Recognising oral diseases - DOC

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Recognising oral diseases - DOC Powered By Docstoc
					CANINE ORAL DISEASES
Dr. Tony Caiafa
University of Melbourne
Veterinary Clinic and Hospital
Princes Highway, Werribee, 3030
Email toothdoc@tpg.com.au


Canine oral diseases can have a significant debilitating effect on the animal’s overall
health.
Diagnosis of oral disease requires a thorough examination of the head, neck and
oral cavity including draining lymph nodes of the head and neck region, assessment
of temporo-mandibular joint function and masticatory muscle function as well as
intraoral structures including the periodontium, the alveolar mucosa, the tongue,
oropharynx and salivary glands.

Paedodontics- The study of oral and dental structures in the immature developing
animal.

      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 Steps

Partial pulpectomy (vital pulpotomy) steps.

Remember- works best in younger dogs (under one year of age) and also less
predictable an outcome, if performed >7 days post trauma. Monitor these patients
post treatment for possible loss of pulpal vitality. Continuing radiographic
assessment 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 or
dentinal bridge formation at the pulp amputation site.
Clinical steps
1. 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 bleeding
stops, or flush with saline or place a paper point over p ulp stump for 5 min. approx.


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3. Place Calcium hydroxide (CaOH2) over non bleeding pulp stump. Can use hard
setting CaOH2 like life or dycal, with a CaOH2 applicator. Can also use a non setting
CaOH2 like pulpdent paste or CaOH2 powder mixed with sterile saline. (about 1mm
thick).
4. Remove any excess CaOH2 on the internal walls of your access hole, and place a
reinforced glass ionomer cement (RGIC) such as Vitrebond over your CaOH2 . This
material is visibly light cured (can purchase light curing machines second hand for
about $400). Can also use a chemically cured GIC like Ketac Fil (you do not need to
light cure this), about 1-2 mm thick. GIC provides a firm base so that you can place
your composite resin without disturbing the CaOH2 .
5. Acid etch the dentine and enamel with 37% phosphoric acid etch and rinse off
after 30 sec and dry thoroughly. Place a light cured primer/adhesive like 3M bond or
another bonding adhesive for composite resin cements.
6. Place your composite resin cement in two stages. Firstly place a flowable
composite 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 up
in 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 composite
finishing burs in the high speed handpiece. You may also use soflex discs (3M) in a
slow speed handpiece. Then place another layer of light c ured adhesive over this to
seal any exposed dentinal tubules at the fracture or amputation site.
8. Monitor the case say at 6 months post surgery, hopefully with a radiograph to
make certain that there is no pulpal necrosis. Also, composite resins are not as
strong as natural tooth structure and can break off. They can be easily replaced
though.
Warn patients- especially in the first 6 months post surgery re No Bones, No Rocks
or Sticks- these can break of your composite resin cement. This is why I put a two
layer composite resin cement closure, so that if the top layer fails, the second layer
will 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 recall

Periodontal disease (PD) is the most common disease in small animal practice today.
A high number of middle aged dogs will have some degree of periodontitis.
However, it is commonly under-diagnosed because, firstly, periodontitis has very few
symptoms, so that owners are unaware of any problems and secondly, practitioners
are not looking for PD during routine examinations i.e. at annual vaccination time.
Periodontal disease is an inflammation and destruction of the teeth’s supporting
structures. The periodontium consists of the cementum, alveolar bone, periodontal
ligament and gingivae. The oral mucosa is unique in that it is made up of an
ectodermal lining, which is pierced by teeth. The dentogingival margin therefore
represents a weak area in the oral mucosa's protective and defensive roles.

Aetiology and natural progression of disease

The primary aetiological factor that causes PD is bacteria. Also, there are seco ndary
factors that can contribute to the severity of the disease. Secondary factors such as


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tooth crowding, retained deciduous teeth, systemic illnesses like renal failure or
diabetes 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, bacterial
products and toxins as well as the body’s own defence mechanisms contribute to the
initiation and continuation of PD. PD is not a continuous non-stop process. It
represents a process that is characterised by periods of active tissue destruction and
then periods of quiescence. It can occur at different locations within the oral cavity,
and not always occurring at the same time (Random burst theory).

