Oral medicine Flashcards
What is though to be the cellular difference with FGS
Inadequate b cell functiton/CD4 t helper cells and increase in CD8 cytotoxic cells. Increase in CD8 causes mismatched CD4/CD8 ratio = bad
Elevated ion CD3+ t lymphocytes and MHCII = increase inflammation
Increase in IgG
Elevation of what type of Ig in saliva
IgG and IgM = increase in saliva
IgA = increase in serum
What percent of cats have elevated globulins with FGS
60
What percent of cats recover completely
30
Feline recombinant interferon omega
Interferons (IFNs) are a family of cytokines generated by cells in response to viral infection and which have the ability to impede viral replication and induce apoptosis of infected cells.
Oral administration of type I IFN may potentiate T-helper 1 (Th1) response.
administration of 0.1 MU rFeIFN-u to refractory cases of FCGS over a 3-month period, 55% of the cats were cured or improved (10% cured, 35% markedly improved, and 10% moderately improved).
A moderate positive correlation was shown between clinical improvement and decreased viral load, suggesting an effect of systemic administration of rFeIFN-u on virus replication
Most effectively used in the group of cats that are FCV positive and are long-term non-responders to full mouth extraction.
Mesenchymal stem cell therapy
Modulate immunity by inhibition of T‐cell proliferation, altering B‐cell function, down‐regulating MHC II, and inhibiting dendritic cell maturation and differentiation.
MSCs are obtained mainly from adipose tissue and bone marrow. Frequency in fat is about 10-fold higher than in bone marrow.
of fresh autologous adipose-derived MSCs resulted in complete clinical remission in 3 cats (42.8%) or substantial clinical improvement in 2 others (29.5%) within 1 and 4 months after the first injection. Minimal to no response was observed in 2 cats (29.5%).
In fresh allogeneic MSCs 57% showed substantial clinical improvement, and 2 cats had minimal to no improvement at 6 months. 2 of the 4 responders showed clinical cure by 18 to 20 months, whereas 2 of the 3 nonresponders were euthanized at 6 to 12 months.
A multi-center clinical trial in the USA reported the result of either autologous or allogeneic adipose-derived MSCs injections in 18 cats with refractory FCGS. Of the 18 cats, 5 (27.8%) showed clinical cure, 8 (44.4%) substantial clinical improvement and 5 (27.8%) no improvement. Clinical response was observed between 3 and 6 months after MSCs therapy.
Clinical improvement or cure were less frequent (60% vs 77%) in cats receiving allogeneic than autologous MSCs.
stopped using autologous adipose-derived MSCs due to the deleterious effect of feline foamy virus on MSCs culture and are now favoring allogeneic adipose-derived MSCs obtained from specific pathogen-free (SPF) cats.
FGS is associated with what other oral disease
Perio
RR
FGS is more prevelent with what association
FCV
multi cat house hold
Gold standard for FGS treatment
Extraction of all teeth or premolar and molar teeth is the currently accepted standard of care for the primary management of FCGS (no difference has been shown between full-mouth extraction and subtotal-mouth extraction (premolar/molar teeth additional teeth)
Improvement = 67-80%
What percent of cats according to jennings JAVMA 2015 showed imrpvment and still needed EMM after extractions
69%
28.4% showed clinical cure
38.9% showed substantial improvement
32.6% were little or not improved.54
68.8% of cats showing clinical cure or substantial improvement required extended medical treatment
Cylcosporine in FGS
Cyclosporine is a calcineurin inhibitor licensed for the management of chronic allergic dermatitis in cats and dogs. It exerts its immunomodulatory effect on the cell mediated immune system through the inhibition of T lymphocyte function and proliferation and has been shown to induce apoptosis of lymphocytes.
Kissing lesions
Discrete areas of mucosal inflammation, both with and without ulceration are common in dogs at sites of tooth contact;
Dogs most commonly seen with CCUS
Greyhound
Maltese
CKCS
Causes of CCUS
Increase in IgG
lichenoid and perivascular infiltrates of plasma cells and lymphocytes, often in large numbers.
