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Recognising oral diseases

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Recognising oral diseases

  1. 1. CANINE ORAL DISEASESDr. Tony CaiafaUniversity of MelbourneVeterinary Clinic and HospitalPrinces Highway, Werribee, 3030Email toothdoc@tpg.com.auCanine oral diseases can have a significant debilitating effect on the animal’s overallhealth.Diagnosis of oral disease requires a thorough examination of the head, neck andoral cavity including draining lymph nodes of the head and neck region, assessmentof temporo-mandibular joint function and masticatory muscle function as well asintraoral structures including the periodontium, the alveolar mucosa, the tongue,oropharynx and salivary glands.Paedodontics- The study of oral and dental structures in the immature developinganimal. • Retained deciduous teeth- often retained deciduous incisors and canines especially in smaller breeds of dogs. Retention may be environmental or genetic, and may result in malocclusion of permanent teeth. Also, retained deciduous teeth can lead to increased plaque accumulation and periodontal disease. • Missing teeth (oligodontia)- especially missing permanent premolar teeth in some larger breeds. If uncertain re the presence or absence of the permanent tooth, take a radiograph. • Interceptive orthodontics (see later) • Vital pulpotomy therapy  for fractured immature permanent teeth.  for base narrow condition.Vital pulpotomy StepsPartial pulpectomy (vital pulpotomy) steps.Remember- works best in younger dogs (under one year of age) and also lesspredictable an outcome, if performed >7 days post trauma. Monitor these patientspost treatment for possible loss of pulpal vitality. Continuing radiographicassessment required for 1. pulpal necrosis (periapical radiolucency around tooth apex), or 2. ceased development of the tooth (no further dentine formation or apical closure in a young dog), or 3. clinically, an external draining sinus.Signs of success are indicated by continuing dentine development, apical closure ordentinal bridge formation at the pulp amputation site.Clinical steps1. Amputate part of crown (for base narrow canines, or traumatic occlusions only).For trauma cases skip this step.2. Drill out about 5mm of pulp. Flush pulp with sodium hypochlorite until bleedingstops, or flush with saline or place a paper point over pulp stump for 5 min. approx. 1
  2. 2. 3. Place Calcium hydroxide (CaOH2) over non bleeding pulp stump. Can use hardsetting CaOH2 like life or dycal, with a CaOH2 applicator. Can also use a non settingCaOH2 like pulpdent paste or CaOH2 powder mixed with sterile saline. (about 1mmthick).4. Remove any excess CaOH2 on the internal walls of your access hole, and place areinforced glass ionomer cement (RGIC) such as Vitrebond over your CaOH2 . Thismaterial is visibly light cured (can purchase light curing machines second hand forabout $400). Can also use a chemically cured GIC like Ketac Fil (you do not need tolight cure this), about 1-2 mm thick. GIC provides a firm base so that you can placeyour composite resin without disturbing the CaOH2.5. Acid etch the dentine and enamel with 37% phosphoric acid etch and rinse offafter 30 sec and dry thoroughly. Place a light cured primer/adhesive like 3M bond oranother bonding adhesive for composite resin cements.6. Place your composite resin cement in two stages. Firstly place a flowablecomposite as a base. Then use a hybrid type of composite resin cement like Z250(3M) and use a whiter shade like B1. It is a close match to canine enamel. Build it upin 2 mm increments up to the level of your crown amputation or level of the fracture(light cure this).7. Finally, finish and smoothe over your composite resin cement with compositefinishing burs in the high speed handpiece. You may also use soflex discs (3M) in aslow speed handpiece. Then place another layer of light cured adhesive over this toseal any exposed dentinal tubules at the fracture or amputation site.8. Monitor the case say at 6 months post surgery, hopefully with a radiograph tomake certain that there is no pulpal necrosis. Also, composite resins are not asstrong as natural tooth structure and can break off. They can be easily replacedthough.Warn patients- especially in the first 6 months post surgery re No Bones, No Rocksor Sticks- these can break of your composite resin cement. This is why I put a twolayer composite resin cement closure, so that if the top layer fails, the second layerwill still protect the pulp.Periodontal disease  Recognising the symptoms and signs of periodontitis  Formulating a treatment plan based on the