Pathogenesis

For PD to occur, one needs bacteria. Bacteria attach to the tooth surface by
adhering to the tooth pellicle (Salivary glycoproteins). The pellicle is firmly attached
to the teeth and even after ultrasonic scaling /polishing; it will reform on the tooth
surface within minutes.
Once attached, plaque can only be removed from the tooth surface by mechanical
means 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 swells
and lifts away from the tooth (chronic marginal gingivitis). Chronic marginal gingivitis
is defined as inflammation of the marginal gingival tissues and is characterised by
redness, swelling and bleeding. Gingivitis, if treated correctly, is reversible and the
health of the periodontium can be restored to normal. If the plaque is left undisturbed,
it eventually penetrates sub-gingivally. The bacterial composition of the plaque then
changes to a predominantly gram negative anaerobic motile flora. This flora is
responsible for the initiation of PD. The principle bacteria incriminated in PD are
Bacteroides and Fusobacterium spp.
The bacteria and their toxins penetrate the sulcular and junctional epithelium and
initiate a rapid acute inflammatory response by the body. The end result of this
process is periodontal soft tissue damage and alveolar bone resorption. This leads to
deep pocket formation as well as to tooth mobility and e ventual tooth loss. PD is not
only a localised disease but can also cause bacteraemia and possibly systemic
disease.
Bacterial plaque is often attached to calculus. Calculus is merely mineralised plaque
and in itself is not harmful. However, it provides a roughened surface for plaque to
adhere to.
Saliva contains phosphoproteins which normally prevent the formation of calculus on
teeth. But, plaque bacteria produce proteases which break down these
phosphoproteins and allow the mineralisation of the plaque. This is why calculus is
often heaviest around the duct openings of the major salivary glands.

Diagnosis

Periodontal probing, with a blunt ended probe, measures attachment loss and pocket
depth. Probing provides a practical way of assessing periodontal health.
Radiographs will also indicate the state of the periodontal tissues by showing
alveolar bone levels as well as the presence of sub-gingival calculus. The use of
subtraction radiography is popular in human periodontic therapy to assess alveolar
bone loss or its stabilisation.
Attachment loss (AL) can be used to assess the extent of disease by using a
veterinary periodontal disease index (Wiggs and Loprise). AL is measured from the
cemento-enamel junction to the depth of the periodontal pocket.


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Stage 0 is classified as normal gingiva, stage 1 is gingivitis (0% AL), stage 2 is early
PD (<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 thorough
supra and sub-gingival cleaning and on-going reassessment.
In humans, the severity of PD is based on attachment loss measurements, tooth
mobility, bleeding on probing, purulent discharges from pockets and tooth pain. A
prognosis is then assigned to each tooth, and teeth with the poorest prognosis are
often extracted.

Dietary management

Diet does play a role in PD. Soft diets are more likely to remain in the oral cavity for
longer periods of time, unless removed by mechanical brushing. This food debris
provides a substrate for bacterial proliferation. Diets such as Hill’s T/D help in the
removal of plaque. Raw bones do help in preventing plaque accumulation by
stimulating increased saliva flow and through a direct mechanical action, but bones
can cause gastrointestinal upsets as well as fractured teeth. Animals with poor
salivary function are also more prone to PD due to lack of lubricating and cleansing
actions of the saliva as well as the lack of salivary phosphoproteins.

Treatment

Removal of plaque is essential in preventing and controlling PD.
This can be accomplished by a combination of mechanical brushing, dietary
adjustments and regular dental prophylaxis.
Remember that supra-gingival plaque removal does nothing in removing sub-gingival
plaque. 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 be
formulated, that will treat the patient’s problems. The owner’s motivation and ability
to provide homecare must be taken into account before putting a treatment plan into
action.
In summary, periodontal disease is a serious but insidious disease of older dogs. A
high percentage of animals walking into veterinary practices will have one or more
teeth 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 resorption

Endodontic disease

      Trauma- exposure of the pulp with subsequent pulpal inflammation and
       eventual necrosis
      Abrasion/Attrition/acid erosion (see above)


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        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 endodontics

Endodontics 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, the
aetiology, diagnosis, prevention, and treatment of diseases and injuries of the pulp,
and associated peri-radicular conditions.

