Each maxillary cheek tooth has two infundibula that are cement(um)-containing cup-like invaginations of the occlusal enamel extending deep into the dental crown (Figure 1). Mandibular cheek teeth have none. These cylindrical-shaped structures extend almost the full length of the dental crown, from the occlusal surface to the apex (root area), and are up to 90mm deep in recently erupted teeth. Due to normal dental wear, infundibula gradually become shorter and may even become fully worn away in aged horses.
During their development, infundibula should become filled with cementum that is deposited at the occlusal aspect of the infundibulum. Deposition then proceeds in an apical (towards the roots) direction. Simultaneously, cement deposition occurs on the internal enamel walls of the infundibulum and proceeds in an axial (central) direction. As cementum is progressively deposited on the infundibular walls, the soft tissue dental sac remnants containing the infundibular vasculature move centrally.
Ideally, but uncommonly, complete cemental filling of the infundibulum should occur, except for one to two small (circa 1mm diameter) central linear channels (ie sites of former vascular channels) that can be seen occlusally in almost all maxillary cheek teeth. These channels have been termed “vascular channels”.
Aetiopathogenesis of infundibular disease
The developmental failure of complete cemental filling of infundibula (ie infundibular cemental hypoplasia) is a very common disorder, with gross anatomical studies (Kilic et al., 1997; Fitzgibbons et al., 2010), standard computed tomographic (CT) studies (Windley et al., 2009) and micro-CT studies (Horbal et al., 2019a, 2019b) showing some degree of cemental hypoplasia to be present in circa 90 percent of all infundibula.
The developmental failure involving the incomplete cemental filling of infundibula is a very common disorder
Infundibular cemental hypoplasia commonly affects the apical region of the infundibulum, where it is termed “apical cemental hypoplasia”. Another common pattern is the presence of long central linear defects (ie central linear cemental hypoplasia), and some teeth have both central linear and apical cemental defects (Figure 2).
Due to normal dental wear, defective areas of cementum in the apical aspects of the infundibula eventually become exposed occlusally, often when horses are between 10 and 15 years old (Figure 3). The exposed cemental defects then become impacted with food. In contrast, wide (eg over 10mm diameter) central linear cemental hypoplasia defects can become impacted with food and then develop infundibular caries in young horses.
Following impaction with food, subsequent fermentation of carbohydrates by acidogenic bacteria leads to acid formation with the development of infundibular caries, with the dissolution of calcified tissue and destruction of its soft tissue components.
Acid demineralisation (and thus caries) occurs in cementum after a minimal drop in pH, ie at pH 6.7 (as compared to enamel demineralisation that occurs at pH 5.5). Consequently, infundibular cementum (but less so infundibular enamel) is very prone to caries. Small, often full-length central linear defects, including the “normal” small “vascular channels”, develop limited food impaction that seldom lead to clinical caries.
Impact of auxiliary blood supply
Multiple studies have shown the maxillary Triadan 09s (4th cheek tooth) to have the highest prevalence of infundibular cemental disorders. Fitzgibbon et al. (2010) showed the 09s to have five times more severe infundibular caries than the other Triadan positions.
During dental development, the main blood supply to the infundibulum comes from the fleshy overlying dental sac that fully encloses the dental bud. When the tooth erupts, the soft dental sac, and thus the main infundibular blood supply, is quickly lost. However, Suske et al. (2016) have recently shown the presence of accessory blood supplies to the infundibula – one at the rostral (mesial) and one at the caudal (distal) aspect of the teeth. These continue to function after dental eruption.
The mesial (rostral) infundibulum retains its accessory blood supply for a shorter period. Thus it has a higher prevalence of infundibular cemental hypoplasia (and thus caries) than the distal (caudal) infundibulum, whose accessory blood supply lasts longer, for possibly up to two years post-eruption.
Grading infundibular disease
As noted, all infundibular caries lesions are believed to be secondary to pre-existing infundibular cemental hypoplasia. Caries that affect cementum only (termed “grade 1” caries) do not necessarily cause any clinical problem unless they are extensive and deep (Figure 4). The extension of caries from the cementum to infundibular enamel (grade 2; Figure 5) can sometimes allow for the extension of caries to adjacent dentine (grade 3; Figure 6), which often causes serious clinical problems, including the development of sagittal fractures (grade 4; Figure 7) and apical infections (Borkent and Dixon 2017).
Grade 3 caries can lead to the coalescence of both infundibula, causing structural weakness in the tooth (Figure 7A) and the subsequent development of midline sagittal fractures (termed “grade 4” caries) (Figure 7B). Infection of the apex of the tooth inevitably develops in such teeth and often leads to infection of the overlying paranasal sinuses (Figure 8).
In addition to a predisposition to sagittal fractures, caries of dentine (grade 3) can allow cariogenic bacteria to extend into and cause infection of adjacent pulp horns (Figure 9). This pulpar infection usually spreads to the apical region, causing apical infections, ie infection of the apical aspects of the periodontal membranes and alveolus. Apical infection often leads to infection of adjacent anatomical structures, including empyema of the maxillary sinuses (Figure 8) or, less commonly, infection of the rostral maxillary bones (usually with involvement of Triadan 06s to 07s) (Borkent and Dixon 2017).
The prevalence of infundibular caries varies greatly (from 13 percent to 100 percent) between earlier studies. These large differences are due to the definition of caries used in each study, for example if small central defects, “vascular channels”, were termed infundibular caries. It also depends on the age of the horses examined (there is a much higher prevalence in older horses) and variations between different equine populations.
A recent UK epidemiological study using standardised classification guidelines found a prevalence of infundibular caries of 23 percent in three- to five-year-old horses, which increased to 69 percent in horses over 20 years old (Borkent et al., 2017).
Being able to recognise cheek teeth with infundibular caries susceptible to the development of sagittal fractures or apical infections should be an integral part of an effective equine dental examination. This is because this allows for their subsequent treatment if necessary. For example, the fractured tooth should be extracted if horses develop a caries-related sagittal fracture of a maxillary cheek tooth. Additionally, the other maxillary cheek teeth (especially the contralateral teeth – usually a Triadan 09) need to be examined for evidence of advanced caries, and affected teeth should be restored to hopefully prevent them from fracturing or developing an apical infection.
Being able to recognise cheek teeth with infundibular caries susceptible to the development of sagittal fractures or apical infections should be an integral part of an effective equine dental examination
Most teeth with grade 1 and localised grade 2 caries do not need any restorative treatment but should be monitored annually or biannually to detect possible worsening. This is especially relevant in young teenage horses, ie when apical cemental defects become exposed on the occlusal surfaces due to normal dental wear.
Ex-vivo and long-term clinical studies (Pearce and Brooks, 2022) have shown effective debridement of carious infundibula using files and dental drills, with restoration using composite dental materials. These specialist techniques are described in detail by Pearce and Horbal (2022).
|The author would like to thank Dewi Borkent for reviewing this manuscript.