severity of disease, age of the patient and willingness of owner to instigate home-care  Monitoring and recallPeriodontal disease (PD) is the most common disease in small animal practicetoday.A high number of middle aged dogs will have some degree of periodontitis.However, it is commonly under-diagnosed because, firstly, periodontitis has very fewsymptoms, so that owners are unaware of any problems and secondly, practitionersare not looking for PD during routine examinations i.e. at annual vaccination time.Periodontal disease is an inflammation and destruction of the teeth’s supportingstructures. The periodontium consists of the cementum, alveolar bone, periodontalligament and gingivae. The oral mucosa is unique in that it is made up of anectodermal lining, which is pierced by teeth. The dentogingival margin thereforerepresents a weak area in the oral mucosas protective and defensive roles.Aetiology and natural progression of diseaseThe primary aetiological factor that causes PD is bacteria. Also, there are secondaryfactors that can contribute to the severity of the disease. Secondary factors such as 2
  3. 3. tooth crowding, retained deciduous teeth, systemic illnesses like renal failure ordiabetes mellitus, Smoking in man, will also increase the risk of PD.It is within the gingival sulcus, that the bacteria that cause PD live. Bacteria, bacterialproducts and toxins as well as the body’s own defence mechanisms contribute to theinitiation and continuation of PD. PD is not a continuous non-stop process. Itrepresents a process that is characterised by periods of active tissue destruction andthen periods of quiescence. It can occur at different locations within the oral cavity,and not always occurring at the same time (Random burst theory).PathogenesisFor PD to occur, one needs bacteria. Bacteria attach to the tooth surface byadhering to the tooth pellicle (Salivary glycoproteins). The pellicle is firmly attachedto the teeth and even after ultrasonic scaling/polishing; it will reform on the toothsurface within minutes.Once attached, plaque can only be removed from the tooth surface by mechanicalmeans i.e. tooth brushing.Initially, gram positive aerobic bacteria attach to the tooth surface supragingivally(often seen as a thin white film covering the teeth).But over a period of time, as the gingiva becomes irritated by this plaque, it swellsand lifts away from the tooth (chronic marginal gingivitis). Chronic marginal gingivitisis defined as inflammation of the marginal gingival tissues and is characterised byredness, swelling and bleeding. Gingivitis, if treated correctly, is reversible and thehealth of the periodontium can be restored to normal. If the plaque is leftundisturbed, it eventually penetrates sub-gingivally. The bacterial composition of theplaque then changes to a predominantly gram negative anaerobic motile flora. Thisflora is responsible for the initiation of PD. The principle bacteria incriminated in PDare Bacteroides and Fusobacterium spp.The bacteria and their toxins penetrate the sulcular and junctional epithelium andinitiate a rapid acute inflammatory response by the body. The end result of thisprocess is periodontal soft tissue damage and alveolar bone resorption. This leads todeep pocket formation as well as to tooth mobility and eventual tooth loss. PD is notonly a localised disease but can also cause bacteraemia and possibly systemicdisease.Bacterial plaque is often attached to calculus. Calculus is merely mineralised plaqueand in itself is not harmful. However, it provides a roughened surface for plaque toadhere to.Saliva contains phosphoproteins which normally prevent the formation of calculus onteeth. But, plaque bacteria produce proteases which break down thesephosphoproteins and allow the mineralisation of the plaque. This is why calculus isoften heaviest around the duct openings of the major salivary glands.DiagnosisPeriodontal probing, with a blunt ended probe, measures attachment loss and pocketdepth. Probing provides a practical way of assessing periodontal health.Radiographs will also indicate the state of the periodontal tissues by showingalveolar bone levels as well as the presence of sub-gingival calculus. The use ofsubtraction radiography is popular in human periodontic therapy to assess alveolarbone loss or its stabilisation.Attachment loss (AL) can be used to assess the extent of disease by using aveterinary periodontal disease index (Wiggs and Loprise). AL is measured from thecemento-enamel junction to the depth of the periodontal pocket. 3
