Diagnosis and Treatment of Unusual Oral Lesions
Sandra Manfra Marretta, DVM, Diplomate,
Unusual oral lesions that are a diagnostic and therapeutic challenge include: canine osteomyelitis and bone sequestra, feline mandibular swelling, bilateral pathologic caudal mandibular fractures, dentigerous cysts, renal secondary hyperparathyroidism, hypoplasia or congenital absence of the soft palate, pharyngeal mucoceles, nasopharyngeal stenosis, choanal atresia, and inability to open or close the mouth. Thorough physical examination, clinicopathologic testing, histopathologic evaluation, and oral radiography are essential in the diagnosis of these problems. Once an accurate diagnosis is determined appropriate surgical and other therapeutic modalities can be instituted.
Osteomyelitis and Bone Sequestra
Osteomyelitis and bone sequestra are infrequently diagnosed in the oral cavity. Osteomyelitis and bone sequestra may be a complication of severe periodontal disease, extractions, or jaw fractures.1,2 Osteomyelitis or bone sequestra following extractions and jaw fractures may be caused by retained tooth roots, exposed alveolar bone, or operator-induced osseous necrosis. A bone sequestra may develop when a piece of alveolar bone is fractured off during a dental extraction and left in the extraction site. Several cases of severe osteomyelitis with secondary necrosis of bone have occurred in Cocker Spaniels and may be related to an inappropriate immune response in this breed. Dogs with osteomyelitis or bone sequestra are usually examined because of fetid breath, severe oral pain, facial swelling, reluctance or inability to eat and have severe purulent nasal discharge if the osteomyelitis or bone sequestra is located in the maxilla. Dental radiographic examination is performed to assist in the diagnosis. Teeth in the necrotic bone or retained tooth roots and bony sequestra are removed and necrotic bone curettaged to the level of healthy, bleeding bone. Intraoperative bacterial culture and sensitivity testing is performed. Tissue is submitted for histopathologic examination to rule out an underlying neoplasia. The area is liberally flushed with sterile saline solution and closed with a mucoperiosteal flap using 3-0 polydioxanone. Broad-spectrum antibiotic therapy such as amoxicillin-clavulanic acid (Clavamox, Pfizer Animal Health) is initiated until bacterial culture and sensitivity results are available.
Feline Mandibular Swelling
Feline mandibular swelling can be difficult to diagnose because of the ventral location of the mandible and the inability to recognize this problem during cursory physical examination. Mandibular swellings in cats secondary to malignant neoplasia has been recognized for years. Nonmalignant mandibular swellings, osteomyelitis, in cats caused by dental disease has not been described until recently. A one year prospective study was performed at The Animal Medical Center involving 24 cats with mandibular swellings.3 Clinical signs on physical examination include excessive salivation, oral bleeding, halitosis, loose teeth, anorexia, change in food preferences, weight loss, and behavioral change. Diagnosis in these cases is based on oral radiography and histopathologic examination. The most common cause for malignant feline mandibular swelling is squamous cell carcinoma. The most common cause of benign feline mandibular swelling is retained roots secondary to end-stage external root resorptive lesions. Periodontal disease and fractured teeth also result in benign feline mandibular swelling. In man, dental infection is the most common cause of osteomyelitis of the mandible. Cats with osteomyelitis secondary to retained roots, periodontal disease or endodontic disease are treated by extraction of the affected teeth followed by curettage of the bone, flushing the area with sterile saline, and closure of the gingiva over the exposed mandible. Cats with benign mandibular swelling secondary to dental disease have a rapid return to normal function following appropriate treatment. Recognition and treatment of dental disease in the early stages may prevent osteomyelitis of the mandible in cats.
Bilateral Pathologic Caudal Mandibular Fractures
Bilateral pathologic caudal mandibular fractures can be an infrequent but severe complication of advanced periodontal disease. These pathologic fractures may occur in the region of the first mandibular molars and often occur following minimal bony stress. These types of fractures tend to occur most frequently in geriatric, small breed dogs and have been described as "orthopedic disasters." Various techniques for repair of these fractures have been utilized including tape muzzles, acrylic splints, percutaneous skeletal fixation devices, bone plates, pins and cerclage wires with variable success. A salvage procedure for the management of these difficult cases has been reported.4 It is recommended that this technique be reserved for bilateral mandibular fractures with poor bone quality in the region of the first molars. All diseased teeth should be extracted and the avascular ends of the exposed hemimandibles are removed with rongeurs resulting in 1-2 centimeters of bone loss bilaterally. The fracture sites are flushed and mucoperiosteal flaps are elevated and sutured over the exposed bone ends using 3-0 polyglactin 910. The mandibular and maxillary lip margins are removed from the level of the commissures of the lip to the distal aspect of the mandibular canine extraction sites. The buccal mucosa is closed bilaterally in a simple interrupted pattern using 3-0 polyglactin 910. The skin is closed with 3-0 nylon in a simple interrupted pattern. This advances the commissures of the lips to the previous location of the distal aspect of the mandibular canine teeth. Postoperatively a soft gruel is recommended for approximately 2 weeks after which time a canned dog food diet may be feed. It is recommended that this salvage procedure involving bilateral partial central hemimandibulectomies with bilateral advancement of the commissures of the lips be limited to those cases in which more conservative mandibular fracture repair techniques have been unsuccessful.
