Salivary gland disease Flashcards
(155 cards)
1
Q
What are the major and minor salivary glands?
A
Major includes parotid, submandibular and sublingual.
Minor glands are throughout the mouth.
2
Q
What are the parotid glands, their location and structure?
A
They are large, bilateral and in the preauricular region, overlying and fitting behind the ramus of the mandible. There is a superficial lobe which is flat and separated from the deep lobe (pyramid) and it can have accessory lobes. The facial nerve (cranial nerve VII) passes through it. The parotid gland is driven by parasympathetic secretomotor drive from otic ganglion. It delivers through stensons duct which runs along the cheek, perforating buccinator and emerging in the buccal mucosa approximately next to the first upper molar. It produces mainly serous secretion and contributes 20-40% of total saliva. It accounts for 60%of total salivary gland tissue.
3
Q
What are the submandibular glands, their location and structure?
A
They are smaller and they are paired glands which are walnut sized. They are found in the upper neck, curving around the posterior edge of the mylohyoid muscle. They have long ducts called Wartons duct which emerges either side of the base of the lingual frenum (punctum). They are palpable if dilated or if containing a stone. The lingual nerve twists around the submandibular duct and the hypoglossus so the lingual nerve needs to be protected. The facial artery runs through it from behind digastric, emerging at the lower border of the mandible at the site of VIIm branch. It has a secretomotor supply from the submandibular ganglion which is suspended off the elbow of the lingual nerve. They produce mixed saliva (mucous and serous). It contributes 60-70% of total saliva. It accounts for 30% of total salivary gland tissue.
4
Q
What are the sublingual glands, their location and structure?
A
The sublingual glands are the smallest and they are bilateral glands located in the floor of the mouth under the tongue, suspended from the submandibular duct. They secrete into the ducts of rivinus (10 small ducts) some of which drain into the submandibular duct. It has secretomotor supply via chorda tympani (VII nerve, submandibular ganglion). It has mixed secretion but mainly mucous and contributes 10%. Removal of the sublingual ducts is rarely indicated except in ranula which is a risk to the lingual nerve. They account for 5% of total salivary gland tissue.
5
Q
What are the minor salivary glands?
A
Minor salivary glands are found throughout the mouth mainly in the lips, cheeks, palate and tongue. There are approximately 800+ in total. There is parasympathetic supply from the otic ganglion and they have mucous secretion (one exception – posterior lateral tongue). They contribute 5-10% of saliva. They are commonly seen in the lip vermillion. They can become traumatised and blocked. They account for 5% of total salivary gland tissue.
6
Q
What is the organisational structure of salivary glands and their function?
A
You produce between 1-2L of saliva per 24 hours. The organisational structure includes acini which are saliva producing cells and demilunes. The initial fluid is secreted into the ductal system and there are intercalated/striated and secretory ducts. Protein and ion content is modified within the duct and there is ion exchange in striated ducts. Increasing diameter ductules drain into the main duct. Myoepithelial cells squeeze product at peak demand. Saliva components include proteins, calcium, phosphate, mucins, immunoglobulins and enzymes. The function of saliva is remineralisation, inhibition of demineralisation, anti-bacterial/fungal/viral, bolus, taste, digestion, buffering and lubrication. All components are critical for full oral health. Drugs, disease and radiation can affect.
7
Q
How should you examine the salivary glands?
A
- Feel outline, texture, size relative to opposite side, feel for a lump
- Bidigital exam of glands
- Look for and identify punctum/orifice
- Dry with gauze
- Swipe with pressure along malar or press up in neck – any product/quality/pus/blood
- Microswab/salivary protein/flow rate
- Ask about pain, dry mouth, mealtime syndrome (common, due to stone, stricture or debris sludge), mass effects, cranial nerve neuropathy (VII), ask about intermittent vs increasing
8
Q
What should you use to diagnose salivary gland disease?
A
- Clinical history, thorough general and specific examination
- Suitable imaging – USS/MRI/possible CT
- Sialography only indicative
- Histology – direct biopsy, FNA, core needle biopsy – gold standard, don’t do FNA
- Immuno may add to plain histological diagnosis
- Unusual or secondary tumours may need further histological examination/specialist referral
9
Q
What are the non-neoplastic lesions of salivary glands?
A
- Developmental anomalies
- Inflammatory - sialoadenitis
- Obstruction and trauma
10
Q
What are developmental anomalies?
A
They are very rare. You may see aplasia which is usually associated with other anomalies or syndromes. There is occasionally heterotopic salivary tissue where it is present somewhere it shouldn’t be. Stafne’s bone cavity presents close to the angle of the mandible and appears as a round radiolucency.
11
Q
What are the types of sialoadenitis and the causes?
A
Acute: - Bacterial - Viral Chronic: - Bacterial - Post-irradiation - Autoimmune e.g. Sjogren's syndrome - General debility/dehydration/terminal illness/diabetes mellitus/alcohol
12
Q
What is bacterial sialoadenitis?