  4. 4. Stage 0 is classified as normal gingiva, stage 1 is gingivitis (0% AL), stage 2 is earlyPD (<25% AL), stage 3 is moderate PPD (25-50% AL), and stage 4 is severe PD(>50% AL).Once PD has been diagnosed, it cannot be reversed but only controlled by thoroughsupra and sub-gingival cleaning and on-going reassessment.In humans, the severity of PD is based on attachment loss measurements, toothmobility, bleeding on probing, purulent discharges from pockets and tooth pain. Aprognosis is then assigned to each tooth, and teeth with the poorest prognosis areoften extracted.Dietary managementDiet does play a role in PD. Soft diets are more likely to remain in the oral cavity forlonger periods of time, unless removed by mechanical brushing. This food debrisprovides a substrate for bacterial proliferation. Diets such as Hill’s T/D help in theremoval of plaque. Raw bones do help in preventing plaque accumulation bystimulating increased saliva flow and through a direct mechanical action, but bonescan cause gastrointestinal upsets as well as fractured teeth. Animals with poorsalivary function are also more prone to PD due to lack of lubricating and cleansingactions of the saliva as well as the lack of salivary phosphoproteins.TreatmentRemoval of plaque is essential in preventing and controlling PD.This can be accomplished by a combination of mechanical brushing, dietaryadjustments and regular dental prophylaxis.Remember that supra-gingival plaque removal does nothing in removing sub-gingivalplaque. Pockets deeper > 3-4mm (dogs) require root planing and curettage.Continual assessment is essential for the correct management of PD.Therefore, at the onset of the oral examination, a treatment plan should beformulated, that will treat the patient’s problems. The owner’s motivation and abilityto provide homecare must be taken into account before putting a treatment plan intoaction.In summary, periodontal disease is a serious but insidious disease of older dogs. Ahigh percentage of animals walking into veterinary practices will have one or moreteeth affected by PD.Diseases of the tooth surface  Abrasions- pathological wear due to friction of a foreign body independent of the occlusion.  Attrition- tooth wear due to tooth to tooth contact ie.malocclusions  Erosion- loss of tooth substance due to non bacterial intrinsic/extrinsic acid attack.  Genetic/environmental disorders- enamel hypoplasia, amelogenesis imperfecta etc.  External/internal tooth resorptionEndodontic disease  Trauma- exposure of the pulp with subsequent pulpal inflammation and eventual necrosis  Abrasion/Attrition/acid erosion (see above) 4
  5. 5.  Perio-endo lesions- characterised by both endodontic disease and periodontitis. Both diseases need to be treated to preserve the tooth. Extraction of the tooth if the degree of periodontitis is severe and the tooth has a guarded prognosis.Definition of endodonticsEndodontics is a branch of dentistry dealing with diseases of pulpal and peri-radicular tissues. It encompasses the study of the biology of the normal pulp, theaetiology, diagnosis, prevention, and treatment of diseases and injuries of the pulp,and associated peri-radicular conditions.Pulpal anatomyDental pulp is loose connective tissue, which occupies the pulpal chamber.It is the mature form of the dental papilla. It is present in each root canal of singleand multi-rooted teeth.At the apical constriction (apical delta) of the root canal, the pulp becomescontinuous with the periodontal ligament. The pulp contains odontoblasts,fibroblasts, defense cells, and neurovascular tissues. The neurovascular supplyenters the pulp via the apical foramina of the roots. Usually there are many foramina(6-90 openings) entering each root canal, forming an apical delta. The pulp also hasa lymphatic drainage system.As the pulp ages, there is decreasing cellularity and increasing fibrosity of the pulp.The vasculature and nerve supply also diminishes.The odontoblasts lining the pulp produce dentine throughout the life of the tooth andthis results in thicker dentinal walls and a smaller pulp.The odontoblasts also respond to injury by producing reparative dentine, which isdesigned to protect and shield the pulp.Neural tissues consist mainly of A-delta myelinated nerve fibres (sharp, localisedpain- ie.dentinal pain) and C non-myelinated nerve fibres (dull throbbing pain, slowerconducting and more resistant to pulpal ischaemia than A-delta fibres).Functions of the dental pulp1. Formation of dentine (coronal and radicular)2. Maintenance of tooth (fluid environment)3. Defence mechanism (secondary dentine, reparative dentine, fluid flow)4. Age changes (peri-tubular dentine, more solid tooth)5. Sensation (pain)6. ProprioceptionAetiology of pulp and periapical diseaseA. Bacteria -coronal ingress through tooth fractures, cracks, leaking restorations (i.e. after vital pulpotomy) Radicular ingress- periodontal disease, cracks, fractures, breakdown of RCTB. Trauma- Accidental: tooth fracture, luxation, avulsion (cage biting, road trauma, animal fights, rock chewing). Physiological: attrition, abrasion, occlusal trauma.C. Iatrogenic- cavity preparation (heat ,depth, dehydration, exposure of tubules) - surgical trauma to adjacent teeth 5
