Achieve Predictability in Complex Restorations With Crown Lengthening

Complex restorative situations often require an interdisciplinary approach to diagnosis and treatment. The predictability of tooth-borne restorations is based on a healthy, biologic foundation. The relationship of the hard and soft tissues must be upheld to preserve the dimensions of tissue and epithelial attachments around teeth; namely, the supracrestal attached tissues (formerly biologic width).¹

Crown lengthening procedures can provide both functional and esthetic benefits to natural and restored teeth and help create facial harmony. The surgical workflow largely depends on the appropriate diagnosis and restorative plan. Otherwise, the original gingival apparatus simply reestablishes itself — or, worse, breaks down in light of supracrestal attached tissue impingement. Learning to properly identify and treat crown lengthening cases can improve long-term health and patient outcomes.

During active eruption, the tooth emerges into the oral cavity and coronally advances until it meets its antagonist. Then, passive eruption begins, as the secondary epithelial attachment splits and recedes apically to establish a new dentogingival junction.² Ideally, the supracrestal tissue attachment includes 1.07 mm of connective tissue, and 0.97 mm of junctional epithelium, with a sulcus depth of 0.69 mm.³

However, tooth eruption does not always create the right biologic dimensions, leading to the appearance of thick, fibrotic gingiva and short clinical crowns. The failure of the free gingival margin to migrate past the cervical convexity of the crown is known as altered passive eruption (APE). Occlusal interferences during active eruption, thick, flat phenotypes, genetic predisposition, and orthodontic and endodontic trauma have been proposed etiologies.² Clinically, APE presents in 12% of the population. There is a statistically significant association between gingival phenotype and prevalence of APE, with a greater prevalence in those with a thick, flat gingival phenotype.⁴ The anatomical difference can predispose the sulcus to anaerobic bacteria and limit hygienic and restorative access.⁵

References

1. Caton JG, Armitage G, Berglundh T, et al. A new classification scheme for periodontal and peri-implant diseases and conditions — Introduction and key changes from the 1999 classification. J Periodontol. 2018;89(Suppl 1):S1–S8.
2. Goldman HM, Cohen DW. Periodontal Therapy. 4th ed. St. Louis: Mosby; 1968.
3. Gargiulo A, Wentz FM, Orban B. Dimensions and relations of the dentogingival junction in humans. J Periodontol. 1961;32:261–267.
4. Nart J, Carrio N, Valles C, et al. Prevalence of altered passive eruption in orthodontically treated and untreated patients. J Periodontol. 2014;85:e348–e353.
5. Volchansky A, Cleaton-Jones PE. Delayed passive eruption. A predisposing factor to Vincent’s infection? J Dent Asso S Africa. 1974;29:291–294.

This information originally appeared in Saltz AE, Antonella AB. Decision-Making in Esthetic and Functional Crown Lengthening. Decisions in Dentistry. March 2022;8(3)30-33.