A
Bacterial sialoadenitits predominantly involves the parotid gland and is termed acute (ascending) parotitis. It is an ascending infection caused by oral bacteria (s.aureus). You get acute swelling, heat and pain. Pus exudes from ducts. It is usually secondary to a dry mouth which may be due to radiotherapy, Sjogren’s syndrome or drug-induced.
13
Q
What are the two forms of recurrent parotitis?
A
- In adults - recurrent infection secondary to dry mouth
- In children - recurrent parotitis of childhood
- Both forms appear to be associated with ascending infection, often staph aureus
14
Q
What is recurrent parotitis in adults?
A
It occurs at 40-60 years and more in females. It is often unilateral. It is secondary to xerostomia. It is due to recurrent ascending infections. It is often secondary to Sjogren’s syndrome, drug induced dry mouth and radiation damage.
15
Q
What is recurrent parotitis of childhood?
A
It occurs at ages 4 months-15 years. Males and females are equal. It may resolve at puberty. There are bilateral parotid swellings with a sudden onset. It has days-week duration with periods of quiescence. Its not suppurative. There is no obvious cause or predisposing factors. There may be evidence of infection such as pain, redness and fever. Sialography will show punctate sialectasis radiographically which appears like leaves on a tree. There is gradual destruction of acinar elements and reduced flow. Histologically acini cells are damages and this is irreversible. There will be lots of inflammation.
16
Q
What is the prevalence and incubation period of viral sialoadenitis?
A
It is mumps (epidemic parotitis). It is caused by the mumps virus (paramyxovirus). It is now quite rare and there are less than 1000 cases per year. There was a 2006-08 epidemic. The incubation period is 2-3 weeks and it has direct or droplet spread. The numbers were quite high until 1988 until MMR vaccine was introduced and since then numbers have decreased.
17
Q
What is mumps?
A
It is acute bilateral parotid swelling which can be unilateral. It is usually in children. It is very painful and there is malaise and fever. It is self-limiting in 10-14 days. It may spread to other glands/organs.
18
Q
What are the complications of mumps?
A
- Orchitis in 30%
- Meningitis in 10%
- Oopohoritis 5%
- Pancreatitis 5%
- Cranial nerve palsies
VIII nerve deafness
19
Q
What is chronic sialoadenitis and where does it usually occur?
A
Chronic sialoadenitis is the most commonly seen and it is usually secondary to duct obstruction due to calculi. Salivary calculi is an accumulation of calcium and phosphate salts which deposit in the salivary ducts or gland. Histologically calculus is seen as a concentric accumulation of calcium salts around cellular debris and mucous. It is usually unilateral. The male to female ratio is 2:1. It is 80% seen in the submandibular gland, 20% in the parotid and 1-15% in the minor salivary glands. 35% is seen in the floor of mouth, 35% in the posterior duct and 30% in the gland itself so it is evenly distributed.
20
Q
How can a duct become blocked?
A
There can be narrowing of the duct or thickening of saliva. This leads to obstruction by calculus leading to saliva retention and inflammation. This leads to swelling and fibrosis and therefore loss of function. Fibrous tissue narrows the ducts. This is most common in submandibular gland as it has mucous saliva which is thicker and the duct is not straight so obstruction is more common. The submandibular gland is also pushing the saliva against gravity. There will be less acini and lots of lymphocytes. The swollen painful gland can occur at mealtimes or when thinking/smelling food.
21
Q
What colour are serous and mucous acini histologically?
A
Serous acini are darker purple and mucous acini are lighter.
22
Q
What is radiation sialoadenitis?
A
It occurs at doses over about 20Gy. There is a high risk of permanent damage over 30Gy and severe damage over 50Gy. Serous acini are most sensitive. There is inflammation and fibrosis of glands. There is loss of function. It is an important consideration in cancer patients. Histologically you still see ducts but hardly any acini and lots of inflammatory cells.
23
Q
What is the most common cause of sialoadenitis and what can this result in?
A
The most common cause is obstruction and trauma. As a result you can get salivary calculi (stones), mucous cysts (mucoceles) and necrotising sialometaplasia.
24
Q
What is sialolithiasis and the treatment options?
A
Sialolithiasis is the formation of stones within ducts of the major salivary glands. There are many myths relating to aetiology such as dehydration. There is a likely nidus around which calcium salts are deposited. It is affected by confirmation of the duct and flow rate. There is the ball valve effect with obstruction and temporary flow restriction. There will be expansion and pain from the gland capsule and the stone may travel, exfoliate at the duct orifice or become larger. Sialolithotripsy/basket retrieval/laser fragmentation/local release are more conservative treatment options compared to whole gland excision.
25
What is sialosis and the treatment?
Sialosis is bilateral, painless swelling of the parotid glands. There is reduced function and the patient will get xerostomia. It can be due to diabetes, drugs or alcohol. There should be supportive treatment or excision.
26
What are mucoceles and the types?
They are painless swellings which rupture and recur. The lower lip is the most common site and it is most common in children. The types are mucous extravasation cyst and mucous retention cyst. The most common is mucous extravasation cyst. Mucoceles can also raise on the palate, tongue and cheeks but it is not very common. Excise under LA with the minor salivary gland. There will be a scar so care with the vermillion border.