  6. 6. - orthodontic movement - periodontal treatment - radiation therapy for cancerD. Others - Aging - Internal resorption - ORLPulpal pathology due to bacteriaThe pulp space is capable of containing millions of bacteria. The bacteria producetoxins (especially endotoxins) which diffuse through dental tissues into the peri-radicular tissues. Bacterial by-products act on host tissues in two ways: a) enzymes and metabolic products can exert a direct tissue toxic effect, and b) Components from the bacterial cell i.e. endotoxin can trigger inflammatory defence reactions.Pulpal response to injuryThe response of the pulp to injury depends on the status of the pulp at that time (i.e.inflamed or not).With mild injury, odontoblasts die and there is acute inflammation in the sub-odontoblastic layer, but resolution will occur, and cells in the sub-odontoblastic layerwill differentiate into odontoblasts and instigate reparative dentine.With major injury, some pulpal tissue dies, and there is acute inflammation inadjacent tissues- a walling off of affected tissues and subsequent fibrosis. However ifthere is continuing inflammation-there will be further necrosis, eventually involvingthe whole pulp.Some of the theories about the causes of pulpal necrosis include1. limited drainage from the pulp2. limited access for repair ( from one direction only- the apical end)3. pulp is surrounded by nonflexible tissue ( i.e. like the brain encased in bone)The aims of endodontic treatmentBiological aims:a) to remove from the root canal system all organic matter that is capable of either decomposing into tissue destructive by- products or that can support bacterial growth;b) To remove or destroy all bacteria present in the root canal system.Mechanical aims:c) to prepare the root canal space to a form which allows complete three dimensional filling; andd) To fill the prepared space with a bio-compatible filling material in order to completely seal the coronal and apical ends of the canal. The apical end of the root canal filling should be placed as close to the cemento-dentinal junction. Finally, a complete coronal seal should be placed.Methods used to accomplish theses aims 6
  7. 7. a) Aseptic techniqueb) Debridement of the root canal systemc) Irrigation with disinfecting agentsd) Medication if required with antimicrobial dressings.e) ObturationFollow upAll endodontic cases should be reviewed to assess whether the treatment has beensuccessful.Success can be based on clinical examination as well as radiographs (not alwayspractical).If radiographs are taken, there should be no further loss of peri-radicular bone andthere should be healing of any radiolucent areas that were present prior to treatment.Oral neoplasia/growths  Squamous cell carcinoma  Fibrosarcoma  Malignant melanoma  EpulidesOral TumoursAre those tumours that arise from the gingiva, oral mucosa, tongue, tonsil, bone ordental structures.Odontogenic (those tumours arising from elements involved in tooth development) vsnon-odontogenic tumours (arising from non dental tissues of the oral cavity).Oral tumours account for approx. 5% of all malignant tumours in dogs.Epulides (odontogenic tumours) are benign and account for 30% of all canine oraltumours.Most common site for oral tumours: gingiva, buccal mucosa, hard/soft palate andtongue (Hoyt and Withrow, 1984).The most common malignant canine tumours are Malignant Melanoma (MM),Squamous Cell Carcinoma (SCC), and Fibrosarcoma (FS).Smaller breeds (<23 Kg) see MM more, larger breeds (>23 Kg) see FS and SCCmore often.SCC is the most common malignant feline oral tumour, followed by Fibrosarcoma.Symptoms/clinical signs  Facial swelling  Dyspnoea- tonsillar or caudal lingual tumours  Regional lymphadenopathy  Weight loss  Exophthalmos  Persistent haemorrhage from mouth  Dysphagia  Tooth loss/mobility. History of recent tooth extraction!Malignant melanoma (MM)  Most common canine oral malignancy (33%)  Rapidly growing 7
