Update on the Etiology of Tooth Resorption in Domestic Cats

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vet clin small anim 35 (2005) 913–942 update on the etiology of..compared with cats without forl [5], indicating that multiple tooth resorption..all rights reserved. doi:10.1016/j.cvsm.2005.03.006 vetsmall.theclinics.com 914 reiter et al surface, where mononuclear cells fuse with other...

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Update on the Etiology of Tooth Resorption in Domestic Cats pdf

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Update on the Etiology of Tooth Resorption in Domestic Cats - page 1
Vet Clin Small Anim 35 (2005) 913–942 Update on the Etiology of Tooth Resorption in Domestic Cats Alexander M. Reiter, Dipl Tzt, Dr Med Vet a, *, John R. Lewis, VMD a , Ayako Okuda, DVM, PhD b,c Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, 3900 Delancey Street, Philadelphia, PA 19104–6010, USA b Department of Anatomy, School of Veterinary Medicine, Azabu University, Fuchinobe, Japan c Vettec Dentistry, Tokyo, Japan a Feline odontoclastic resorptive lesions (FORL) were first recognized and histologically differentiated from caries in the 1920s [1,2]. Some anecdotal reports describing caries-like lesions at the cervical region of feline teeth followed in the 1950s and 1960s, until two microscopic studies in the 1970s again revealed that FORL were not caries but a type of tooth resorption [3,4]. A recent study showed that cats with FORL have a significantly lower urine specific gravity and significantly higher serum concentration of 25- hydroxyvitamin D (25OHD) compared with cats without FORL [5], indicating that multiple tooth resorption in domestic cats could be the manifestation of some systemic insult rather than a local cause. In this article, the histologic and radiographic appearance of FORL and certain other peculiarities of feline teeth are reviewed. An attempt is then made to compare these findings with changes of the periodontium induced by administration of excess vitamin D or vitamin D metabolites in experi- mental animals. Histologic and radiographic features of feline odontoclastic resorptive lesions Tooth resorption is caused by odontoclasts. Their precursors derive from hematopoietic stem cells of bone marrow or spleen and migrate from blood vessels of the alveolar bone or periodontal ligament toward the external root * Corresponding author. E-mail address: reiter@vet.upenn.edu (A.M. Reiter). 0195-5616/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.cvsm.2005.03.006 vetsmall.theclinics.com
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Update on the Etiology of Tooth Resorption in Domestic Cats - page 2
914 REITER et al surface, where mononuclear cells fuse with other cells to become multinucleated mature odontoclasts [6,7]. One important fact to understand is that FORL develop anywhere on the root surface and not just close to the cementoenamel junction [8]. Resorption of enamel as the initial event is only rarely observed [9]. Resorption may also start on the same tooth at various root surfaces simultaneously, progressing from cementum coronally into crown dentin as well as apically into root dentin. As the resorption progresses into crown dentin, the enamel often becomes undermined and a pink discoloration may be observed at the crown surface [10]. FORL that emerge at the gingival margin were originally referred to as neck lesions (Fig. 1) [4]. Exposure to periodontal inflammation, which is caused and maintained by bacterial infection, results in the formation of highly vascular and inflamed granulation tissue [11–16]. These defects may be painful and bleed easily when probed with a dental instrument [10]. One characteristic feature of inflammatory root resorption is that the alveolar bone adjacent to the tooth defect is also resorbed [17]. Such root lesions have been categorized as type I root lesions if unaffected root areas are surrounded by a radiographically visible periodontal space (Fig. 2) [18]. Although pulp involvement may be seen in advanced stages of FORL [19,20], the cervical root resorption in human beings typically proceeds laterally and in an apical and coronal direction, surrounding a thin shell of dentin and predentin, and envelops the root canal, leaving an apple core appearance of the cervical area of the tooth [21]. It has been demonstrated in several studies in human beings that superficial external resorption is common and usually self-limiting [22]. Spontaneously repaired defects of cementum and superficial dentin are called surface resorptions, in which the anatomic contour of the root surface is restored [17]. Most clinically evident FORL appear histologically to be in resorptive and reparative phases simultaneously [14]. Although attempts at repair can be noted by production of bone, cellular cementum, and bone- cementum [12–14,19,20,23], tooth resorption in cats is usually progressive Fig. 1. Classic ‘‘neck lesions’’ at the right lower third (*) and fourth premolar teeth (arrowheads).