27
What are mucous extravasation cysts?
They are 85% of mucoceles and occur in a younger age group the peak of which is 20-30 years. The lower lip is the most common site (in 50%+). You get them as there is a break in the salivary duct so saliva leaks and pools in the connective tissue. It has a wall of fibrous and granulation tissue and not an epithelial lining. Histologically the lumen is lined with mucous, there are macrophages filled with mucous, lining of inflamed compressed granulation tissue.
28
What are mucous retention cysts?
They are 15% of mucoceles so not as common. They are seen in older age groups often over 40 years. The peak age is 50-60 years. They are seen in the floor of mouth and buccal mucosa so a different site. The retention cyst is caused due to a blocked duct so saliva cannot get out, there is backpressure and the duct swells and enlarges. It is lined by duct epithelium. Histologically the lumen is lined with mucous and it has a lining of ductal epithelium. The cyst wall is fibrous tissue with glands and not as much epithelium.
29
What is a ranula?
They arise in the floor of the mouth and are usually extravasation cysts. They arise from the sublingual gland and are painless swellings. They rupture and recur and are usually 2-3cm. They are usually seen in children. The management is surgical excision and possible exploration of the neck, excision with sublingual gland or decompression and ligation (new) where you take the roof off and ligate the base.
30
What is necrotising sialometaplasia?
It is important as it can be mistaken for malignancy. It presents as an indurated, ulcerated swelling. It is usually seen on the palate and often biopsied as malignant. It heals spontaneously in 4-8 weeks. It is benign inflammatory disease. Histologically it may look like a carcinoma due to proliferation of stratified squamous epithelium. You get squamous metaplasia of salivary ducts and islands of squamous epithelium deep in connective tissues. But you also see necrosis of acini with ghosts of normal structures.
31
What are the most common salivary epithelial tumours?
```
They are classified by WHO 2017 and there are 35+ tumours. The most common ones:
Benign:
- Pleomorphic adenoma
- Warthin tumour
- Cystadenoma
- Basal cell adenoma
- Canalicular adenoma
Malignant:
- Mucoepidermoid carcinoma
- Acinic cell carcinoma
- Polymorphous adenocarcinoma
- Adenoid cystic carcinoma
- Carcinoma ex pleomorphic adenoma
```
32
What is the difference between adenomas and carcinomas?
Epithelial tumours are divided into adenomas or carcinomas. Adenomas develop from glandular tissue and carcinoma develops in tissues that line the inner or outer surfaces of the body. Adenomas are benign and carcinomas are malignant. Adenomas can affect people of any age and carcinomas rarely affect children.
33
What are the non-epithelial tumours?
- Soft tissue tumours
- Malignant lymphomas
- Secondary tumours
- Unclassified tumours
- Tumour like lesions
34
What is the epidemiology of salivary gland tumours?
There are approximately 1000 malignant salivary gland tumours per year in the UK. 70% of tumours are parotid, 9% submandibular and 1% sublingual so 80% are seen in the major salivary glands. 70% are pleomorphic adenomas and 90% are benign. Only 20% are in the minor glands. Minor gland tumours are more commonly malignant (50%). Sublingual tumours are 99% malignant. There is a wide age distribution of salivary gland tumours and mostly in older patients. 80% of tumours in major glands are benign.
35
What is the site distribution in minor glands?
- Palate 55%
- Lips 15% (95% of these in upper lip and almost always benign, more likely to be malignant in lower lip)
- Cheek 10%
- Tongue 10%
- Other 10%
36
What is a pleomorphic adenoma and the epidemiology?
It is the most common salivary gland tumour. The parotid is the most common site and the palate is the next common. It is 70% of major gland tumours and 45% of minor gland tumours. The age range is 30-60 and male and female are equal. It is benign, grows steadily and can become very large and entangled in the facial nerve. If fit and well excise the adenoma as it can have malignant change. A wide excision is critical the first time as any residual capsule may contain elements of tumour. It may recur, recurrence may be late, extensive or 'scattergun'. It is difficult to treat if multiple recurrences occur, especially outside the gland.
37
What is the histopathology of a pleomorphic adenoma?
- It has a mixed pleomorphic pattern with a variety of appearances and patterns
- Islands and strands of epithelial cells
- Ductal structures are common
- Myxoid, mucoid or chondroid stroma
- It is encapsulated and lobules are within a capsule
- Often lobular pattern
- Infiltration of tumour into capsule may be seen
- Stroma surrounding tumour is abnormal - bluish appearance (myxoid), can see cartilage sometimes (chondroid) and this is the only tumour that shows this
38
What is a Warthins tumour, the epidemiology and histology?
It is 10% of benign salivary gland tumours and is always in the parotid gland. It is completely benign and is sometimes bilateral or multifocal. It is more common in males (60:40), smokers and occurs later (60 years). Histologically you see irregular cysts, lined by oncocytic duct epithelium (pink and two nuclei), the stroma is composed of lymphoid tissue which is dense.
