Proceedings of VetFest 2020 Fechney, A - How vital is that tooth anyway?

How vital is that tooth anyway?

Dr Angus Fechney Massey University Veterinary Teaching Hospital

Palmerston North, New Zealand

Introduction Determining dental pulp vitality, and therefore providing good advice to our clients, can be a challenge in clinical practice. Understanding the anatomical and physiological composition of the pulp-dentine complex aids understanding surrounding the changes that may occur in response to various noxious stimuli and facilitates discussion around treatment options. Treatment of immature nonvital permanent teeth can be particularly challenging. The final part of the lecture will discuss options for immature nonvital permanent teeth with a brief segue into regenerative endodontics Pulpal anatomy and response to injury The dental pulp is loosely arranged fibrovascular tissue with rich innervation. Older teeth have less abundant pulp due to deposition of secondary or tertiary dentine that narrows the pulp canal. Pulp is composed of four layers: 1) Odontoblastic layer which produces secondary dentine throughout the life of the tooth and tertiary dentine in response to injury and irritation; 2) Cell free zone of Weil (subodontoblastic nerve plexus of Raschkow); 3) Cell rich zone – containing undifferentiated mesenchymal cells and fibroblasts; 4) Pulp proper – major vessels, nerves and connective tissue1

The stroma within the central pulp chamber is primarily responsible for providing nutrition for the layer of odontoblasts that produce this dentine and line the outer surface of the pulp chamber. These cells are also responsible for physiological regulation of the dentine matrix via cytoplasmic extensions that travel along the dentinal tubules.2 There are three main types of dentine: Primary dentine is produced during development of the tooth, after the enamel has formed but before the tooth erupts. Secondary dentine is produced after eruption and throughout the life of a vital tooth and is therefore responsible for the reducing width of the pulp chamber as it ages. Tertiary dentine or reparative dentine is produced as a response to noxious insult to the odontoblast. Unlike primary and secondary dentine, tertiary dentine is denser and disorganized with no dentinal tubules and therefore insensitive. Despite distinctive histologic features, dentine and pulp are related embryologically and functionally and should be considered together. This unity is exemplified by the classic functions of pulp: it is 1) formative in that it produces the dentine that surrounds it; 2) nutritive in that it nourishes the avascular dentine; 3) protective, in that it carries nerves that give dentine its sensitivity; 4) reparative in that it is capable of producing new dentine when required.1 Common causes of pulpitis in animals include traumatic injury, extension of local infection and tooth fracture, severe attrition or tooth resorption that results in pulp exposure.

Pulpitis may be septic or sterile and response to this inflammation may cause an increase pressure within the pulp chamber and thereby exacerbate injury through ischemia, particularly as the pulp chamber narrows. Pulp injury generally results in accumulation of inflammatory cells, fibrosis, calcification +/- necrosis (depending on whether the pulpitis is

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Proceedings of VetFest 2020 Fechney, A - How vital is that tooth anyway?

reversible or irreversible).2 Where there are no signs of a complicated crown fracture, clinical signs of pulpitis may only include pain and tooth discoloration however irreversible pulpitis and pulp necrosis may sometimes be asymptomatic.3

Histologically tertiary dentine is often seen lining an infected or non-vital tooth, indicating pulpitis or pulp necrosis maybe sufficient injury to trigger transition from secondary dentinogenesis to tertiary dentinogenesis. Chronic degenerative changes may also occur in injured teeth in the absence of pulpitis or pulp necrosis manifesting as pulpal fibrosis, pulpal calcification, atrophy and/or loss of odontoblasts.2 Any chronic degenerative change may lead to pulp sclerosis within the pulp where bone-like osteodentin may fill all or part of the pulp chamber (Figure 1). Endodontically, this presents a further challenge when attempting to save teeth with this degree of change. If attempting to save these teeth, endodontic treatment (root canal therapy) can be problematic.

Figure 1 – Pulp sclerosis at the mid-point Figure 2 – Apical lucency in a young dog of the pulp chamber in a 10 year associated with chronic infection of

old Cheetah. Note the wide an immature non-vital tooth. Note the blunderbuss shaped region of the thin dentinal walls when compared to canal apically. surrounding teeth Radiographic evidence of endodontic disease includes: periapical lucency, increased width of apical periodontal ligament space, root tip resorption, arrested tooth maturation, and accelerated tooth maturation (Figure 2).3 Careful radiographic studies can alert the practitioner to subgingival changes and help guide the decision-making process with the client. Treatment of immature nonvital permanent teeth can be particularly challenging. If the stimulus is temporary and minor and without exposure to infection, the pulpitis can be reversible, especially in the young patient. However, when the pulpitis is irreversible, standard root canal therapy may be contraindicated in young dogs with thin walled and immature teeth that have open apices. The root canal procedure cannot seal the open apex adequately and removing the pulp tissue prevents continues growth of dentine. This may further weaken the tooth.4,5 Historically, outside extraction, the treatment options for these nonvital teeth were either a surgical root canal with retrograde filling or apexification: stimulation of root closure so that eventually a standard root canal procedure could be performed.6

Regenerative endodontic procedures are described as biologically based procedures designed to repair or replace damaged structures, including dentine and root structure, as well as cells of the pulp-dentin complex.7 These procedures have shown to be able not only to resolve pain and apical periodontitis but continued root development, thus increasing the thickness and strength of the previously thin and fracture-prone roots.8

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Proceedings of VetFest 2020 Fechney, A - How vital is that tooth anyway?

Summary Due to the extensive innervation within the root canal (as well as in the periodontal ligament), treatment of pulpitis is imperative. When irreversible pulpitis is diagnosed, treatment via endodontics or exodontics/extraction should be strongly advised. Given the limited external signs of pain exhibited by animal patients, radiography is a crucial diagnostic step in the assessment of endodontic trauma. Although extraction of teeth is a potential and viable treatment for traumatically damaged teeth, other treatments are available to preserve these teeth, maintaining both their important structure and function within the oral cavity, and eliminating the need for painful extraction. References

1. Nanci A and Ten Cate AR (2018). Ten Cate’s Oral Histology: Development, Structure and Function, 9e. St Louis, MO: Mosby Elsevier

2. Murphy BG, Bell CM, Soukup JW (2020). Veterinary Oral and Maxillofacial Pathology, 1e. Hoboken, NJ: Wiley Blackwell

3. Feigin K, (2019) Fifty shades of grey: contemporary understanding of the intrinsically stained dog teeth. Proceedings of the 33rd Annual Veterinary Dental Forum.

4. Wiggs RB, Lobprise HB Clinical oral pathology Wiggs RB, Lobprise HB (1997). Veterinary Dentistry – Principles and Practice, 1e. Philadelphia, PA: Lippincott-Raven

5. Wiggs RB, Lobprise HB Basic endodontic therapies Wiggs RB, Lobprise HB (1997). Veterinary Dentistry – Principles and Practice, 1e. Philadelphia, PA: Lippincott-Raven

6. Wiggs RB, Lobprise HB Advanced endodontic therapies In: Wiggs RB, Lobprise HB (1997). Veterinary Dentistry – Principles and Practice, 1e. Philadelphia, PA: Lippincott-Raven

7. Murray PE, Garcia-Godoy F, Hargreaves KM. Regenerative endodontics: a review of current status and a call for action. J Endod. 2007 Apr;33(4):377-90.

8. Feigin K, Shope B. Regenerative endodontics J Vet Dent. 2017 Sep;34(3):161-178.

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