Update on the Etiology of Tooth Resorption in Domestic Cats - page 3
TOOTH RESORPTION IN DOMESTIC CATS 915 Fig. 2. Radiograph of teeth in Fig. 1; note that inflammatory root resorption is associated with adjacent alveolar bone resorption (dotted line outlining the alveolar margin). and continues until the roots are completely resorbed or the crown breaks off, leaving root remnants behind [10]. Most previous research focused on FORL emerging at the gingival margin. The commonly observed fusion of roots of feline teeth with alveolar bone (dentoalveolar ankylosis) has not received the same investigative attention. It has previously been reported that the periodontal space is quite narrow in mandibular premolars and molars of adult cats [24]. In a recent histologic study, clinically and radiographically healthy teeth from cats with FORL on other teeth were evaluated. These apparently ‘‘healthy’’ teeth showed hyperemia, edema, and degeneration of the periodontal ligament, with marked fiber disorientation, increased osteoid formation along alveolar bone surfaces (hyperosteoidosis), gradual narrowing of the periodontal space, and areas of ankylotic fusion between the tooth and alveolar bone (Fig. 3) [25]. These findings demonstrate events that occur before resorption and suggest that the early FORL may be noninflammatory in nature [25]. Ankylosed roots are at risk of being incorporated into the normal process of bone remodeling, and the tooth substance is gradually resorbed and replaced by bone (replacement resorption) (Fig. 4) [10]. Ankylosed roots and those with replacement resorption have been categorized radiographically as type II root lesions [18]. Peculiarities of feline permanent teeth It has previously been suggested that there is a need for further microscopic research to differentiate histopathologic findings of FORL from normal anatomy of feline teeth [26]. Several peculiarities can be noted in permanent teeth of cats that could represent separate pathologic entities or be associated with FORL. Cementum is an avascular bone-like tissue covering the roots of mammalian teeth. It normally covers the cervical root surface as a thin
Update on the Etiology of Tooth Resorption in Domestic Cats - page 4
916 REITER et al
Update on the Etiology of Tooth Resorption in Domestic Cats - page 5
TOOTH RESORPTION IN DOMESTIC CATS 917 Fig. 4. Radiograph of dentoalveolar ankylosis and root replacement resorption of mandibular canine teeth (dotted line outlining original root contour); also note the bulbous enlargement of crestal alveolar bone (arrowheads). layer that gradually becomes wider apically. Two types of cementum (acellular and cellular) are usually recognized, which can be further subdivided depending on the presence and origin of collagen fibers (afibrillar, intrinsic, or extrinsic). Cementum formation beyond physiologic deposition is called hypercementosis and can commonly be observed in teeth of cats with FORL [12]. In one study, hypercementosis was demonstrated in all investigated feline teeth [14]. Excessive amounts of cellular cementum are deposited particularly at apical and midroot surfaces, sometimes causing bulbous root apices (Fig. 5), whereas an abnormal thickening of acellular cementum can be found on cervical root surfaces (Fig. 6) [25]. In other species, hypercementosis has been observed in unerupted, hypofunctional, and extruding teeth without opposing antagonists [27–30] and in certain conditions, such as hyperthyroidism [31], hyperpituitarism [32–34], Paget’s : Fig. 3. Histopathologic pictures of a feline premolar tooth with a normal furcation area (A) and a premolar tooth of a cat with feline odontoclastic resorptive lesions on other teeth showing degeneration of the periodontal ligament, narrowing of the periodontal space, and dentoalveolar ankylosis (B). Close-up of apical area of tooth root showing periodontal ligament degeneration and two areas of ankylotic fusion (arrows) between cementum (C) and alveolar bone (B).
