Published in IVIS with the permission of the AAEP Close this window to return to IVIS Applied Equine Dental Development Kirstie Dacre, BVMS, MSc, Cert EM (Int Med), PhD Author s address: Veterinary Teaching Hospital, Massey University, Palmerston North, New Zealand. Equine Dental Embryology During dentogenesis the tooth germ undergoes a sequential process of events termed the initiating, morphogenetic and cytodifferentiating phases. Importantly, in hypsodont teeth there is delayed termination of the latter two stages at the apical region thus allowing continued eruption of the tooth and root development following eruption. Tooth formation begins with the bud stage during which the dental lamina (derived from epithelial tissue) produces a series of tooth buds along its buccal margin. This is followed by the cap stage in which a coned structure, termed the enamel organ, is formed by an invagination of mesenchymal tissue into the tooth bud. All deciduous teeth and permanent molars are derived from the enamel organ of the dental laminae, however, permanent incisors, canines and premolars are formed from a lingual extension of the dental laminae of the temporary teeth. As a result, permanent incisors force the temporary teeth labially during eruption. The proliferating invaginated mesenchymal tissue forms a structure termed the dental papilla which ultimately produces dentine and pulp. The mesenchymal tissue also extends peripherally to form the dental sac which protects and nourishes the develop enamel organ. 1 The dental sac, dental papilla and enamel organ are together termed the tooth germ. Continued proliferation of the enamel organ and dental papilla cause the tooth germ to assume a bell shape which is termed the bell stage of development. The infundibula of incisor and maxillary cheek teeth are formed at this stage by an invagination of the enamel epithelium down into the bell shaped structure. Peripheral invaginations of the enamel organ also occur at this stage which will form the peripheral enamel infoldings of the cheek teeth. 2 Cytodifferentiation within the enamel organ leads to the formation of ameloblasts and odontoblasts which begin to lay down enamel and dentine respectively. 3 These substances are formed by the secretion of extracellular matrix mucopolysaccharides and organic fibres which is then mineralised. The ameloblasts form a projection termed Tomes process which secretes enamel prisms and interprismatic enamel. 4 As dentine is laid down, the odontoblasts migrate towards the centre of the dental papilla leaving long thin cytoplasmic extensions, termed odontoblastic processes, around which dentine is formed. These processes occupy the dentinal tubule whilst the cell body sits at the periphery of the pulp cavity. 5
Blood supply to the developing brachydont tooth germ is first maintained by blood vessels in the dental papilla. Once mineralisation of dentine and enamel begins, however, the enamel epithelium is isolated from the dental papilla and is nourished solely by vessels in the overlying dental sac. 5 Following crown formation, the enamel epithelial cells in the neck region of the tooth germ proliferate down over the dental papilla as a double layer of cells known as Hertwig s epithelial root sheath. This induces the underlying tissue to differentiate into odontoblasts and the production of dentine. 5 Subsequent contact between dental sac cells and dentine induces differentiation of dental sac cells into cementoblasts and the production of cementum. 6 In equine teeth cementum is deposited over the entire length of the dental crown, including over the occlusal surface just prior to eruption. 2 Hertwig s root sheath disintegrates when the tooth reaches its complete length such that no further enamel can be produced throughout the lifespan of the tooth. Cementum formation in the infundibula occurs until the dental sac is destroyed following eruption of the tooth. No further cementum can be deposited in the infundibulum following disruption of the vascular supply from the dental sac which is believed to be the reason for incomplete cemental filling of many infundibula and is termed infundibular cemental hypoplasia. Developmental Disorders Abnormalities of Teeth Number Abnormalities of teeth number are termed adontia (absence of teeth), oligodontia (reduced number of teeth) and polydontia (increased number of teeth, i.e. supernumerary teeth). Adontia has not been recorded in the equine. True (congenital) oligognathia, i.e. when one or more dental buds do not develop, is rare but has been reported in the literature. 8,9 When this occurs, the rest of the dental buds migrate such that the dental row is shortened and thus malocclusions and overgrowths develop. In contrast, polydontia is much more commonly observed with a recent study finding 2.8% of cheek teeth cases and 9.1% of incisor cases involving presence of supernumerary teeth. 7,8 Polydontia may be caused by the splitting of dental buds, e.g. by trauma, or the development of additional tooth germs from the dental lamina. The supernumerary teeth are often abnormal in shape or even connated (a double tooth) and do not fit properly in the dental row and consequently cause malocclusions, periodontal disease and overgrowths. Occasionally, horses will have supernumerary cheek teeth in all 4 dental rows, in which case malocclusion is minimal but crowding in the dental row may cause rotation and periodontal disease of the supernumerary teeth.
