Update on the management of equine periodontal disease

Periodontal disease was recognised by the early veterinary authors and was described as the ‘scourge of the working horse’ [1]. Despite this, much remains unknown about the aetiopathogenesis of the disease, and management of the syndrome continues to frustrate. Some light has been shed by recent studies into the histopathology and microbiology of the disease but evidence-based data about efficacy of treatments remain scarce. It is known that the prevalence of periodontal diseases increases with age in horses and donkeys, reaching almost 90% in late-teenaged horses and those of 20 years of age or more [2]. Risk factors are multifactorial and include dental conformation, food type, livery management systems and the presence of other dental diseases. Other data such as breed and geographical location have not been shown to be risk factors. Primary periodontal disease was described as rare by Colyer, but in the vast majority of equine cases periodontal disease is associated with the degradation of food material entrapped between the teeth. This is usually coincidental with the presence of diastemata, which vary in morphology, and progress with age and masticatory wear patterns. Diastemata referred to as ‘valve-type’, where there is occlusal contact but a diastema at the gingival reflection, appear to be most vulnerable to food entrapment and are associated with an acute periodontitis. This type of diastema appears to be particularly painful in young horses. When interproximal food entrapment occurs, putrefaction is accompanied by release of inflammatory mediators that stimulate a periodontitis featuring neutrophilic inflammation, at variable depth depending on the severity of the inflammation [3]. A number of bacteria, including spirochaetes, have been isolated from periodontal pockets in afflicted horses, but their role is unclear [4]. Neutrophilic inflammation deep into the gingiva has been shown histologically and in chronic deep cases, destruction of Sharpey’s fibres and periodontal collagen degradation feature [5]. Chronic cases also show peripheral dental caries, alveolar bone sclerosis and a biofilm. The role of the biofilm, in conjunction with chronic contact with sequestered food substrates and salivary alterations, remains unclear, in contrast to its importance in pathophysiology of the disease in humans. Clinically, periodontal disease is associated with gingival hyperaemia, inflammation and increased depth of the gingival sulcus as a consequence of periodontal collagen lysis. In the face of the inflammation, gingival immune defence appears to be compromised, and affected animals experience pain especially when masticating, which results in alterations in chewing behaviour that over time causes altered occlusal wear patterns. The disease is progressive and ultimately can lead to permanent changes in the occlusal alignment, misalignments, alveolar bone sclerosis, reduction in tooth stability, soft tissue ulceration and weight loss. Diagnostic imaging, including open mouth radiographs and computed tomography, is very helpful to demonstrate chronic or irreversible changes that can inform treatment plans. Currently there are few studies demonstrating efficacy of many current treatments. A series involving treatment using odontoplasty amongst other therapies demonstrated medium to long-term clinical benefit in a retrospective case series [6]. Most treatment protocols aim to reduce pain, reverse periodontal inflammation, restore occlusal conformation and improve masticatory efficiency. Ongoing management is almost invariably necessary. The principal goal is to remove entrapped food (without which all other components of therapy fail to make impact). This facilitates debridement of the gingival ulcer, removal of inflammatory mediators and the possibility of gingival healing. In some cases, widening of the diastemata (interproximal odontoplasty) using a narrow 2–4 mm conical or cylindrical rotating burr has shown efficacy. This can also be performed under visual guidance using a dental unit. Diastema widening is less effective in aged horses with open-type diastemata. Food, biofilm and bacteria are also debrided using manual clearance with picks and forceps, water lavage under pressure and air abrasion. The periodontal lesion can be treated with topical antimicrobials, gelatin sponges, and temporarily protected with PVS material extruded into the diastema as a stent or more permanent bridging material bonded to one interproximal surface after debridement. Anecdotally, combinations of these treatments show promise but systematic validation is lacking [7]. There is a study with multifactorial treatment that showed no significant treatment between the various protocols although there was some selection bias. One study showed some cytotoxicity of depot PVS in vitro although this may not be as important in a clinical setting. Horses can resent treatment due to the pain, and optimal results are achieved with the horse sedated and judicious use of local analgesia; posttreatment, the use of anti-inflammatory therapy is indicated. Odontoplasty is invasive, requires precision and can result in iatrogenic pulp exposure if performed inaccurately, and therefore a clinic situation incorporating oroscopic control enables more precise treatment. However, treatment to a limited degree involving periodontal pocket evacuation and lavage is widely possible in an ambulatory set-up. The appropriate treatment of associated periodontal caries remains debatable. Debridement of diseased peripheral cementum to reduce food adhesion, and possible superficial restoration of deep carious lesions, appears logical. Dietary management, including avoiding low pH diets, compiling diets devoid of coarse fibre forage and maximum grazing time is a component of the overall strategy. The benefit of systemic antimicrobials or perioceuticals is unclear although these may accelerate the subsidence of inflammation in severe cases. Treatment frequency depends on severity but intensive weekly therapy results in the rapid reduction in inflammation, although this is impractical in many cases and 3 or 4-monthly examinations are often utilised. Following effective treatment, improvement in appetite, chewing action and bodyweight are also observed and periodontal inflammation can be seen to recede with reduced periodontal pocket depth and eventual obliteration.

References

1. Colyer, F. (1906) Variations and diseases of the teeth of horses. Trans. Odontol. Soc. Great Britain 39, 154-163.
2. Du Toit, N., Burden, F.A. and Dixon, P.M. (2009) Clinical dental examinations of 357 donkeys in the UK. Part 2: Epidemiological studies on the potential relationships between different dental disorders, and between dental disease and systemic disorders. Equine Vet. J. 41, 395-400.
3. Cox, A., Dixon, P. and Smith, S. (2012) Histopathological lesions associated with equine periodontal disease. Vet. J. 194, 386-391.
4. Kennedy R, Lappin, D.F., Dixon, P.M., Buijs, M.J., Zaura, E., Crielaard, W., O’Donnell, L, Bennett, D., Brandt, B.W. and Riggio, M.P. (2016) The microbiome associated with equine periodontitis and oral health. Vet. Res. 47, 49.
5. Staszyk, C., Wulff, W., Jacob, H.G. and Gasse, H. (2006) The periodontal ligament of equine cheek teeth: the architecture of its collagen fiber apparatus. J. Vet. Dent. 23, 143-147.
6. Dixon, P.M., Barakzai, S., Collins, N. and Yates, J. (2008) Treatment of equine cheek teeth by mechanical widening of diastemata in 60 horses (2000– 2006). Equine Vet. J. 40, 22-28.
7. Jackson, K., Weber, L.M. and Tennant, M. (2012) A retrospective study of the effectiveness of four different treatments of periodontal disease in equine cheek teeth. J. Vet. Dent. 33, 83-89.