Dentigerous cysts occur infrequently in dogs, however, the diagnosis of dentigerous cysts should be a primary consideration in young dogs presenting with oral swellings. Additionally, the possiblity of an iatrogenic dentigerous cyst must be considered in those dogs in which a deciduous tooth was extracted or a traumatic episode has occurred in a puppy and subsequently the permanent tooth fails to erupt.5 Definitive diagnosis of a dentigerous cyst is based on history, physical examination, radiography, and histopathologic examination. Dentigerous cysts arise from the cellular components of the developing dental follicle.6 The cyst contains one or more embedded teeth and usually surrounds the coronal aspect of the tooth. As the tooth bud continues to develop but fails to erupt, the cyst becomes filled with fluid. Fluid pressure within the cyst results in a smooth-bordered radiolucent cavity typically adjacent to the cementoenamel junction as viewed radiographically. The treatment of a dentigerous cyst usually involves surgical extraction of the affected tooth and thorough removal of the entire epithelial lining of the cyst wall which is submitted for histopathologic examination. Complete excision of the tooth and the cystic epithelium is curative.
Renal Secondary Hyperparathyroidism
Hyperparathyroidism results in resorption of calcium from bone as the body attempts to maintain calcium homeostasis. Hyperparathyroidism is most commonly caused by a nutritional deficiency or chronic renal disease. The first bone affected in cases of renal secondary hyperparathyroidism is the mandible followed by the maxilla.7 The initial radiographic finding associated with hyperparathyroidism is loss of the lamina dura which is the cortical plate of the alveolus that surrounds the tooth roots. As the disease progresses there is a loss of density of mandibular trabecular and cortical bone. Failure to successfully treat the underlying chronic renal failure results in the progression of bone loss and eventual death from the underlying renal disease.
Hypoplasia or Congenital Absence of the Soft Palate
Hypoplasia or congenital absence of the soft palate has been previously described.8 This rare condition is diagnosed in puppies with a history of chronic mucopurulent nasal discharge. They may also be presented with a history of coughing, respiratory distress, poor weight gain, and general unthriftiness. Oral examination of puppies with hypoplastic or congenital absence of the soft palate reveals a diminutive soft palate with a midline rump of muscular tissue covered by epithelium. Unlike midline congenital clefts of the hard and soft palates that have a good prognosis with surgical correction of the congenital cleft palate, dogs with a hypoplastic or congenital absence of the soft palate have a poor prognosis because the defect is not amenable to surgical correction. Attempts to surgically correct congenital absence of the soft palate are unsuccessful because of the absence of adequate tissue for repair and lack of proper neuorologic function.
Dogs with pharyngeal mucoceles typically are presented because of difficulty breathing or swallowing. Confirmation of pharyngeal mucoceles is made on oral examination and aspiration of a clear or blood-tinged, ropey fluid that is consistent with saliva. The animal should be preoxygenated prior to induction and entubated rapidly to prevent anoxia secondary to obstruction of the upper airway by the pharyngeal mucocele. Pharyngeal mucoceles are treated by marsupialization of the mucoceles and removal of the ipsilateral mandibular and sublingual salivary glands.
