolars. Am J Orthod Dentofacial Orthop. 2004;125(5):537–43. DOI: https://doi.org/10.1016/j.ajodo.2003.05.009

Kurol J, Thilander B. Infraocclusion of primary molars with aplasia of the permanent successor. A longitudinal study. Angle Orthod. 1984;54(4):283–94. DOI: https://doi.org/10.1093/ejo/6.4.277

Iraqi G, Helal N, Arafa A, Helal F. Retained primary molars and related reasons in Umm Al-Qura University, Makkah: a retrospective study. Open Dent J. 2019;13(1):190–5. DOI: https://doi.org/10.2174/1874210601913010190

Williams R, Park JH, Chae JM, Vaden JL. The congenitally missing second premolar: space closure. A viable option. Am J Orthod Dentofacial Orthop. 2020;157(4):571–83.e16. DOI: https://doi.org/10.1016/j.ajodo.2019.10.015

Alqahtani SM. Tooth hemisection. Case study and literature review. Int J Med Dent. 2019;23(2):272–6.

Northway WM. The nuts and bolts of hemisection treatment: managing congenitally missing mandibular second premolars. Am J Orthod Dentofacial Orthop. 2005;127(5):606–10. DOI: https://doi.org/10.1016/j.ajodo.2004.12.001

Radke U, Kubde R, Paldiwal A. Hemisection: a window of hope for freezing tooth. Case Rep Dent. 2012;2012:390874. DOI: https://doi.org/10.1155/2012/390874

Miller N. Ten Cate’s oral histology. 8th ed. London: Nature Publishing Group UK; 2012. p. 157–92. DOI: https://doi.org/10.1038/sj.bdj.2012.772

Costa VPP, de Queiroz IQD, Lia ÉN. Primary and Permanent Dentitions: Characteristics and Differences. In: Coelho Leal S, Takeshita E, editors. Pediatric Restorative Dentistry. Cham: Springer; 2019. DOI: https://doi.org/10.1007/978-3-319-93426-6_3

Fox AG, Heeley JD. Histological study of pulps of human primary teeth. Arch Oral Biol. 1980;25(2):103–10. DOI: https://doi.org/10.1016/0003-9969(80)90084-9

Nylen M. Electron microscopic studies of odontogenesis. J Indiana Dent Ass. 1960;39:406–21.

Kubota K, Kubota J. On the formation of the so-called cell-rich zone in the human dental pulp. Okajimas Folia Anat Jap. 1961;37(1):29–47. DOI: https://doi.org/10.2535/ofaj1936.37.1_29

Rodd HD, Boissonade FM. Vascular status in human primary and permanent teeth in health and disease. Eur J Oral Sci. 2005;113(2):128–34. DOI: https://doi.org/10.1111/j.1600-0722.2005.00193.x

Raslan N, Wetzel WE. Exposed human pulp caused by trauma and/or caries in primary dentition: a histological evaluation. Dent Traumatol. 2006;22(3):145–53. DOI: https://doi.org/10.1111/j.1600-9657.2006.00410.x

Andreasen FM, Kahler B. Pulpal response after acute dental injury in the permanent dentition: clinical implications – a review. J Endod. 2015;41(3):299–308. DOI: https://doi.org/10.1016/j.joen.2014.11.015

Murray PE, About I, Lumley PJ, Smith G, Franquin JC, Smith AJ. Postoperative pulpal and repair responses. J Am Dent Assoc. 2000;131(3):321–9. DOI: https://doi.org/10.14219/jada.archive.2000.0175

Smith AJ, Scheven BA, Takahashi Y, Ferracane JL, Shelton RM, Cooper PR. Dentine as a bioactive extracellular matrix. Arch Oral Biol. 2012;57(2):109–21. DOI: https://doi.org/10.1016/j.archoralbio.2011.07.008

Smith AJ, Patel M, Graham L, Sloan AJ, Cooper PR. Dentine regeneration: key roles for stem cells and molecular signalling. Oral Biosci Med. 2005;2(2/3):127–32.