39
What is a mucoepidermoid carcinoma, the epidemiology and histology?
It is the most common malignant salivary gland tumour and is 20% of minor and 5% of major gland lesions. The parotid is the most common site, then the palate, cheek and retromolar pad (if a patient thinks they have a mucocele on retromolar pad its not possible so its this). It is seen occasionally in children. It is malignant and about 10-15% metastasise. Histologically there is a mixture of mucous cells (pale blue cells) and epidermoid (squamous cells). Lesions are usually multicystic and high grade lesions may be solid with few mucus cells and occasional lesions have many clear cells.
40
What is an adenoid cystic carcinoma, the epidemiology and histology?
It is the second most common malignant tumour and is 15% of minor and 5% of major gland lesions. The parotid is the most common site and then the palate, cheek and sinuses. It is highly malignant. 75% of patients die within 20 years. Metastasis is via the bloodstream and nerve invasion. Histologically it is an infiltrative tumour with no capsule and has a characteristic multicystic or cribriform pattern (swiss cheese). It infiltrates widely through bone, blood vessels and along nerves.
41
What is a polymorphous adenocarcinoma, the epidemiology and histology?
It used to be called polymorphous low grade adenocarcinoma but the name was changed in 2017. It is similar to mucoepidermoid and it is only found intraorally. It is usually seen in the palate (70%) and in the lips and cheek (30%). It is the third most common intraoral malignancy. It is usually seen in over 50 years. There is infiltrative growth. This and adenoid cystic carcinoma are the most common salivary cancers that infiltrate nerves. It is often misdiagnosed on incisional biopsies as pleomorphic adenoma or adenoid cystic carcinoma. You need great care with small palatal biopsies. The overall survival is over 90% at 5 years and it metastasises in 10-15% of cases. It shows a variable histological pattern including lobules (well demarcated lobular outline), ductal structures, cribriform areas, papillary cystic pattern, single cell filing and washout out nuclei (staining very pale). Perineural infiltration is typical (eye of the storm appearance histologically). There is bland, monotonous cytology. It can be unpredictable and lesions with a papillary cystic pattern and cytological atypia may have worse prognosis.
42
What is an acinic cell carcinoma, the epidemiology and histology?
It is about 5% of salivary gland malignancies. It is seen 80% in the parotid and 15% in minor glands. It has a 30% recurrence rate and 15% metastasise. It has a variable histological appearance: solid, microcystic, papillary cystic and follicular. Lymphoid tissue and germinal centres are common.
43
What is a carcinoma ex pleomorphic adenoma, the epidemiology and histology?
About 10% of pleomorphic adenomas become malignant. It is usually long standing and/or recurrent lesions. It is seen in the elderly (60+). There will be a history of a long term slow growing lesion with a recent increase in size. Histologically it may appear to be a typical pleomorphic adenoma but it will show areas of cytological atypia. Some lesions contain other types of carcinoma - adenoid cystic, adenocarcinoma etc.
44
What is a parotidectomy and extralesional dissection?
Parotidectomy can be conservative, radical or extended. Associated with neck dissection. Extralesional dissection aims to minimise surgical defect and VII nerve risk. Careful nerve function monitoring, no attempt to dissect trunk of nerve. Just removes lump.
45
What are tumour like lesions?
- Oncocytosis
- Necrotising sialometaplasia
- Salivary gland cysts
- Chronic sialoadenitis of submandibular gland
- Lymphoepithelial lesions
46
What is Sjogren's syndrome?
It is an autoimmune disorder characterised by lymphocyte mediated destruction of exocrine glands resulting in dry eyes and mouth. Primary SS is dry eyes and mouth and secondary is dry eyes and/or mouth and connective tissue disease (RA/SLE). It occurs 90% in females in middle age. The oral symptoms are dry mouth (dry mucosa and lobulated tongue), infections (candidosis) and caries. There will be dry eyes (keratoconjunctivitis) and parotid swelling in about 20%.
47
What is the histopathology?
There is lymphocytic infiltrate in salivary glands. In minor glands focal sialoadenitis and in major glands lymphoepithelial lesion. It shows typical lymphoepithelial lesions and the gland is replaced by lymphocytes. Acini disappear but ducts proliferate to form epithelial islands. Epithelial islands are infiltrated by lymphocytes - lymphoepithelial lesion, In about 2-5% of cases these lesions may progress to lymphoma.
48
What are the causes of xerostomia?
There are a range of causes including diabetes (due to raised blood sugar and polyuria), medication (anti-cholinergics, cytotoxics, sympathomimetics, diuretics, anti-depressants), radiotherapy and autoimmune conditions including SS.
49
What does the parotid gland contain which the sublingual and submandibular glands do not?
They contain small lymph nodes within them (submandibular and sublingual do not). During embryological development, the parotid gland is encapsulated after the development of the lymphatic system, whereas the submandibular and sublingual glands encapsulate before lymphatic development. Hence, lymph nodes are found normally within the parotid glands but not in submandibular or sublingual glands. Scalp/ear/haematological cancers can spread to/involve intra-parotid lymph nodes. Accordingly there is always a differential diagnosis for parotid gland masses that includes intra-parotid lymph nodes. The history may point you in the right direction.