Update on the Etiology of Tooth Resorption in Domestic Cats - page 6
918 REITER et al Fig. 5. Radiograph showing bulbous root apices of the right lower fourth premolar and first molar in a cat; note the missing third premolar tooth (*). disease [35–37], and vitamin A deficiency [38,39]. It has also been demon- strated that occlusal trauma does not lead to hypercementosis [40,41]. Some cats seem to exhibit abnormal extrusion of teeth, referred to as supereruption [10]. Supereruption is most commonly observed in maxillary Fig. 6. Histopathologic pictures of a premolar in a cat with thin cervical cementum and normal biologic width (A) and a premolar of a cat with feline odontoclastic resorptive lesions on other teeth showing cervical hypercementosis, bulbous enlargement of crestal alveolar bone, and loss of biologic width (B). B, alveolar bone; C, cementum; D, dentin; G, gingival connective tissue.
Update on the Etiology of Tooth Resorption in Domestic Cats - page 7
TOOTH RESORPTION IN DOMESTIC CATS 919 canine teeth, leading to exposure of the root surface (Fig. 7). Normally, active eruption of brachyodont teeth does not cease when they meet their opposing teeth but continues throughout life; ideally, the rate of eruption keeps pace with tooth wear, preserving the vertical dimension of the dentition [42]. It has been speculated that supereruption in cats may be the result of hypercementosis [43] or increased osteoblastic activity of periapical alveolar bone [44]. Another peculiarity found in cats is a distinct thickening of bone along the alveolar margin or the surfaces of the alveolar plates, alone or in combination with supereruption. This alveolar bone expansion is commonly seen in maxillary canine teeth but occurs with less intensity around other teeth as well (Fig. 8) [10]. In human beings, a similar condition is called ‘‘peripheral buttressing’’ and is believed to be a result of the body’s attempt to compensate for lost bone during the reparative process associated with trauma from occlusion. The condition may present as shelf-like thickening of the alveolar margin, referred to as ‘‘lipping’’, or as a pronounced bulge in the contour of the alveolar bone [45]. Unusual dentin formation has been described in feline teeth. In one study, osteodentin could be demonstrated in most feline premolars and molars, particularly in furcation areas of root dentin close to the root canal [13]. In osteodentin, cellular inclusions (remnants of odontoblasts) can be found between randomly running dentinal tubules. FORL were observed in areas of the tooth in which osteodentin was most typically found [13]. Vasodentin was found in 3 of 10 control teeth and in 6 of 49 teeth with FORL and was most often observed in the outer third of circumpulpal dentin [46]. In vasodentin, dentinal tubules run randomly, with penetration of canals that may contain vascular-like tissue. Another study found vasodentin almost equally in teeth with or without FORL, although the Fig. 7. Clinical picture (A) and radiograph (B) of the left upper canine tooth showing supereruption (arrows and dotted line outlining the cementoenamel junction).