Abdul Jabbar S, Nawaia S, Rughwani V, Hansen K, Naoumova J. Hemisection versus conventional extraction as interceptive treatment in congenitally missing mandibular second premolars: a randomised controlled split-mouth trial. Eur J Orthod. 2025;47(4):cjaf043. DOI: https://doi.org/10.1093/ejo/cjaf043

Haskell EW, Stanley HR. Vital hemisection of a mandibular second molar: a case report. J Am Dent Assoc. 1981;102(4):503–6. DOI: https://doi.org/10.14219/jada.archive.1981.0131

Valencia R, Espinosa R, Torres MA, Saadia M. Long-term histological response of hemisectioned exposed primary pulps: an in vivo study. J Clin Pediatr Dent. 2009 Fall;34(1):19–24. DOI: https://doi.org/10.17796/jcpd.34.1.n51v8102r8j7821m

Edwall L, Kindlová M. The effect of sympathetic nerve stimulation on the rate of disappearance of tracers from various oral tissues. Acta Odontol Scand. 1971;29(4):387–400. DOI: https://doi.org/10.3109/00016357109026527

Kuratate M, Yoshiba K, Shigetani Y, Yoshiba N, Ohshima H, Okiji T. Immunohistochemical analysis of nestin, osteopontin, and proliferating cells in the reparative process of exposed dental pulp capped with mineral trioxide aggregate. J Endod. 2008;34(8):970–4. DOI: https://doi.org/10.1016/j.joen.2008.03.021

Fernandes AM, Silva GA, Lopes N, Jr., Napimoga MH, Benatti BB, Alves JB. Direct capping of human pulps with a dentin bonding system and calcium hydroxide: an immunohistochemical analysis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008;105(3):385–90. DOI: https://doi.org/10.1016/j.tripleo.2007.08.031

Masuda-Murakami Y, Kobayashi M, Wang X, Yamada Y, Kimura Y, Hossain M, et al. Effects of mineral trioxide aggregate on the differentiation of rat dental pulp cells. Acta Histochem. 2010;112(5):452–8. DOI: https://doi.org/10.1016/j.acthis.2009.05.001

Simon S, Cooper P, Smith A, Picard B, Naulin Ifi C, Berdal A. Evaluation of a new laboratory model for pulp healing: preliminary study. Int Endod J. 2008;41(9):781–90. DOI: https://doi.org/10.1111/j.1365-2591.2008.01433.x

Moghaddame-Jafari S, Mantellini MG, Botero TM, McDonald NJ, Nör JE. Effect of ProRoot MTA on pulp cell apoptosis and proliferation in vitro. J Endod. 2005;31(5):387–91. DOI: https://doi.org/10.1097/01.don.0000145423.89539.d7

Nowicka A, Wilk G, Lipski M, Kołecki J, Buczkowska-Radlińska J. Tomographic evaluation of reparative dentin formation after direct pulp capping with Ca(OH)2, MTA, biodentine, and dentin bonding system in human teeth. J Endod. 2015;41(8):1234–40. DOI: https://doi.org/10.1016/j.joen.2015.03.017

Edanami N, Yoshiba K, Ibn Belal RS, Yoshiba N, Takenaka S, Ohkura N, et al. Role of dystrophic calcification in reparative dentinogenesis after rat molar pulpotomy. Int J Mol Sci. 2025;26(15):7130. DOI: https://doi.org/10.3390/ijms26157130

Hosoya A, Nakamura H. Ability of stem and progenitor cells in the dental pulp to form hard tissue. Jap Dent Sci Rev. 2015;51(3):75–83. DOI: https://doi.org/10.1016/j.jdsr.2015.03.002

Nanci A. Ten Cate's Oral Histology: Development, Structure, and Function. 7th ed. St. Louis (MO): Mosby Elsevier; 2007. p. 411.

Nelson‐Filho P, Borsatto MC, De Oliveira PT, Da Silva RAB. Partial replacement of the dentin–pulp complex by periodontal supporting tissues in a traumatically intruded primary maxillary incisor. Dent Traumatol. 2008;24(5):553–5. DOI: https://doi.org/10.1111/j.1600-9657.2007.00549.x

Published

2026-07-01