50
What imaging can be used for dry mouth, painful swollen gland and a lump in the gland?
For a dry mouth ultrasound is the first line imaging test if you suspect Sjogren's syndrome and occasionally sialography can be useful.
For a painful and swollen gland plain radiography can be used usually followed by sialography.
For a lump in the gland ultrasound with a core biopsy for tissue diagnosis. For malignant tumours this is followed up with an MRI.
51
What is the only cause of a dry mouth that can be identified on imaging?
Sjogren's syndrome. The disease process destroys the gland parenchyma producing a typical pattern of changes on imaging. Appears more speckled.
52
Why is sublingual gland obstruction rare?
Because it lacks a single duct and there are multiple tiny openings into the floor of the mouth.
53
Can ultrasounds be used for salivary stones?
They can identify some stones but are not as sensitive as a sialogram.
54
What imaging would be used for a submandibular obstruction and parotid obstruction?
. For a submandibular obstruction, a lower true 90 degree occlusal and a posterior oblique occlusal film are needed, possibly with a sectional OPT. For a parotid obstruction, an AP extra-oral film plus a small dental film inside the cheek are useful.
55
What is sialography?
Sialography involves injecting iodinated contrast along the submandibular or parotid ducts. The iodine in the contrast makes it densely radiopaque: stones are less dense than the contrast and they appear as radiolucent filling defects on the image.
56
What is the treatment for submandibular calculi?
- If visible in the anterior third of the duct then surgical excision usually under local anaesthetic via an intraoral approach
- If small, mobile and anterior to the mylohyoid bend then basket removal is indicated
- If beyond the mylohyoid bend or too big to remove with a basket then excision of the submandibular gland via an extraoral approach
57
What is basket removal of submandibular calculi?
It is an intraductal technique done under local anaesthetic. A helical wire basket is inserted into the duct opening (closed). Advance past the calculus and open the basket. Calculus is snared within the basket and drawn to the duct opening. It is released from the duct with a small papillotomy incision. No suturing is required (causes stenosis).
58
What are the complications of basket retrieval?
- Pain and swelling is to be expected post procedure
- Failing to remove the stone
- Getting the basket stuck in the duct (stone adherent to duct wall, needs to be mobile on sialogram)
- Persistent symptoms despite removing the calculus (ductal stenosis post incision?)
59
What is the treatment for parotid obstruction?
For strictures balloon dilation is used if it is in the extraglandular duct (most common), otherwise superficial parotidectomy.
For stones:
- If visible at the duct opening then simple surgical excision
- If in the extra-glandular duct, anterior to the posterior border of the ramus, small and mobile, then basket retrieval as per submandibular stones
- If in the gland parenchyma or too large to pass down the duct, lithotripsy (shattered with sound waves) or superficial parotidectomy
60
What is balloon dilation of ductal strictures?
It is an intra-ductal technique which is done under local anaesthesia: typically articaine down the duct mixed with iodinated contrast, this produces topical anaesthesia and enables identification of the stricture site. Also submucosal buccal lidocaine is injected along the course of the duct. There is dilation of the parotid papilla with a lacrimal probe followed by insertion of a 2 or 3mm angioplasty balloon along the duct. The uninflated balloon is positioned across the stricture under X-ray guidance and then inflated to 15psi for 90s. Two or three inflations can be needed.
61
What are the complications of balloon dilation?
- In some cases the stricture is too tight to pass the balloon even when a fine guide wire is used for navigation
- Despite the local anaesthetic dilation of parotid duct strictures is uncomfortable when the balloon is inflated
- Some strictures will not dilate even after several balloon inflations
- About a third of dilated parotid strictures will re-stenose within 2 years of treatment and will require a repeat procedure
62
What is the success rate of basket retrieval and balloon dilation?
Baskets overall 68% successful. Balloons overall 76% successful which reduces to 50% after 2 years.
63
What are the features of a malignant tumour?
Some features are more predictive of a malignant tumour, such as rapid growth, fixation to skin or underlying tissues, pain and in the case of parotid gland tumours, facial nerve weakness. As a rule of thumb, the smaller the gland the greater the likelihood that a salivary tumour is malignant. High grade malignant salivary neoplasms have infiltrative, spiculated margin that is ill-defined, which helps distinguish them from benign tumours on imaging. Benign salivary neoplasms are typically well defined solid masses with smooth/lobulated margins.
64
What are two consequences of salivary gland surgery?
- Freys syndrome
| - Facial nerve injury
65
What is freys syndrome?
Preauricular surgery (parotid) cuts across numerous small nerve branches and as it heals you can get cross function between parasympathetic (cholinergic neurotransmitter) and sympathetic (adrenergic transmitter) which is normally impossible. The exception to the rule is that sympathetic sudomotor supply for sweat glands is cholinergic so healing across salivary gland secretomotor nerves and skin nerves leads to freys syndrome. You see food and start sweating and flushing in preauricular region. There is flushing, redness, skin sweating on tasting/eating food. The treatment is botox into skin used with LA (intradermal) which inhibits cholinergic drive to muscles. You dust iodine on skin and then starch and give the patient peppermint. When sweat occurs skin will go black and this is where you put botox (minors starch iodine test), repeat test and there should be no black staining of skin.