Update on the Etiology of Tooth Resorption in Domestic Cats - page 8
920 REITER et al Fig. 8. Radiographs of alveolar bone expansion (arrowheads) of upper (A) and lower canine teeth (B) in cats with missing teeth and feline odontoclastic resorptive lesions on other teeth. locations of vasodentin and FORL differed [13]. Furcation canals connecting the pulp chamber and the periodontal ligament were found in deciduous premolar teeth in kittens as well as in teeth of adult cats [47,48]. After experimental pulp injury, changes in the periodontal ligament at the opening of the furcation canal and resorption of dental tissues and alveolar bone in the furcation area took place [48]. In a more recent study, patent furcation canals were found in 27% of permanent carnassial teeth in adult cats [49]. Irregularities in dentin formation are generally considered to be evidence of deficient mineralization during dentinogenesis [50]. The inclusion of
Update on the Etiology of Tooth Resorption in Domestic Cats - page 9
TOOTH RESORPTION IN DOMESTIC CATS 921 odontoblasts or pulp tissue into dentin may also be attributable to times of rapid mineralization of newly formed dentin matrix, however. This view is supported by the observation that the layer of predentin appeared extremely thin or was not present in teeth of cats with FORL [51]. Increased vitamin D activity in cats with feline odontoclastic resorptive lesions Although FORL may have occurred more than 800 years ago [52], retro- spective studies of zoologic collections of feline skulls showed a low prevalence of FORL before the 1960s [53,54]. It was suggested that the increased prev- alence of FORL might be associated with aspects of domestication, such as altered feeding practices, vaccination, and neutering programs [10]. Unlike bone that undergoes resorption and apposition as part of a continual remodeling process, the roots of permanent teeth are normally not resorbed because of resorption-inhibiting characteristics of unmineral- ized layers on external and internal root surfaces (eg, periodontal ligament, cementoblasts and cementoid, odontoblasts and predentin) [10,17]. Odon- toclasts may be attracted only to, or can attach only to, mineralized tissue. It has been postulated that removal or mineralization of the organic matrix of the root covering would make it possible for odontoclasts to recognize the mineral component [10,17]. Measurement of biochemical markers of bone turnover, bone alkaline phosphatase (BAP) and deoxypyridinoline (DPD), did not show significant differences between cats with and without FORL [55]. It has recently been demonstrated that cats with FORL expressed a significantly higher mean serum concentration of 25OHD compared with cats without FORL, how- ever [5]. Furthermore, the mean serum concentrations of blood urea nitro- gen and phosphorus were significantly higher and the mean urine specific gravity and mean calcium-phosphorus ratio were significantly lower in cats with FORL compared with cats without FORL [5]. Although the mean values of renal parameters remained within physiologic range, the results suggest the possibility of gradual impairment of renal function in cats with FORL. Using a human radioimmunoassay not yet validated for use in cats, calcitonin was significantly more often detected in blood sera of cats with FORL, which may be an expression of protective secretion during times of transient mild hypercalcemia [5]. It was also demonstrated that cats with FORL vomited significantly more often than cats without FORL [5,56]. The diet represents the only source of vitamin D in cats because they are unable to produce vitamin D in the skin [57]. Based on feeding studies in the 1950s, the National Research Council proposed a minimum vitamin D requirement for growing kittens of 500 IU/kg of dietary dry matter [58]. Later studies demonstrated that kittens given a diet with vitamin D 3 per kilogram of dry matter at a rate of 250 or 125 IU did not show clinical signs
Update on the Etiology of Tooth Resorption in Domestic Cats - page 10
922 REITER et al Table 1 Changes in dental and periodontal tissues of experimental animals receiving excess vitamin D or vitamin D metabolites Age/weight at start of experiment 127–182 g Reference no. [103] Species Rats Type of vitamin D Vit D (nfd) Dose 307,000–1,860,000 IU (once); killed after 48 h Route of administration SC Additional methods n/a Diagnostic tools H [108] Dogs 39 d irrad D2 or D3 10,000 IU/kg BW  9.5 mo Food Some dogs also given excess vit A R þ H [109,119] Dogs 29 or 34 d irrad D2 450,000 IU (once); killed at 2.5, 4, or 9 mo of age 10,000 IU/kg BW/d  6 mo (intermittently) (total 1,270,000 and 1,450,000 IU); killed after additional 5 mo of ‘‘recovery period’’ 500,000 IU (once); killed after 6 d PO n/a R þ H [110,114] Dogs 2 mo D2 or D3 Food n/a R þ H [105] Rats 21 d (w100 g) D2 P n/a R þ H (I þ M) [97] Rats 40–50 g D2 100,000 IU on 1st, 4th, 7th, 10th, and 14th d; killed on 15th d IP Some rats also given a collagen- damaging lathyrogen n/a H (M) [121] Rats 50–150 g D2 50,000–200,000 IU  2–4/wk; sacrifice after 1–12 wk PO H (LM þ EM) [111] Rats 154 g D2 1.25 mio IU/kg of diet  6 wk Food n/a H (M) [112] Hamsters 4 mo D2 5,000 IU twice/wk  8 wk IP n/a H (M) [102] Pigs 5d D3 45,000–162,000 IU/d  17–48 d PO n/a H
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