  8. 8.  Appear white-grey to brown-black and are firm and vascular  Gingiva, followed by buccal/labial mucosa, hard/soft palate and tongue.  Commonly affected breeds include Poodles, Dachshunds, Scottish terriers and Golden retrievers.  Local bone invasion and local/distant metastasis common. Check for lesions in tonsils/regional lymph nodes  Metastasis occur in > 80% of cases.  Lung metastasis slow growing- difficult to pick up on radiograph at time of surgery  Tumours < 2cm in size have better prognosis if lymph nodes are clear.  Mitotic index of > 3/hpf and increased cellular pleomorphism associated with poorer Prognosis.  Confusing histopathological picture if the biopsy specimen does not contain melanin (third of all cases).  Wide surgical excision (>2cm) is recommended.  Intratumoural chemotherapy: Adrenaline/cisplatin has been used in MM with some success.  Immunotherapy: MM is a relatively immunogenic tumour. The use of monocyte-macrophage system activators may show some promise.  1 yr survival rate of < 20% after surgery. Euthanasia due to recurrence or metastasis.Squamous cell carcinoma  Non tonsillar SCC is the 2nd. most common oral malignancy in dogs (20%)  SCC is the most common oral malignancy in cat and man  Larger dog breeds more often  Most tumours found rostral to the canines  In dogs, often seen on gingiva of rostral mandible and caudal maxilla.  Gingival masses often invade bone  Can also occur on tongue and sublingual area (common in cats)  Metastasis in the dog is very site-dependent with the rostral oral cavity having a low metastatic rate and the caudal tongue and tonsil having a high metastatic potential.  Abdominal metastasis has been reported with tonsillar SCC  One year survival rates of non-tonsillar SCC in dogs: 50-91% after surgery.Fibrosarcoma  Third most common oral malignancy (17%) in dogs, 2nd most common in cats.  Most commonly seen on gingiva followed by hard/soft palate, labial/buccal mucosa and tongue  Gingival mass often on maxilla between canine and PM4  Usually firm and non-ulcerated  Males>females  Higher % (25%) in animals under 5 yrs. old compared to MM and SCC.  Large breeds- esp. Golden retriever  Fibrosarcoma is very invasive locally but metastasises in < 20% of cases (usually lungs)  Aggressive surgery required  Poorly responsive to chemotherapy  Radiotherapy combined with hyperthermia?  Local recurrence is common 8
  9. 9.  1 yr survival rate of 25-40% after excisionOverall prognosis following surgery:  Surgery may allow local control and offer either cure or palliation  SCC: good-rostral; poor-caudal  Fibrosarcoma: Poor-fair  Malignant Melanoma: Poor-fair  Acanthomatous Epulis: excellentPostoperative care  Access to blood transfusions, ICU, and analgesics  Owner satisfaction with cosmetic/functional results: good.  Radiation therapy- where available is useful either alone or post surgery in canine SCC or Acanthomatous Epulis (AE). Use for lymph node disease theoretically helpful.  Chemotherapy- Most oral tumours considered chemo-resistant. Intralesional chemo. has been used in SCC, Fibrosarcoma and AE with mixed results.  Feeding tubes may be considered post surgery  Wound dehiscence/bleeding considered major post –op complications.  Early aggressive surgery for oral malignancy best chance of cure Surgery  Subtotal/total maxillectomy/mandibulectomy for those tumours invading bone.  Caudal tumours or those crossing the midline may be non-resectable  Tumours invading into sublingual musculature /caudal pharynx may not be resectable  May require pharyngotomy endotracheal intubation  Maxillectomy/mandibulectomy may be palliative only and not cure the disease.EpulidesThe epulides are similar to gingival hyperplasia in appearance and are usuallyconfined to the gingival margin. They are often slow growing, firm, and generallycovered by intact epithelium. “Benign” masses such as focal fibrous/generalisedgingival hyperplasia and the epulides are by far the most common “growths”encountered in the oral cavity of dogs. Focal fibrous hyperplasia (localised gingivalhyperplasia) is usually a reactive growth due to a long standing underlying irritantsuch as plaque/calculus. It is often clinically and histo-pathologically misdiagnosedas an epulis.The treatment of gingival hyperplasia is by local excision and management of theunderlying cause. Epulides tend to be rare in the cat.There is also a drug induced form of generalised gingival hyperplasia seen in dogson cyclosporin medication, as well as a familial hyperplastic lesion reported in Boxerdogs.Many “benign” gingival masses in old dogs go unreported, so that gingivalhyperplasia and fibromatous/ossifying epulis are underreported in surgical biopsyspecimens. However, in one survey of oral biopsy specimens submitted to aveterinary pathology laboratory, the epulides still made up approx. 36% of samplessubmitted. 9