B cells, T cells, CD3 negative IL171 cells, macrophages, and mast cells and FoxP3
Pentoxifyline
Reduction of the production of inflammatory cytokines (especially TNF) by phagocytes stimulated with a variety of microbial products (eg, endotoxin)
Inhibits, in particular, the production of proinflammatory interleukin 17 (IL-17), interleukin 2 (IL-2), and interferon-gamma.
20mg/kg BID
Doxycycline
Broad spectrum ABX
5mg/kg BID
Niacinamide
Vitamin B3
200-250mg BID
Cyclosporine
An effective immunosuppressive agent, inhibits T-cell function and suppresses cell-mediated immune responses.
Mechanism of action: binds to intracellular cyclophilin A forming a cyclosporine-cyclophilin complex, which inhibits calcineurin, an enzyme critical to the synthesis of CKs such as IL-2, IL-4, TNF-ɑ and INF-Ɣ by T-cells.
Also inhibits the production of IL-17 by memory Th17 cells.
5mg/kg SID
Whole blood trough levels >300
Metronidazole
decreases leukocyte-endothelial cell adhesion and migration from the bloodstream into tissue, dampens down the proliferation of lymphocytes by causing damage to lymphocyte DNA, reduces the number and function of macrophages
Because metronidazole decreases the levels of IL-2 and INF gamma produced by T cells and significantly inhibits antibody production by B lymphocytes, this provides a proposed mechanism to control CCUS.
15mg/kg SID
genetic predisposition in the Siamese, Somali, Maine Coon, Persian, and Abyssinian.
occurs around the time of tooth eruption. Susceptibility decreases by around two years of age.
Juvenile gingivitis
Eosinophilic granuloma complex in the cat
association with various allergies (flea saliva, food proteins and environmental allergens, possibly feline self-allergens to Fel d 1 protein in saliva)
common sites are the dorsal surface of the tongue, the palate, and the mucocutaneous junction of the rostral lips.
lesions are well demarcated, flat or nodular, usually ulcerated, and variable in color from bright pink to yellow.
Classically, “eosinophilic ulcers” are flat, ulcerated lesions and “eosinophilic granulomas” are proliferative.
Young cats 2-8yo
Eosinophilic stomatitis in the dog
In dogs, lesions tend to be palatal, with less frequent involvement of the tongue, lips or other mucosal sites. Cavalier King Charles spaniels and Siberian husky breeds are over-represented.
Oral eosinophilic granuloma in Siberian huskies
Believed to be hereditary or familial condition
usually on the tongue, can also be seen on the palatal mucosa
lingual lesions = halitosis and oral discomfort
palatal lesions = no clinical signs.
young animals (1–7 years of age)
70% of asymptomatic dogs resolved without medication.
** see study for further information
Wegnerrs granulomatosis
An uncommon canine autoimmune inflammatory disorder affecting the gingiva, oral mucosa, and underlying alveolar bone.
Complement system inhibition with C5a has an important role in Pathogenesis.
Clinically, the gingival lesion can be multifocal, bruised, and erythematous in appearance, expansile, and friable. In all regards, it looks like a neoplasm. Radiographically the lesion is associated with severe alveolar bone loss. The key to a correct diagnosis is in the presence of granulomatous inflammation that is, not secondary to fungal or infectious disease.
Masticatory muscle myositis
Immune-mediated syndrome; impacts muscles innervated by the mandibular branch of the trigeminal nerve (masseter, temporalis, pterygoids)2 M fibers
Features:
inability to open the jaws (trismus), jaw pain and masticatory muscle atrophy, with occasional exophthalmos
More chronic presentations will show the atrophy with or without restricted jaw mobility.
