Chronic Incisor Periodontal Disease with Cemental Hyperplasia and Hypoplasia in Horses

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1 Published in IVIS with the permission of the AAEP Close this window to return to IVIS Chronic Incisor Periodontal Disease with Cemental Hyperplasia and Hypoplasia in Horses Robert C. Gregory, DVM; Joanne Fehr, DVM, MS, Diplomate ACVS; Jim Bryant, DVM, Diplomate ACVS Authors address: Pilchuck Veterinary Hospital, nd Street SE, Snohomish, WA Take Home Message Aged horses suffering from periodontal disease of the incisors often have cemental hyperplasia and hypoplasia of the affected teeth and osteomyelitis of surrounding bone that can be detected radiographically. Introduction Four aged horses from twenty-three to twenty-nine years of age were admitted to Pilchuck Veterinary Hospital in Snohomish, Washington from January of 2002 to December of 2005 for oral examination because of disease of the incisors. Each presented symptoms of gingival inflammation combined with swelling of the maxilla and or mandible. During radiographic examination of the affected incisors of all four horses, cemental lysis and proliferation and signs of osteomyelitis were observed. The disease process present is not well understood, and these case reports are presented to open discussion on the possible pathology Horse 1 A twenty-six year-old Holsteiner gelding was admitted because of enlargement of the maxillae. The horse had been quidding for one month prior to admission. The owner reported that for the last two years, the horse had shown signs of pain when oral examination was attempted. Hematologic abnormalities included a white blood count of 3,300 cells/mm and 6% eosinophils. The horse would not permit its mouth to be examined, even after it was sedated with detomidine HCL (20mcg/kg, IV) and butorphanol tartrate (0.1mg/kg, IV). Consequently, the horse s mouth was examined while the horse was anesthetized with a short-acting anesthetic agent. During oral examination, thickening of the premaxillae and rostral aspect of the mandible (Fig.1) was observed. Radiographic examination revealed both lytic and proliferative changes in the tertiary cementum. Stage 2 periodontal disease (2) characterized by gingival recession, gingival sulci-greater than or equal to 5-8mm deep, trapped food particles, decay of supra and sub gingival cementum with visible tooth mobility stage 1 was observed. The horse was euthanized after it developed signs of colic 12 hours after examination. Post mortem examination

2 Figure 1. Lateral radiographic projection of the rostral portion of the mandible and premaxillae of a twenty-six year-old horse suffering from severe periodontal disease of the premaxillary and madbular incisors. showed that signs of colic were caused by spontaneous rupture of the small colon. The diseased premaxillae and mandible were not available for histological examination. Horse 2 A twenty-nine year-old Thoroughbred gelding was presented to the clinic because of choke. During oral examination, severe disease of the incisors was observed. Stage 4 periodontal disease was present, and the gingiva surrounding all incisors was nearly completely recessed and was ulcerated and edematous. The tooth roots were exposed. Sulcular epithelium was necrotic, and a purulent discharge was present between the teeth. Teeth 101, 102, and 403 (Triadan numbering system) were moderately to severely mobile. Abnormalities noted during radiographic examination of teeth and surrounding tissues include loss of alveolar bone, apical blunting, and lytic and proliferative changes in subgingival crown and root (Fig. 2). The horse was treated by extracting teeth 101, 201, and 403 while the horse was anesthetized with a short-acting anesthetic agent. Remaining incisors were reduced to improve alignment, and the cheek teeth were floated to partially correct a wave mouth that was present. The horse was administered trimethoprim-sulfa (24mg/kg), q 8h for 28 days. 0.12% chlorhexidine Rinse was applied to the coronal-gingival margin with a soft brush twice daily. Histological examination of gingiva and bone revealed chronic gingivitis, and unidentified osteomyelitis as a bacterial culture did not indicate a specific agent. A six month re-check exam showed improvement of the periodontal disease in the remaining teeth 101 and 201.

3 Figure 2. Dorsoventral radiographic projection of the premaxillae of a twenty-nine year-old horse suffering from severe periodontal disease of the premaxillary incisors. Figure 3. Dorsoventral radiographic projection of the premaxillae of a 25-year-old horse affected with severe periodontal disease of the incisors. Horse 3 A twenty-five year-old Thoroughbred mare, which had not received an oral exam for two years, was examined because it had difficulty chewing. A parasagittal buccal fracture of both the was observed. Secondarily to the fracture, remodeling of the premaxilla 10 to 15 mm above the exposed maxillary incisor root was observed. Tooth 203 the left corner incisor was affected by stage 2 periodontal disease. Radiographic examination revealed both lysis and proliferation changes in the sub-gingival coronal cementum (Fig. 3). The horse was treated with trimethoprim-sulfa (24mg/kg, q12h, orally) for 14 days and 0.12% chlorhexidine rinse for 14 days. Horse 4 A twenty-three year-old Throughbred mare was referred to Pilchuck Veterinary Hospital because of signs of infections of the right paranasal sinuses and for removal of a 110 buccal fracture fragment of tooth. During oral examination, caries were observed in 109, 209 and a fractured mandibular incisor (403). Radiographic examination of the rostral aspect of the mandible revealed severe cemental hypoplasia of teeth 402, 403 and moderate lysis in teeth 302 and 303 (Fig. 4). Teeth 403 and 303 were removed using gingival tissue flaps to cover the alveolus and the horse was treated with trimethoprim-sulfa (24mg/kg, q 12h, orally) for 28 days and phenylbutazone (2.2mg/kg, q 12h, orally) for 5 days. A bacterial culture of alveolar tissue was negative for aerobic and anaerobic bacteria. Histopathologic examination of the bone of the rostral portion of the mandible indicated periosteal proliferation and chronic fibrosis.

4 Figure 4. Ventrodorsal radiographic projection of the rostral aspect of the mandible of a 23-year-old horse. Discussion Cemental hypoplasia and cemental hyperplasia were observed radiographically in premaxillary and mandibular incisors of these four aged horses. Histopathological examination and bacterial culture of biopsies of affected tissue in two of these horses did not identify the etiology of the disease. Halicephaliobus deletrix, a saprophytic organism found in decaying humus, was found by Ruggles et al 1 to be a causative agent of osteolytic change of the mandible or maxilla in a horse. The parasite has been reported to infect the maxilla, mandible, the kidneys and the CNS. No kidney disease or disease of the CNS was observed in the four horses in this study, and no parasites were observed during histological examination of tissue, including bone, that was removed from the affected premaxillae or mandible of two of these horses. Changes in the cementum observed radiographically maybe a response by the cementum to severe inflammation. 2 Cementum is a living tissue and contains two types of epithelium. 2 Perhaps one type of epithelium becomes hypoplastic when inflamed and the other becomes hyperplastic. Research to determine the response of cementum to inflammation may lead to a reason for these radiographic findings.

5 References 1. Ruggles AJ, Beech J, Gillett DM, Midal LT, Reef VB, Freeman DE. Disseminated Halicephalobus deletrix infection in a horse. JAVMA 203(4) Klugh DO, et al. Equine Periodontal Disease. Clinical Techniques in Equine Practice 4(2); , 2005.