66
What is facial nerve injury?
• In patients with facial nerve injury you get droop of forehead, eyelid ptosis, weak cheek and corner of mouth, incompetence of lips, dry eyes aesthetic detriment, similar to stroke effects. The treatment is endoscopic browlift, lid surgery, eye weights, static slings to commissure, dynamic slings using temporalis.
67
What are the connective tissue disorders?
- Rheumatoid arthritis
- Systemic and discoid lupus erythmatosus
- Systemic sclerosis
- Sjogren's syndrome
- Mixed connective tissue disorder
68
What is rheumatoid arthritis and the cause?
It is a multisystem inflammatory disease of synovium and adjacent tissues. It is autoimmine and often familial. HLA-DR4 (60%), genetic factors account for 50%. There are rheumatoid arthritis associated autoantibodies. There will be IgM class antibodies (rheumatoid factor) to Fc protein of IgG but these are not disease specific. Anti-cyclic citrullinated protein antibody (anti-CCP) is highly disease specific. There is a significant risk of mortality.
69
What is the epidemiology of rheumatoid arthritis?
It affects 3 cases per 10000 and 1-2% of the population. It affects females more than males 3:1. The peak incidence is 35-50 years. 40% of individuals are unable to work and disabled 10 years post onset.
70
What are the clinical signs of rheumatoid arthritis?
It has insidious onset. There is pain and stiffness of small joints and muscle weakness and wasting. Other symptoms:
- Fatigue and malaise
- Anaemia
- Weight loss
- Neurological effects - carpel tunnel syndrome
- Lymphadenopathy
- Lung problems - pleural effusion, pleural nodules, interstitial fibrosis
- 15% of cases have Sjogren's syndrome
- TMJ damage in juvenile rheumatoid arthritis
71
What joints are most commonly affected by rheumatoid arthritis?
- Metacarpophalangeal/proximal interphalangeal 90%
- Metatarsophalangeal 90%
- Wrist 80%
- Ankle 80%
- Knee 80%
- Shoulder 60%
- Elbow 50%
- Hip 50%
- Cervical spine 40%
- TMJ 30%
The relevance to dentistry is hands and wrists for the use of tepe brushes, OH. An electric toothbrush is easier for these patients. If affecting the TMJ this will cause difficulty with mouth opening at the dentist. If affecting cervical this will affect lying the chair back.
72
What are the extra-articular manifestations of rheumatoid arthritis?
- Weight loss
- Malaise
- Fever
- Lymphadenopathy
- Rheumatoid nodules (seen on joints e.g. elbows)
- Felty's syndrome (RA, splenomegaly, neutropenia)
- Amyloidosis
- Sjogren's syndrome
73
How is rheumatoid arthritis diagnosed?
- Clinical
- Radiographic changes
- Anaemia
- Raised ESR, CRP
Anti-CCP positive (80%)
- Rheumatoid factor positive 80%
- ANA positive 30%
74
What ways can rheumatoid arthritis be managed?
With general measures following NICE guidelines or with pharmacotherapy.
75
What are the general measures for rheumatoid arthritis?
(NICE guidelines)
- Education - empower with self management programmes
- Exercise - maintenance of general fitness and maintain muscle bulk
- Physio/OT - individual needs to be identified
- Surgery - for progressive deformity etc
- Dietary advice - weight reduction (3 omega fatty acids)
76
What pharmacotherapy can be used to treat rheumatoid arthritis?
Ask the patient about injections, inhalers, creams as they may forget.
- DMARDs - disease modifying anti-rheumatic drugs
- Corticosteroids - IA/IM/PO
- Biological agents
- Anti-TNFa ' biological agents' e.g. etanercept, infliximab
- Non-TNF agents e.g. rituximab, anakinra
- Symptomatic relief - NSAIDs, COX-2 inhibitors
- Surgical treatment (synovectomy, tenosynovectomy, reconstructive surgery)
77
What are the side effects of NSAIDs?
- Stomatitis
- Erythema multiforme
- Gastrointestinal bleeding leading to anaemia leading to depapillated tongue, burning tongue, candidosis
78
What are the oral effects of different DMARDs?
- Methotrexate can cause oral ulceration
- Gold can cause lichenoid reactions
- Penicillamine can cause loss of taste perception, lichenoid reaction and severe oral ulceration
- Hydroxychloroquine can cause lichenoid reactions
- Cyclosporin can cause gingival hyperplasia
79
What are the oral effects of different biologics?
- Adalimumab (Humira) oral relevance is TB, oral candidosis, erythema multiforme, lichenoid reactions, oral SCC
- Etanercept (Enbrel) oral relevance is oral candidosis, sarcoid nodules to face, erythema multiforme, oral SCC
- Infliximab (remicade) oral relevance is histoplasmosis infection, OLP, mandibular osteomyelitis, parotid swelling, ulceration, erythema multiforme
- Rituximab oral relevance is candidosis, ulceration
80
What are the orofacial aspects of rheumatoid arthritis?
