Based on the history, oral examination and radiographic documentation the working diagnosis is made and a subsequent treatment plan is initiated. An attempt at classifying the underlying etiology of the disease is made.
Based on the history, oral examination and radiographic documentation the working diagnosis is made and a subsequent treatment plan is initiated. An attempt at classifying the underlying etiology of the disease is made. The approach to treatment can be dramatically dissimilar if for example you are treating a suspected jaw swelling as an osteomyelitis when in reality it is due to a neoplasia. The end result of treatment should be an amelioration of the clinical symptoms and either an improvement of the radiographic signs if involving periodontal or endodontic disease or verification of a post-surgical procedure i.e. extraction or mass resection.
For purposes of treatment rationale, oral pathology can be classified according to the causal etiology and the tissues being primarily affected. For purposes of time constraints our discussion will exclude genetic disease and neoplastic maladies and cover those oral diseases which have development causes These are further divided into those that affect the teeth gingiva and bone and fall into the following categories: dental eruption disorders, inflammatory / infectious disease, and traumatic injuries.
Dental eruption disorders encompass teeth that are either partially or completely impacted, or misaligned. The brachiocephalic breeds like the Boxers, Shih Tzu, Lhasa Apso and the Maltese are more prone to this development due to crowding from inadequate jaw space to accommodate the full complement of teeth. In contrary, other breeds have impactions due to tooth malformation or transposition of the adult tooth buds which then lead to eruption problems.
In the case of partial or total impaction, clinically the normal eruption times for deciduous and adult teeth are prolonged. Either individual or groups of teeth may be affected. Often the clinical crowns might be present but dramatically reduced in height or tipped in their axis when compared to the teeth of the contralateral side. Frequently, in place of the tooth is a large fluctuant purplish swelling. The animals are usually not affected in their behavior or eating habits. Depending on the encountered pathology the end result of impactions usually is cyst development.
In the case of partial eruptions clinically visible is that the horizontal axis of the crown becomes tipped. Radiographically the axes of the roots of the affected teeth develop abnormal curvatures or dilacerations to accommodate for this restricted coronal growth. In the human literature they attribute dilacerations possibly to trauma. It is further hypothesized that this confinement impacts the development of the endodontic system which, depending on the severity of the curvature may lead to vascular compromise and pulpal necrosis. Often visible under the affected teeth are periapical lucencies due to the leaching of the devitalized pulpal tissue into the surrounding bone. These teeth need to be treated either endodontically i.e. with a root canal or surgically extracted due to the danger of bone loss and fracture.
Contrary to a partial impaction or incomplete eruption, is the sequellae associated with a total impaction of the adult tooth. In the literature, Odontogenic cysts often result from lack of eruption. These cysts are classified into: Periapical or radicular cysts, Dentigerous or follicular cysts and Eruption cysts. The definition of the true cyst is an epithelium-lined pathologic cavity.
Periapical cysts develop usually from non-vital teeth and necrotic pulp. The apical inflammation results in the formation of a dental granuloma. The degradation products of the pulpal necrosis stimulate the epithelial rests of Malassez which are located in the periodontal ligaments. This epithelial proliferation leads to a periapical cyst which as more debris develops within the cyst there is an increase of osmotic pressure. The pressure increase draws fluid within the cyst and a stimulation of the surrounding osteoclasts to break down more bone of the surrounding bone leading to cystic enlargement. If the cyst ruptures and hemorrhage forms within the cyst, dystrophic calcification can occur. In people the radicular cysts are usually asymptomatic and cannot be differentiated radiographically from the granuloma. If they are long-standing cysts they can cause root resorption of the offending teeth and adjacent teeth. The treatment is usually to extract the non-vital tooth and curette the apical zone. An alternative would be to do an apicoectomy and direct lesional curettage.
The calcifying odontogenic cyst is believed to be derived from odontogenic epithelial remnants within the gingiva or within the mandible or maxilla. The cyst usually consists of a single cavity in which the fibrous wall encloses an epithelial lining which is irregular in structure. The basal cell layer consists of ameloblast-like cells. The most characteristic of this cyst is the keratinized, anucleate "ghost" cells which form small foci within the epithelial lining or larger keratin masses which extend into the cystic lumen. Mineralization of these ghost cells is common and calcified masses of variable sizes are seen. The cysts usually are solid and are amenable to simple excision.
In contrast to the above impaction cysts are eruption problems that are due to either inadequate jaw growth or transposition of the adult tooth buds. Both lead to teeth that erupt into a malocclusion with the opposing arches' teeth. When teeth hit or traumatize other teeth or soft tissue the resulting defects can lead to either a devitalization of the maloccluding teeth or a breakdown of their periodontal ligaments causing periodontitis and loss of the tooth. When the lower canine teeth malerupt in a "base narrow" or more lingual they traumatize the hard palate and this eventually leads to a permanent oro-nasal fistula.
The malocclusions can usually be dealt with by extraction of the lesser important tooth. As alternatives to this, teeth can orthodontically be moved into a more anatomic position or reduced in their height by crown reducing and vital pulpectomies. The latter procedure involves reducing the crown and removing 5-8 mm of the pulp. This is then covered with calcium hydroxide which will stimulate the odontoblasts to lay down secondary dentin. The procedure allows for the retention of the tooth and maintenance of the alveolar ridge. It is less invasive than the surgical extraction and less after care then performing orthodontic movement.