Diagnosis:
the gold standard is Type 2M fiber (muscle fiber unique to masticatory muscles) antibody detection, these autoantibodies are more likely to be found in the active phase of the disease
Trigeminal Neuropathy
Other names: mandibular neuropraxia
Occurrence: dogs
Cause: idiopathic, based on resolution of clinical signs and lack of long-term neuropathy
Features:
open mouth that can be closed passively with little effort
Treatment:
Recovery in idiopathic cases usually occurs in two to four weeks with rest and conservative support
Use of corticosteroids had no effect on the clinical course of the disease
Osteomyelitis
Occurrence: common site in the mandible
Cause:
Usually bacterial infection, but fungi can also be responsible
Bone infections can result from three possible routes of inoculation – hematogenous, implantation, or local extension.
Infectious agents include: Staphylococcus spp., Streptococcus sp., Fusobacterium necrophorum, Truperella pyogenes, Nocardia spp., and several different fungal agents including Coccidioides immitis (cats, and dogs), Cryptococcus neoformans (cats), Aspergillus spp., Candida spp. and occasionally Pythium insidiosum.
The most common form of bacterial inoculation is via local extension from an infection of the tooth or periodontal tissues.
Clinical presentation:
large and firm swelling, often painful on palpation
Radiographically there may be a zone of bony destruction surrounded by a region of increased density or sclerosis.
sequestration may be present
proliferative reaction of the periosteum at the periphery of the lesion with lysis of the associated cortical and alveolar bone.
Endosteal or periosteal scalloping of the cortex, or a moth-eaten pattern of bone destruction is often evident.
Periodontal osteomyelitis
Attachment loss exposes the periodontal apparatus to the plaque-associated microflora, resulting in bacterial periodontitis. The presence of microorganisms stimulates osteoblasts and inflammatory cells to produce inflammatory cytokines like TNF alpha, IL1, and IL6. These mediators stimulate osteoclasts, resulting in bone and tooth root resorption.
Osteonecrosis
Definitions: exposed necrotic bone in the maxillofacial region that fails to heal after 6 to 8 weeks (up to 44 days before noticing)
Subtypes:
Radiation induced: Predisposed to breakdown and delayed healing. Risk of dehiscence and progressive extension of the osteonecrosis. Difficult to differentiate from recurrent malignant disease. Risk of recurrence is higher. Prognosis is fair to guarded.
Traumatic: treat by localization and surgical removal of the bone sequestrum. Prognosis is excellent.
Non-traumatic (infectious): removal of the bone sequestrum, appropriate bone debridement and long-term appropriate medical therapy.
Idiopathic: A disproportionate number of cocker spaniels have been reported. May recur at the same location or other sites. Prognosis is fair to good.
Hyperparathyroidism
- Nutritional secondary hyperparathyroidism can occur as a result of diets with a low calcium-to-phosphorous ratio, such as all meat. This leads to a transient hypocalcemia, which stimulates the secretion of parathyroid hormone.
- In renal secondary hyperparathyroidism, the reabsorption of phosphate is impaired, which results in hyperphosphatemia. This in turn leads to a lower blood calcium concentration, which stimulates parathyroid gland activity. Concurrent with secondary hyperparathyroidism, the synthesis of 1,25-dihydroxyvitamin D in the kidney is also decreased. This leads to a decrease in intestinal calcium absorption and impaired mineralization of osteoid. The combined effect of renal secondary hyperparathyroidism and the decreased 1,25-dihydroxyvitamin D is often referred to as renal osteodystrophy.
Features of hyperparathyroidism
Features:
The first radiographic sign is loss of the lamina dura, followed by loss of density of mandibular trabecular and cortical bone. Teeth may appear almost unsupported by bone.
most likely to become clinically evident in growing dogs but rarely in cats.
The first bone affected is the mandible, followed by the maxilla, then the other bones of the skull, and finally the long bones.
the bones of the jaws may become swollen and malleable.
Histo: Histologically, bone resorption and replacement with fibrous tissue is seen, which is often referred to as osteitis fibrosa cystica. In addition, osteomalacia, or poorly mineralized osteoid, may be seen.