  10. 10. The term epulis is a clinically descriptive term referring to a localised non-specificexophytic growth on the gingiva. Most epulides are benign non-neoplastic lesions,containing remnants of the dental lamina located in the periodontal ligament orgingival epithelium, but an excised epulis should always be submitted forhistopathology to determine the true nature of the lesion. Epulides have apredilection for the rostral (anterior) mandible/maxilla and maxillary fourth premolarregion, but can occur anywhere on the gingival mucosa.Epulides contain dental lamina cells from the periodontal ligament or gingivalepithelium and are divided into mainly three types, namely fibromatous (fibrous)epulis, ossifying epulis and the locally invasive acanthomatous epulis. A fourthtype, namely the pyogenic granuloma is rare, and will not be discussed here.Fibromatous epulis can be single or multiple and usually has a smooth, pinksurface, although it can become erythematous and ulcerated due to occlusal ormasticatory forces. If large enough it can cause pain and interfere with mastication. Itdoes not invade bone.Ossifying epulis is probably of periodontal ligament/gingival epithelium origin.These growths show metaplastic bone formation, and varying amounts of osteoidmaterial can be seen within them. This osteoid material may appear on radiographs.In addition, strands of odontogenic epithelium are often present in varying amounts.Recently, there has been a push to reclassify fibromatous/ ossifying epulides asperipheral odontogenic fibromas.Fibromatous /ossifying epulides are best treated by local scalpel excision orcryosurgery, although attempts to superficially remove the lesion without extendingmargins to the underlying bone or into periodontal ligament often results inrecurrence. The tooth in the vicinity of the growth may or may not need to beextracted depending on the extent of the epulis and any localised periodontitis.Acanthomatous epulis, although classified as benign, can be locally aggressive,displace teeth, invade into bone and is considered the most common invasivetumour of the dog jaw. When 40% or more of the cortex is destroyed, bone lysis maybe observed. However, apparently normal radiographs do not rule out bone invasion.If a tumour appears fixed to the underlying bone, then it can generally be assumedthat there is microscopic invasion of the bone. Fortunately, acanthomatous epulisdoes not metastasize and can be controlled by wide local excision. There has beenone report of hypercalcemia being associated with this tumour.Acanthomatous epulis may be referred to as a peripheral ameloblastoma orbasal cell carcinoma in some of the veterinary literature. The tumour often consistsof sheets and anastomosing bands (palisades) of pleomorphic epithelial cells ofodontogenic origin. These cells exhibit reverse polarity of the nuclei similar toameloblasts. The tumour shows a biologic behaviour similar to intraosseousameloblastoma in humans and the term canine acanthomatous ameloblastoma hasbeen suggested by some.Current treatment recommendations include aggressive surgical resection, radiationtherapy or a combination of the two. Other treatments that have been used withvariable success include intralesional anti-cancer drugs (esp. bleomycin ) andsurgical debulking followed by aggressive ablation with CO2 laser.At present, radical surgery (up to one cm. margins, based on radiographs) offers thebest results with less than 5% recurrence.Radiation therapy is also effective, but there have been reports of malignant tumourtransformation at the irradiated site in approximately 20% of cases treated withirradiation. This can develop years after the original epulis removal.  Others- including cysts- dentigerous cysts, radicular cysts, residual cysts.Orthodontics 10
  11. 11. Orthodontics is concerned with the study and treatment of dento-skeletal anomalies assoc. with growth and function of the dento-facial tissues. The ultimate goal of orthodontic treatment is an occlusion that functions normally, maintains oral health and is pain-free. Orthodontic treatment involves thorough assessment of the malocclusion including the aetiology of the malocclusion. Malocclusions can be described as being genetic or environmental (local/systemic) in origin or both. Genetic or hereditary factors will affect the shape and size of the jaws and teeth. There may also be variations in the no. of teeth present. A genetic defect such as cleft lip/palate is often assoc. with altered tooth morphology and number of teeth. Environmental factors may include systemic influences such as infections, nutritional