Pathology of the supporting tooth structures, called the periodontium, is defined as periodontitis. The clinical symptomology of inflammation: redness, bleeding, edema, gingival recession and bone destruction is brought on by the host's reaction to the bacterial colonization of supragingival plaque. As the disease progresses there is a continued loss of the alveolar bone and the periodontal ligaments. Radiographically this is seen as a reduction in height of the crestal bone. Exposure of the roots and further bony pocketing around the teeth allow for the subgingival plaque and calculus to develop. The ultimate loss of the tooth's attachment apparatus occurs and eventually the tooth becomes mobile as more of the supporting bone is eroded. Since the teeth of the mandible occupy much of the jaw space, in toy breeds often idiopathic jaw fractures occur as the periodontal disease becomes more rampant.
Depending on the grade of severity, periodontal disease is classified into Class I –Class V. The higher the number the more severe the symptoms are. In Class V disease greater than 50% of the alveolar bone is lost and there is increased tooth mobility. Seen on the radiograph is widening of the periodontal space and often signs of concurrent endodontic disease (periapical lysis) and root resorption. Depending on this classification, the treatment ranges from a thorough dental scaling and polishing in Class I-II disease. Class III involves closed curettage of the gingiva, root planing of the root and pocket treatment with doxycycline gel. Class IV disease treatment, due to the increased pocket depth, involves laying a gingival flap and open curettage and root planning. Any infrabony lesions between the teeth and the supporting alveolar bone are treated with alveoloplasty to smooth any rough bony contours, possibly bone grafting and apical reposition flaps. Sometimes at this stage in order to provide stability to the mobile teeth an interdental splint is placed. Usually in Class V disease the teeth are severely affected and need to be extracted. Since in periodontal disease many stages are present in one animal, the treatment involves multiple techniques in order to bring about appropriate healing.
Any etiology which leads to an insult of the pulpal chamber and root canal will develop into a pulpitis. In the case of blunt trauma there often is no open fractured tooth. The inflammation of the inside pulp tissue occurs and the intra-dental pressure builds. This forces the blood pigment through the dentin tubules which turn the tooth clinically pink. Since the space for expansion of these inflamed tissues is limited, the pulp starts to undergo necrosis and eventually the tooth devitalizes. The blood pigment breaks down to form hemosiderin and the tooth changes in color to grey. Radiographic appearance of pulpitis that has occurred to young growing teeth shows disproportionately large root canals and often significant periapical rarification of the affected tooth. This latter effect is due to the abundance of necrotic pulp tissue which seeps out the tooth's apex and inflames the periapical bone. Periapical cysts or granulomas can form. In the case of the former, as it grows more of the surrounding bone becomes from the pressure demineralized. The treatment rationale is to either extract the tooth and curette out the alveolus or perform a root canal therapy. In the later treatment an access hole is drilled in the tooth and all of the pulpal elements in the canal is removed with meticulous filing and flushing. The so prepared canal is then filled or obturated with an inert substance. This will prevent leakage out the apex. The root canal access hole is then filled to prevent microleakage from the oral cavity.
If the traumatized tooth is fractured the exposed pulp will be infected. The rate of infection and ultimate devitalization is dependent on the following factors: age of animal (younger has greater resistance to infection), length of exposure duration and type of microorganisms in the mouth. In the last factor, if the animal is coprophagic, the devitalization is extremely rapid. The treatment option for a freshly exposed (within 72 hours) vital tooth is a vital pulpectomy and pulp capping with calcium hydroxide. Unlike the utilization of this procedure for malocclusions where the tooth is reduced under sterile situations, the traumatized open fractured tooth has a higher degree of failure. As an alternative either extraction or root canal therapy can be tried.
These events are often encountered as a sequella to perforating wounds of the oral cavity with sticks or thorns and inoculation of the deeper lying tissue with noxious bacterium. These wounds quickly develop into draining tracts. Radiographic documentation can be challenging and often fistulograms fail. Clinically the bone looses its white appearance and becomes yellowish in color. It does not bleed. Radiographic appearance of dead bone appears sclerotic. More often the case for osteomyelitis and subsequent bone sequestration is as a result of improper forceful tooth extraction. The overzealous operator with too much pressure separates underlying tissue from its blood supply. The tissue often isn't sutured over the bone. The subsequently exposed alveolus blood clot breaks down and a dry socket ensues. Devoid of the necessary clot for healing the bone quickly devitalizes. The animal is clinically in extreme pain from this alveolitis. The treatment of choice is to remove any devitalized bone to bleeding tissue. This is then covered with a mucosal flap to protect the developing clot.
Depending on the extent, type and angle of external forces generated on the bones of the skull, this will lead to either simple or compound, closed or open fractures. Clinically depending on which bones are involved adjacent structures can be compromised. Not uncommon is ocular contusions and perforation of the tympanic membrane in maxillary fractures. Epistaxis, oral hemorrhage and respiratory dyspnea are routinely present with palatal bone disruption. Mandibular lateralization occurs to the ipsilateral side of mandibular ramus fractures and fractures of the TMJ condyle. Lateralization occurs to the contralateral side of a dorso cranial TMJ luxation.
Fractures can be self inflicted as in the case of mandibular avulsion fractures when animals stick their mouths in cages, panic and try to pull back suddenly. Due to the fact that the mandibular canines occupy more than 80 % of the jaw, fractures behind this tooth routinely occur. Iatrogenically induced fractures are as a result of improper extraction technique on severely compromised tissue. Often due to the fact that prior to extractions, radiographs are not taken, underlying disease states are often missed.
Therapeutic osseous repair must take into consideration any dental elements which are involved with the fracture site. Combination of wiring and acrylic bonding techniques should be utilized for stabilization. Any teeth within the fracture site should be removed immediately or subsequently root-canalled after the primary bone callus has formed. Any bone fragments that have been separated from their blood supply should be removed. All exposed bone needs to be covered with mucosal flaps in order to speed healing.