- Access - individual with RA less likely to visit dentist
- Atlanto-axial joint dislocation - physical support, pillows, short appointments
- Impaired manual dexterity - electric toothpaste more effective than manual
- TMJ - commonly affected but one of the last joints involved, may lead to open bite
- Secondary sjogrens syndrome
- Felty's syndrome - RA, splenomegaly and lymphadenopathy, increased risk of infection (chronic sinusitis), oral ulceration, angular cheilitis
81
What is lupus erythematosus and the two types?
It is an immunologically mediated condition and the types are discoid lupus erythematosus DLE and systemic lupus erythematosus SLE.
82
What is the cause of lupus erythematosus?
- Genetic predisposition
- Environmental trigger (UV, microbes, drugs)
- T cell dysregulation of B cell activity
- Possible defect in clearance of apoptotic cells
83
What is discoid lupus erythematosus?
It affects the skin and oral mucosa. It affects females more than males and has a peak incidence of 40 years. Oral lesions are similar to lichen planus in appearance. The diagnosis is based on clinical/biopsy/immunology.
84
What are the features of skin lesions in DLE?
- Scaly, erythematosus patches
- Atrophic, hypopigmented areas
- Occur on exposed surfaces
- May be premalignant
85
How is DLE diagnosed?
- Clinical appearance
- Biopsy
- Circulating autoantibodies - ANA (anti-nuclear antibodies), dsDNA may be positive
86
How is DLE managed?
Treat as for lichen planus. Try to improve pain with difflam mouthwash/spray, lidocaine gel, steroidal mouthwash (betamethasone 0.5mg dropped in water, hold in mouth against ulcer for 3-4 minutes, do not rinse, eat/drink for 30 mins), immunosuppressants.
87
What is the age of onset and male to female ratio for SLE?
The age of onset is approximately 30 years. The female to male ratio is 8:1.
88
What are the systemic features of SLE?
- Malar rash
- Polyarthritis
- Photosensitivity
- Oral lesions
- Lymphadenopathy/anaemia
- Renal/cardiac/haematological/neurological
- Up to 40% with oral lesions
- Unilateral or bilateral white patches with central area of erythema or ulceration
- May involve the palate
- May be extensive
89
How is SLE diagnosed?
- Clinical
| - Immunological ( hypergammaglobulinaemia, hypocomplimentaemia, ANA (DNA and ENA) 90%, RF (30%)
90
What is the SLE pharmacological management?
There is 85% survival for 10 years.
- NSAIDs
- Hydroxychloroquine
- Corticosteroids
- Cytotoxic drugs (cyclophosphamide, azathioprine, methotrexate, mycophenolate (mofetil), cyclosporin)
- Dapsone, thalidomide, tacrolimus
91
What is the SLE prognosis?
- Depends on extent of disorder
- Death due to renal involvement
- Males> females
92
What drugs give lupus like drug reactions?
- Carbamazepine
- Hydralazine
- Methyldopa
- Penicillamine
- Procainamide
93
What is systemic sclerosis and the age range?
It is an autoimmune disorder where dense collagen is deposited in the tissues of the body. Clinical features include Raynauds phenomenon. It affects mainly females 20-50 years.
94
What are the types of systemic sclerosis?
- Localised cutaneous - it is limited to the skin on the face, hands and feet, the 10 year survival is 75% and less than 10% develop pulmonary arterial hypertension after 10-20 years.
- Diffuse cutaneous - it has more extensive skin involvement, may progress to the visceral organs, there is a 10 year survival of 55% and death is most often from pulmonary, heart and kidney involvement.
- CREST syndrome - a collection of symptoms seen in limited cutaneous (another name for it)
95
What are the clinical features of CREST syndrome?
- Calcinosis
- Raynauds phenomenon
- O(E)sophageal dysfunction
- Sclerodactyly
- Telangiectasia
(Spells CREST)
96
What are the orofacial manifestations of systemic sclerosis?
- Facial skin rigidity
- Sharp nose
- Thinning of lips
- Loss of facial wrinkles
- Microstomia (poor access for oral hygiene, increased incidence of dental caries, increased incidence of periodontal disease due to abnormal immunoregulation and obliterative microvasculopathy)
- Hypomobile tongue
- Dysphagia and xerostomia
- Periodontal ligament widened on xray
- Pseudoankylosis of TMJ
- Speech
- Eating
- Deteriorating quality of life
97
How is systemic sclerosis diagnosed?
It is difficult and essentially clinical.
- Skin biopsy
- Scl-70 autoantibodies
- Cardiac and pulmonary investigations
- Periodontal widening on radiograph (30%)
98
How is systemic sclerosis managed?
It is difficult to manage and the aims are to reduce the symptoms, slow down the progression of disease, prevent complications and to minimise disability.