imbalances, and endocrine disorders. Local factors include trauma- jaw or tooth fracture, early loss of primary or permanent teeth, damage to permanent tooth buds, and altered tooth/root shape. Habits such as cage biting, rock chewing may also cause malocclusions in the developing animal. Jaw length, jaw width and height, tooth bud position and tooth size are inherited. The development of the maxilla, mandible and teeth are independently regulated genetically. Disharmony in the regulation of these 3 structures results in a malocclusion. As a general rule, tooth crowding and rotation in the premolar/molar area indicates a jaw that is shorter than normal.Malocclusions causing  Crowding leading to periodontitis  Oral trauma I.e. Base narrow canines  Anterior crossbite –ethical dilemma!TerminologyScissor bite: Mx incisors overlap Md incisors, whose incisal edges rest on the lingualcingulum of the Mx incisors.Level bite: when incisor teeth meet edge to edge.Open bite: When a part or all of the teeth are prevented from closing into theirnormal occlusal relationship.Wry bite: The result of unequal arch development. There is a centre linedisplacement and the midline is not confluent between the upper and lower arch.May occur to trauma and slowed growth on one side of the face.Anterior crossbite: cusps of 1 or more anterior teeth (Incisors) are positioned labiallyor lingually to their normal cuspal relationship (undershot)Posterior crossbite: cusps of 1 or more posterior teeth (PMs/Ms) are positionedbucally/lingually to their normal cuspal relationship.Overbite: is the overlap of the lower incisor crown height by the upper incisor.Overjet: the horizontal distance between the upper and lower incisors measuredparallel to the occlusal plane.Types of tooth movementTipping: is the movement of the crown without changing the position of the root apex.Tipping usually requires minimal force.Translation: involves the bodily movement of the tooth without any tipping or rotation. 11
  12. 12. Rotation, extrusion and intrusion: involve rotation around the apico-incisal axis, orthe movement of the tooth coronally or apically.Most tooth movements in veterinary orthodontics involve a combination of tippingand translation.All tooth movements cause some degree of pain to the animal.Treatment optionsOrthodontic treatment can be divided into 3 areas  Preventive: owners are given advise on correct chew toys, oral exercises to prevent fractured, avulsed teeth in the young animal. Counseling for genetic faults also.  Interceptive: action taken to intercept a potential problem. Usually done in the deciduous or mixed dentition  Corrective: Treatment of a existing malocclusion in the permanent dentitionA reasonable approach as to whether a malocclusion is inherited would be:Skeletal malocclusions are inherited unless a developmental cause can be reliablyidentifiedRetained deciduous teeth may be inherited or environmental in origin.Pure dental malocclusions, unless known to have a breed or family predisposition,are judged to be not inherited. (Hennet, 1995)Other oral pathology  CUPS- Chronic ulcerative paradental stomatitis. A localised inflammation of oral mucosa where it contacts an area of plaque/calculus accumulation on the tooth.  Oral papillomatosis- caused by a papovavirus and spreads by horizontal transmission between animals. See wart like lesions and often multiple involving the oral cavity and face. Tends to be self limiting, but may require debulking if traumatised.  Focal/generalised gingival hyperplasia- see in Epulides sectionSystemic diseases with oral manifestations  Renal disease- uraemic ulcers, primary/2nd hyperparathyroidism- osteodystrophy  FIV- FIV induced periodontitis  Immune mediated diseases- Pemphigus, Lupus.  Diabetes mellitus- dehydration, neutrophil dysfunction leading to periodontitis.  Feline Calici virus- acute oral ulceration.Tooth abnormalities  Supernumerary teeth- extra teeth. Often seen in the premolar area.  Impacted teeth- beware of dentigerous cyst formation. Will present as a missing tooth- take a radiograph.  Oligodontia- Not a full complement of teeth  Dilacerated teeth- A permanent distortion of the root or crown possibly due to trauma. 12
  13. 13. SummaryThe detection of oral disease often is simply a matter of lifting the lip andlooking in the mouth. Remember that many oral diseases do not show markedsymptoms until they are well advanced.Early detection of disease will improve the outcome in most cases. There would bevery few animals that present to a veterinary practice today that will not have somedegree of oral disease. So, it is only a matter of looking for it. 13