Nasopharyngeal Stenosis in Cats
Diagnosis and treatment of acquired nasopharyngeal stenosis in cats has been previously described.9,10 Cats with acquired nasopharyngeal stenosis usually present with a history of nasal obstruction of several months' duration. The most significant clinical sign in these cats is a stertorous or wheezing upper respiratory noise. However, when the cat's mouth is held open the respiratory noise and distress are relieved indicating that the clinical signs are nasal in origin. Definitive diagnosis of nasopharyngeal stenosis is confirmed with a small-bore, flexible fiberoptic endoscope. The endoscope is placed dorsal to the caudal edge of the soft palate and directed rostrally. In normal cats the caudal nares are seen at approximately the level of the hard palate and form an ovoid orifice measuring about 6mm dorsoventrally and 5mm laterally in the adult cat. In cats with acquired nasopharyngeal stenosis the caudal nares is reduced to a pinhole-sized orifice by the presence of a thin but tough membrane. Attempts to pass a thin catheter from the external nares through the ventral meatus on each side will be unsuccessful in cats with nasopharyngeal stenosis. The treatment of choice for acquired nasopharyngeal stenosis is surgery. The cat is placed in dorsal recumbency with the mouth taped open. A midline incision is made in the soft palate and the cut edges are retracted laterally. The stenotic nasopharyngeal opening is enlarged by carefully excising the abnormal membrane with a fine iris scissors. The soft palate is sutured with 4-0 polydioxone suture in two layers. Prognosis is good following removal of the nasopharyngeal web.
Bilateral choanal atresia has been recently reported in the dog and has a similiar presentation to cats with nasopharyngeal stenosis.11 Surgical excision of the obstruction through a ventral rhinotomy is recommended. If an obstruction occurs secondary to scar tissue formation a permanent tracheostomy may be considered to bypass the upper airway obstruction.
Inability to Open/Close Mouth
There are several muscles that are involved in opening and closing the mouth. These muscles include the digastricus muscle which opens the mouth while the temporal, masseter and pterygoid muscles close the mouth. The muscles of mastication are innervated by the mandibular branch of the trigeminal nerve (cranial nerve V) except for the caudal belly of the digastricus muscle which receives innervation by the facial nerve (cranial nerve VII).
Several pathologic conditions in the dog can cause a dog to be unable to open the mouth. These conditions include masticatory muscle myositis and adhesion of the zygomatic arch to the ramus of the mandible following trauma.
Masticatory muscle myositis includes the conditions known as eosinophilic myositis and atrophic myositis. It is an immune-mediated disease. The condition occurs most frequently in adult, large-breed dogs, particularly German shepherds and related breeds. Swelling of the temporal and masseter muscles may rarely be recognized by the owner but more frequently the condition is recognized later in the course of the disease when trismus occurs which may progress to a total inability to open the jaws even 1 mm. Diagnosis may be confirmed with a biopsy of affected muscle and with immuno-cytochemical methods both within the muscle biopsy sections and indirectly in the serum of dogs with masticatory muscle myositis. Treatment consists of immunosuppressant medication and if necessary forceful opening of the mouth under general anesthesia by sequental placement of multiple tongue depressors placed between the teeth.
Trauma to the ramus of the mandible and/or zygomatic arch may result in the inability to open the mouth. The condition is confirmed with skull radiographs or CT scan. This condition is treated by surgical removal of the zygomatic arch and a caudal hemi-mandibulectomy. Postoperative physical therapy and anti-inflammatory drugs may help prevent recurrence of clinical signs.
Several pathologic conditions in the dog can cause a dog to be unable to close the mouth. These conditions include idiopathic trigeminal neuropathy also known as canine dropped jaw syndrome and displacement of the coronoid process laterad to the rostral part of the zygomatic arch in dogs with dysplastic temporomandibular joints.
The clinical signs in patients with idiopathic trigeminal neuropathy include acute or peracute inability to close the mouth. Sensory nerves are not affected. The pathogenesis of this condition is unknown and appears to occur more frequently in the fall. Rabies is the principal differential diagnosis. Idiopathic trigeminal neuoropathy is diagnosed with electromyography. Therapy for this condition is supportive including hand feeding. The prognosis is excellent and recovery occurs within 4-8 weeks.
Displacement of the coronoid process laterad to the rostral part of the zygomatic arch may occur in dogs with dysplastic temporomandibular joints. Treatment of recurrent locking episodes is by surgical resection of the zygomatic arch where the coronoid process hits the zygoma.
Diagnosis and treatment of unusual oral lesions such as canine osteomyelitis and bone sequestra, feline mandibular swelling, bilateral pathologic caudal mandibular fractures, dentigerous cysts, renal secondary hyperparathyroidism, hypoplasia or congenital absence of the soft palate, pharyngeal mucoceles, nasopharyngeal stenosis, choanal atresia, and inability to open/close the mouth can be challenging. However, thorough physical examination, clinicopathologic testing, histopathologic evaluation, and oral radiography can provide an accurate diagnosis resulting in the institution of appropriate surgical and other therapeutic modalities providing a successful outcome in most cases.
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