Pulpal anatomy

Dental 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 single
and multi-rooted teeth.
At the apical constriction (apical delta) of the root canal, the pulp becomes
continuous with the periodontal ligament. The pulp contains odontoblasts, fibroblasts,
defense cells, and neurovascular tissues. The neurovascular supply enters 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 has a 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 and
this results in thicker dentinal walls and a smaller pulp.
The odontoblasts also respond to injury by producing reparative dentine, which is
designed to protect and shield the pulp.
Neural tissues consist mainly of A-delta myelinated nerve fibres (sharp, localised
pain- ie.dentinal pain) and C non-myelinated nerve fibres (dull throbbing pain, slower
conducting and more resistant to pulpal ischaemia than A-delta fibres).

Functions of the dental pulp

1.   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.   Proprioception



Aetiology of pulp and periapical disease

A. Bacteria -coronal ingress through tooth fractures, cracks, leaking restorations (i.e.
   after vital pulpotomy)
   Radicular ingress- periodontal disease, cracks, fractures, breakdown of RCT
B. 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
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           - orthodontic movement
           - periodontal treatment
           - radiation therapy for cancer
D. Others - Aging
           - Internal resorption
           - ORL

Pulpal pathology due to bacteria

The pulp space is capable of containing millions of bacteria. The bacteria produce
toxins (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 injury

The 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 layer
will differentiate into odontoblasts and instigate reparative dentine.
With major injury, some pulpal tissue dies, and there is acute inflammation in
adjacent tissues- a walling off of affected tissues and subseque nt fibrosis. However if
there is continuing inflammation-there will be further necrosis, eventually involving
the whole pulp.
Some of the theories about the causes of pulpal necrosis include
1. limited drainage from the pulp
2. 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 treatment

Biological 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; and
d) 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



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a)   Aseptic technique
b)   Debridement of the root canal system
c)   Irrigation with disinfecting agents
d)   Medication if required with antimicrobial dressings.
e)   Obturation

Follow up

All endodontic cases should be reviewed to assess whether the treatment has been
successful.
Success can be based on clinical examination as well as radiographs (not always
practical).
If radiographs are taken, there should be no further loss of peri-radicular bone and
there should be healing of any radiolucent areas that were present prior to treatment.

Oral neoplasia/growths

        Squamous cell carcinoma
        Fibrosarcoma
        Malignant melanoma
        Epulides

Oral Tumours

Are those tumours that arise from the gingiva, oral mucosa, tongue, tonsil, bone or
dental structures.
Odontogenic (those tumours arising from elements involved in tooth development) vs
non-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 oral
tumours.
Most common site for oral tumours: gingiva, buccal mucosa, hard/soft palate and
tongue (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 SCC
more 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
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     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
     1 yr survival rate of 25-40% after excision
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Overall 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: excellent

Postoperative 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.