3 parts of the tongue
- The root, attached to the basihyoid bones by the extrinsic muscles
- The body, the middle portion, attached to the floor of the mouth by the lingual frenulum
- The apex, which is the rostral, unattached, and mobile portion of the tongue.
Lesions of the tongue
Electrocution: Non-cardiogenic pulmonary edema also possible, must be addressed first. Then, wait till necrosis is over to debride (days to weeks) + same supportive tx as above.
Chewing lesions: sx, may recur
Glossitis 2ndry to plant FB (e.g. burdock plant): Prevention, otherwise anti-inflammatory and pain control, removal of burs if able to visualize
Ranula: Sialoadenectomy, can attempt marsupialization first
Linear FB: Trim + GI sx
Canine eosinophilic granuloma: a rare idiopathic condition that causes plaques or proliferative masses on the lateral or ventral aspects of the tongue.
alcinosis circumscripta: idiopathic deposition of calcium salts into soft tissues. Most commonly found in young, large-breed dogs. Slightly raised, nodular, white-to-grey areas on the lingual and/or buccal tissues. TX: excision
Papilloma virus
Calicivirus
Neoplasia – Melanoma>SSC
Pemphigus Vulgaris
Occurrence: rare, middle-aged dogs, severe.
Features: Affect keratinized oral epithelium (hard palate, gingiva, dorsal tongue). The majority of cases have oral involvement (up to 90% of patients, frequently at the mucocutaneous junctions, with some mucous membrane ulceration). Oral lesions occur before skin lesions in about 50 % of cases. Fragile vesicles. Patchy areas of ulceration, crusting and inflammation quickly follow when vesicles rupture and slough.
Ossifying fibroma vs fibrous dysplasia
OF: Other names: cementifying fibroma
Features:
local asympotomatic swellings of the jaw generally with distinct margins.
A predilection for the mandible appears to be present in dogs.
FD: Other names: craniofacial FD
Features:
dysplastic rather than neoplastic process
can be locally destructive, generally self-limiting.
May present in the canine zygomatic bone.
Hyperdontia
Supernumerary teeth (twinning). Develop from continued proliferation of permanent or deciduous dental lamina to form a third tooth germ or from disturbances during tooth development
More common in permanent teeth, maxilla>mandible. Usually incisors, PMs.
Common in Greyhound, Boxer, Bulldog, Rottie, dolichocephalic breeds.
More than 1/3 Greyhounds had T/SN, usually PM1
Boxer and Bulldogs: supernum incisors
Tooth agenesis
Failure to develop
Hypodontia
hypodontia: absence of 1-6 teeth
Oligodontia
absence of >6 teeth
Anodontia
all teeth missing
Common findings with agenesis
More common in permanent dentition, however, if deciduous absent, permanent likely to be absent also.
Cats: MxPM2 freq absent (incidence 3-28%)
Dogs: assoc w Kerry Blue, Affenpinscher, hairless dogs, large dolico, small breed, mini poodle
peg tooth
crown as abnormal conical shape
Gemination vs fusion vs concerescence
Gemination (aka schizodontism)
Single tooth germ attempted to divide into two separate teeth.
