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tvpjournal.com | January/February 2016 | Today's VeTerinary PracTice exTernal TooTh resorPTion in caTs Peer reviewed 21 Surface Resorption In humans, surface resorption occurs secondary to minor trauma (eg, mastication, orthodontic therapy) to the root's cementum. Clastic cells resorb the cementum for several days when osteoclast-activating factors are released at the site of injury. When the resorption stops, cells from the periodontal ligament proliferate and populate the resorbed area, resulting in deposition of reparative tissue. In humans, surface resorption is self-limiting and reversible but can eventually progress to become destructive. Infammatory Resorption Infammatory root (cementum, dentin) resorption is thought to be triggered by a variety of factors, including periodontal infammation. These painful lesions often begin in the gingival sulcus around the neck (cervical portion near the cementoenamel junction) of the tooth. Infammatory cells in the lesion may recognize osteoclast-activating factors of the bare root surface (due to removal of cementum), initiating the resorptive process just apical to the marginal gingiva. Alveolar bone adjacent to an infammatory root resorption lesion is usually also resorbed. Two subtypes of infammatory root resorption have been recognized: 1. Transient resorption followed by formation of reparative tissue 2. Progressive resorption due to continued release of infammatory mediators. When resorption progresses coronally, enamel is undermined, breaks off, or is resorbed. Pathogenesis of this subset of resorptions may be due to an inherent local defect of the cementum and defciency in the protective property of the periodontal ligament. 6 Replacement (Noninfammatory) Resorption Tooth resorption that occurs in cats can be infammatory but, more commonly, is characterized by noninfammatory dentoalveolar ankylosis and replacement resorption of unknown cause. Once the root has fused to the bone, the tooth becomes part of the alveolar bone remodeling process and eventually resorbs, which may take years. This can be somewhat seen as a form of healing. When the resorptive process is complete, osteoblasts form bone in the resorbed area. Thus, the dental hard tissue is gradually replaced by bone. These lesions are not considered to be painful as long as they remain sealed below the gingival sulcus. This process is asymptomatic (based on what we know from human dentistry). Replacement resorption does not exclude the presence of a viable pulp, nor is it confned to the root. The lesion generally starts at the cementum, located at the cementoenamel junction, and progresses apically and coronally. PATHOGENESIS Tooth resorption occurs secondary to the activity of multinucleated odontoclastic cells, which resorb the dental hard tissues. Resorption typically starts in the cementum, anywhere along the root surface, and then progresses into dentin apically or coronally. The location of the initial area of resorption usually dictates the outcome. Tooth resorption is considered progressive. • With coronal advancement into crown dentin, enamel may undergo resorption, exposing the lesion to the oral cavity and bacteria. • For resorptions that begin on the root surface deep in the alveolus, a gradual noninflammatory process replaces the periodontal ligament and root with bone- or cementum-like tissue. • Some noninflammatory lesions do not progress and stay apical to the cementoenamel junction. Histologically, clastic cells are responsible for mineralized tissue resorption. Bone-resorbing cells are usually called osteoclasts; however, when these cells resorb mineralized dental tissues or mineralized cartilage, they are called odontoclasts or chondroclasts, respectively. Resorption and repair are regulated by adhesion molecules associated with mineralized tissues (bone sialoprotein and osteopontin) and an associated integrin, alpha-v beta-3, at resorption sites. The progression of infammatory tooth resorption has 2 distinct stages: 1. Acute phase: Odontoclasts create resorptive lacunae in the dentin. If there is an infammatory stimulus, increased numbers of blood vessels will populate the tissues covering the excavated dentin. The pulp and adjacent hard tissue are normal in the acute phase. 2. Chronic remodeling (reparative) phase: Cementoblast- or osteoblast-like cells populate the area, producing a cementum- or bone- like tissue on top of the excavated dentin. The periodontal ligament and adjacent alveolar bone are destroyed. The acute and chronic phases can coexist in a single lesion, with both destruction and repair occurring simultaneously.