Mineralisation Defects Areas of enamel hypoplasia have been identified in both healthy teeth and teeth with periapical abscessation where it is believed to have been clinically significant. 10 Enamel hypoplasia results in a lack of corresponding coronal cementum. Cemental hypoplasia is seen in the infundibulum of all incisors and occurs commonly in that of maxillary cheek teeth. There is no evidence to suggest that this is pathological in incisor teeth and is often insignificant in cheek teeth, although it has been associated with apical abscessation, infundibular caries and saggital fractures of the teeth. 10 Importantly, the significance of cemental hypoplasia can not be determined from the occlusal surface. Theoretically, the premature removal of deciduous cheek teeth caps leads to premature disruption of the dental sac and its blood supply to the infundibular cementum and thus may predispose infundibular cemental hypoplasia. Wry Nose Wry nose, or campylorrhinus lateralis, is a major congenital deformity resulting in varying degrees of lateral deviation of the rostral face (premaxilla and maxilla) to the dysplastic side. Mild cases suffer no adverse effects however severe cases have nasal septal deviation and nasal occlusion. Facial reconstruction can be performed in milder cases severe cases with nasal obstruction are usually euthanased at an early age. Brachygnathism (parrot mouth) Brachygnathism occurs when there is overjet or overbite of the upper jaw in comparison to the lower jaw. There is some lack of agreement whether this results from an overgrowth of the premaxilla or an undergrowth of the mandible. Brachygnathism is a common disorder, reportedly present in approximately 20% of horses. 11 Mild cases are rarely problematic and may benefit from feeding from the floor which encourages rostrocaudal movement of the temporomandibular joint. More severe cases which lead to overgrowth of the upper incisors may benefit from incisor rasping although all but the most severe cases will be able to prehend food normally. Brachygnathism can be corrected by surgery and orthodontic devices in young foals but is questionable due to the assumed heritability of the disorder. Prognathism (sow mouth, monkey mouth) Prognathia, where the lower jaw is longer than the upper jaw, is seen much less frequently that brachygnathism but is most common in miniature breeds. Again, most cases are managed conservatively.
Developmental Diastema Developmental diastemata are believed to be due to insufficient angulation of the 1 st, 5 th and 6 th cheek teeth, 8 over-spacing of the primordial dental buds, 5 or insufficient peripheral cementum production. 10 These diastema result in exaggerated transverse ridging on opposed teeth and periodontal disease. In some cases of developmental diastema, resolution will occur following continued eruption and further angulation of the dental row. Dental Impactions Dental impactions most commonly occur with the 3 rd mandibular cheek tooth and are believed to occur due to excessive angulation of the cheek teeth with subsequent delayed eruption of the 4 th premolar, which is the last tooth to erupt. An eruption cyst occurs due to reactive osteolysis of the underlying bone and is commonly seen in young horses on the mandible. These cysts are usually insignificant but are believed to cause pulpar ischaemia and periapical abscessation in some cases. 10 Retained Caps Caps of the deciduous teeth are usually lost during eruption of the permanent teeth. Delayed expulsion of caps may lead to temporary quidding, particularly if the cheek teeth remnants become displaced and cause oral trauma. It is unlikely that caps are implicated in dental impactions and thus should only be removed if loose, displaced or rotated as premature removal results in the disruption of the infundibular cemental vascular supply. Developmental Displacements Developmental displacements occur most commonly in the 4 th and 5 th mandibular cheek teeth and are believed to occur due to overcrowding of the dental row. 8 Rotation as well as displacement of the tooth frequently occurs with resulting periodontal disease of the displaced tooth and focal overgrowths on the opposing dental row. References 1. Berkowitz BKB and Moxham B. (1981) Development of dentition: Early stages of tooth development. In: Dental Anatomy and Embryology, ed. JW Osborn, Blackwell Scientific Publications, Oxford, pp. 166-174. 2. Latshaw WK. (1987) Face, mouth and pharynx. In: Veterinary Developmental Anatomy A clinically Oriented Approach, ed. WK Latshaw, BC Decker, Toronto. 3. Ferguson M. (1990) The dentition throughout life. In: The Dentition and Dental Care, Vol. 3, ed. RJ Elderton, Oxford Heinemann Medical Books, Oxford, pp. 1-18. 4. Eisenmann DR. (1994) Amelogenesis: enamel structure. In: Oral Histology (4 th edition), ed. AR Ten Cate, CV Mosby, St Louis, pp. 218-256.
5. Ten Cate AR. (1994) Development of the tooth and its supporting tissues: hard tissue formation and its destruction: dentinogenesis. In: Oral Histology (4 th edition), ed. AR Ten Cate, CV Mosby, St Louis, pp. 78-103. 6. Warshawsky H. (1983) The teeth. In: Histology (5 th edn), ed. L Weiss, The Macmillan Press, New York, pp. 609-655. 7. Dixon PM, Tremaine WH, Pickles K, Kuhns L, Hawe C, McCann J, McGorum B, Railton DI and Brammer S. (1999a) Equine dental disease part 1: A long term study of 400 cases: disorders of incisor, canine and first premolar teeth. Equine Veterinary Journal 31, pp. 369-377. 8. Dixon PM, Tremaine WH, Pickles K, Kuhns L, Hawe C, McCann J, McGorum B, Railton DI and Brammer S. (1999 b) Equine dental disease part 2: A long term study of 400 cases: disorders of development and eruption and variations in position of the cheek teeth. Equine Veterinary Journal 31, pp. 519-528. 9. Ramzan PHL, Dixon PM, Kempson SA and Rossdale PD. (2001) Dental dysplasia and oligodontia in a thoroughbred colt. Equine Veterinary Journal 33, pp. 99-104. 10. Dacre I. (2005) PhD Thesis, University of Edinburgh. 11. Uhlinger C. (1987) Survey of selected dental abnormalities in 23 horses. In: Proceedings of the American Association of Equine Practitioners 33, 577-583.