Increased frequency in boxers
No tmt required except if grooves extends subgingivally (gingivoplasty, sealant/resin)
Fusion
Clinical appearance similar to germination but one tooth is missing from dental arch
Concrescence
Union of two fully formed teeth by only their cementum (no involvement of dentin/enamel)
From trauma/inflammation. Developmental (trauma/crowding) vs acquired (inflammation-induced HC)
Dentin hypoplasia
Often accompanies enamel hypoplasia/dysplasia
Environmental etiology- seen in dogs with distemper and other unknown causes
vitamin D deficiency, phosphorus deficiency
Infectious, traumatic
No tmt necessary if tooth not mobile, monitor for endodontic pathology
Dilaceration
Sharp bend/curve along the root or crown of a formed tooth (20-90°). Root > crown
Odontodysplasia
Tooth or teeth are abnormally shaped, rough surface with yellow to brown discoloration
MX>MN
Permanent teeth, C/I
Focal enamel hypoplasia
Most common type of dog abnormality seen by the authors
Clinical tooth defect areas of opaque white, yellow or brown discoloration of visibly abnormal enamel to grossly abnormal tooth morphology
Often only one tooth affected
Environmental factors are responsible (trauma to the dental germ in the 1st 8-10wks of life):
Trauma #1 anecdotally
Diffuse enamel hypoplasia
nvolvement of much of the dentition; in the author’s experience often present present as areas with circumferential involvement of the entire crown vs pits or lines
Result of systemic diseases
Pyrexia
Canine Distemper Virus: Epitheliotropic nature of the virus causes direct infection and destruction of the ABs, in addition to pyrexia
Amelogenesis imperfecta
Type of hereditary EH with genetic basis, results from a
disturbance in ectodermal layers of developing teeth
Affects teeth in a more uniform fashion than environmental EH
Italian Greyhound - Hypoplastic type, autosomal recessive ENAM gene1
Samoyed - autosomal recessive SLC24A4 gene2
Standard Poodle - Hypocalcified type, mode of inheritance/gene not investigated3
Molar malformation
Usually bilaterally symmetrical defect in enamel leading to periapical infection, PA/P necessitating extraction in a majority of cases
MPO: Non-neoplastic proliferative bone dz of young large-breed dogs (3-5 mo), during MnM1 eruption
Sex/breed predilection: All dogs in this case series were large breed and male
C/S:
Non-painful firm swelling usually centered around M1. May be fluctuant orally.
Usually unilateral (L>R).
Dx:
Rad: Double mandibular cortex
Tx: Usually self-resolving in weeks t
CMO
AKA Lion jaw, Westie Jaw, Scottie Jaw.
Non-neoplastic, non-inflammatory proliferative bone disease, onset at
3-6mos old and continues until 12mos old (when growth ceases)
Breed/Sex Predilection: West Highland white terriers, Scottish terriers,
and Cairn terriers.
Inheritance:
Terrier breeds: Autosomal dominant, incomplete penetrance. Monogenic mutation in chromosome 5 Gene SLC37A2, a glucose phosphate transporter in osteoclasts.
C/S: PAIN when opening mouth, systemic signs (fever, lymphadenopathy). Masticatory muscle atrophy. TMJ restriction in severe cases. Usually bilaterally symmetric though can be unilateral.
Mandibles and tympanic bullae are most commonly affected.
Tx (Wiggs and Verstraete):
usually self-limiting;
Calvarial hyperostotic syndrome
CHS: Non-neoplastic proliferative bone disease usually affecting bull mastiffs (+ pitbulls?).
Onset at 5-10mos old and continues until growth ceases. No known causes or associations other than possibly familial predisposition.
In this case report, only MALE bull mastiffs were affected
C/S: PAIN when opening mouth or palpating head, fever, lymphadenopathy
Dx: CT = cortical thickening of the calvarium and frontal sinus w irregular, bony proliferation over the frontal, temporal, and occipital bones, tending to be unilateral
Tx: Self-resolving about 80% of the time, supportive NSAIDs if needed
Patellar fracture and dental anomaly syndrome
Feline patellar fractures are rare and most commonly occur spontaneously/atraumatically at the mean age of 28 months, and are postulated to be caused from a primary bone disorder. They most commonly occur at the level of the mid to proximal third of the patella. 50% of cats fracture contralateral patella within 3 months of first fracture, and often sustain fractures of other bones.
Persistent deciduous teeth, hypodontia, root resorption, root malformation and unerupted teeth.
Swellings of the jaw (mimicking neoplasia), osteonecoris/myelitis
surgical extraction of persistent deciduous and unerupted permanent teeth, and debridement of proliferative and necrotic bone appear to be necessary for an improved outcome
Generalised increased bone density in some cases supports that the underlying bone disease in these cats is a form of osteopetrosis
What are the four stages of TR