Epulides

The epulides are similar to gingival hyperplasia in appearance and are usually
confined to the gingival margin. They are often slow growing, firm, and generally
covered by intact epithelium. “Benign” masses such as focal fibrous/generalised
gingival hyperplasia and the epulides are by far the most common “growths”
encountered in the oral cavity of dogs. Focal fibro us hyperplasia (localised gingival
hyperplasia) is usually a reactive growth due to a long standing underlying irritant
such as plaque/calculus. It is often clinically and histo -pathologically misdiagnosed
as an epulis.
The treatment of gingival hyperplasia is by local excision and management of the
underlying cause. Epulides tend to be rare in the cat.
There is also a drug induced form of generalised gingival hyperplasia seen in dogs
on cyclosporin medication, as well as a familial hyperplastic lesion reported in Boxer
dogs.
Many “benign” gingival masses in old dogs go unreported, so that gingival
hyperplasia and fibromatous/ossifying epulis are underreported in surgical biopsy
specimens. However, in one survey of oral biopsy specimens submitted to a
veterinary pathology laboratory, the epulides still made up approx. 36% of samples
submitted.
The term epulis is a clinically descriptive term referring to a localised non-specific
exophytic growth on the gingiva. Most epulides are benign non-neoplastic lesions,
containing remnants of the dental lamina located in the periodontal ligament or
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gingival epithelium, but an excised epulis should always be submitted for
histopathology to determine the true nature of the lesion. Epulides have a
predilection for the rostral (anterior) mandible/maxilla and maxillary fourth premolar
region, but can occur anywhere on the gingival mucosa.
Epulides contain dental lamina cells from the periodontal ligament or gingival
epithelium and are divided into mainly three types, namely fibromatous (fibrous)
epulis, ossifying epulis and the locally invasive acanthomatous epulis. A fourth
type, namely the pyogenic granuloma is rare, and will not be discussed here.
Fibromatous epulis can be single or multiple and usually has a smooth, pink
surface, although it can become erythematous and ulcerated due to occlusal or
masticatory forces. If large enough it can cause pain and interfere with mastication. It
does not invade bone.
Ossifying epulis is probably of periodontal ligament/gingival epithelium origin.
These growths show metaplastic bone formation, and varying amounts of osteoid
material 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 as
peripheral odontogenic fibromas.
Fibromatous /ossifying epulides are best treated by local scalpel excision or
cryosurgery, although attempts to superficially remove the lesion without extending
margins to the underlying bone or into periodontal ligament often results in
recurrence. The tooth in the vicinity of the growth may or may not need to be
extracted 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 invasive
tumour of the dog jaw. When 40% or more of the cortex is destroyed, bone lysis may
be 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 assumed
that there is microscopic invasion of the bone. Fortunately, acanthomatous epulis
does not metastasize and can be controlled by wide local excision. There has been
one report of hypercalcemia being associated with this tumour.
Acanthomatous epulis may be referred to as a peripheral ameloblastoma or
basal cell carcinoma in some of the veterinary literature. The tumour often consists
of sheets and anastomosing bands (palisades) of pleomorphic epithelial cells of
odontogenic origin. These cells exhibit reverse polarity of the nuclei similar to
ameloblasts. The tumour shows a biologic behaviour similar to intraosseous
ameloblastoma in humans and the term canine acanthomatous ameloblastoma has
been suggested by some.
Current treatment recommendations include aggressive surgical resection, radiation
therapy or a combination of the two. Other treatments that have been used with
variable success include intralesional anti-cancer drugs (esp. bleomycin ) and
surgical debulking followed by aggressive ablation with CO 2 laser.
At present, radical surgery (up to one cm. margins, based on radiographs) offers the
best results with less than 5% recurrence.
Radiation therapy is also effective, but there have been reports of malignant tumour
transformation at the irradiated site in approximately 20% of cases treated with
irradiation. This can develop years after the original epulis removal.

      Others- including cysts- dentigerous cysts, radicular cysts, residual cysts.

Orthodontics

   Orthodontics is concerned with the study and treatment of dento-skeletal
   anomalies assoc. with growth and function of the dento-facial tissues.
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   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!

Terminology

Scissor bite: Mx incisors overlap Md incisors, whose incisal edges rest on the lingual
cingulum 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 their
normal occlusal relationship.
Wry bite: The result of unequal arch development. There is a centre line
displacement 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 labially
or lingually to their normal cuspal relationship (undershot)
Posterior crossbite: cusps of 1 or more posterior teeth (PMs/Ms) are positioned
bucally/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 measured
parallel to the occlusal plane.

Types of tooth movement

Tipping: 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.
Rotation, extrusion and intrusion: involve rotation around the apico-incisal axis, or
the movement of the tooth coronally or apically.


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Most tooth movements in veterinary orthodontics involve a combination of tipping
and translation.
All tooth movements cause some degree of pain to the animal.

Treatment options

Orthodontic 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 dentition

A reasonable approach as to whether a malocclusion is inherited would be:

Skeletal malocclusions are inherited unless a developmental cause can be reliably
identified
Retained 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 section

Systemic 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.

Summary

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The detection of oral disease often is simply a matter of lifting the lip and
looking in the mouth. Remember that many oral diseases do not show marked
symptoms until they are well advanced.
Early detection of disease will improve the outcome in most cases. There would be
very few animals that present to a veterinary practice today that will not have some
degree of oral disease. So, it is only a matter of looking for it.




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