- Nifedipine
- D-penicillamine
- Iloprost infusions
- Sildenafil
- Corticosteroids
- DMARDs
99
How is microstomia managed?
- Exercise programme - mouth stretching and oral augmentation
- Iontophoresis and ultrasound
- Sectional dentures
- Implants
- Surgical commissurotomy (high incidence of wound dehiscence)
100
What is Sjogren's syndrome and the epidemiology?
It is autoimmune exocrinopathy due to focal lymphocytic infiltration of salivary and lacrimal glands. The types are primary and secondary (with another systemic autoimmune condition such as RA/SLE). The incidence is 0.5-2% and it affects mainly females. 15% RA patients have secondary SS. 30% SLE patients have secondary SS.
101
What is the aetiology of Sjogren's syndrome?
```
Genetic predisposition:
- HLA-B8
- HLADR3
Viral agents:
- Herpes viruses
- EBV, CMV, HHV-6
- Hepatitis C virus (HCV)
- Retroviruses
- HRV-5, HTLV-1
```
102
What is the pathogenesis of Sjogren's syndrome?
- Lymphocytic infiltration of exocrine glands
- Hypertrophy of ductal epithelium and formation of epimyoepithelial islands
- Acinar atrophy and fibrosis
- Probable hyperactivity of B cells
103
What are the subjective symptoms of xerostomia in patients with Sjogren's syndrome?
- Difficulty swallowing/chewing dry food
- Sensitivity to spicy food
- Altered salty bitter metallic taste
- Burning mucosa
- Lack or diminished taste
- Salivary gland swelling/pain
- Cough
- Voice disturbance
- Nocturnal discomfort
104
What are the oral signs of Sjogren's syndrome?
- Initially often little change
- Oral mucosa - dry, atrophic, wrinkled, ulcerated, increased debris
- Tongue - dry, red, lobulated, loss of papilla
- Teeth - increased caries
- Salivary glands - firm on palpation, if swollen
105
What is the European criteria for Sjogren's syndrome?
Not all patients with dry mouth and autoimmune disease have Sjogren's syndrome.
- I - ocular symptoms
- II - oral symptoms
- III - ocular signs
- IV - histopathology
- V - salivary gland involvement
- VI - autoantibodies ( anti-ro (ssa) and anti-la (ssb))
Take a biopsy from minor salivary glands in lower lip. They are shrunken in someone with Sjogren's so difficult.
106
What are the rules for the European classification?
Primary SS:
- Presence of any 4 of the 6 items as long as either item IV or VI positive
- Presence of any 3 of III, IV, V or VI
Secondary SS:
- Well defined connective tissue disease and the presence of item I or II plus any 2 from III, IV and V
107
What is there an increased risk of with Sjogren's?
Lymphoma (non-Hodgkin). It is predominantly B cell (80% marginal zone of MALT type). The risk is 44x the normal population. It is worse in patients with vasculitis, peripheral neuropathy, anaemia, lymphopenia and chronic glandular swelling.
108
What is the management of Sjogren's syndrome?
```
Palliative:
- Increase lubrication
- Maintain oral/dental health
- Review candida status
Therapeutic:
- Pilocarpine
- Immunomodulating agents
```
109
What is mixed connective tissue disease?
It is sometimes called overlap disorder as there are symptoms from a range of connective tissue diseases such as Sjogren's, SLE and systemic sclerosis. There are clinical signs of a number of autoimmune diseases, often oral lichenoid reactions and trigeminal neuropathy. There is the presence of ANA (antinuclear antibody) speckled and RNP autoantibody.
110
What is xerostomia?
It is a symptoms of oral dryness and it may exist with or without hyposalivation. Hyposalivation is an actual decrease in saliva flow rate.
111
What is the difference between serous and mucous saliva?
Serous is watery secretion and mucous is viscous saliva.
112
What are the components of saliva?
```
It is 99.4% water.
Organic solids:
- Protein
- Gamma globulin
- Amylase
- Lysozyme
- Lactoferrin
- Glucose
- Lipids
- Amino acids
Inorganic solids:
- Sodium
- Potassium
- Calcium
- Magnesium
- Chloride
- Phosphate
- Iodide
- Fluoride
```
113
How is saliva formed?
Salivary gland secretion is mainly under autonomic nervous control and various hormones may modify salivary composition. Increased salivary flow is mainly a result of parasympathetic activity which causes vasodilation of blood vessels within glands. There are two components of saliva which are the fluid and protein components. The fluid component includes ions produced by parasympathetic stimulation. The protein component arises from secretory vesicles in acini which are released in response to sympathetic stimulation. The effects of parasympathetic stimulation are stronger and longer lasting. Parasympathetic stimulation leads to copious saliva of low protein concentration and sympathetic stimulation leads to little saliva but with high protein concentration.
114
What affects the salivary flow rate?
The unstimulated/resting flow rate is 0.3ml/minute. During sleep it is 0.1ml/minute. During eating/chewing it is 4-5ml/minute. Smell and taste increase salivary flow and anxiety decreases salivary flow. In unstimulated conditions 60-65% of saliva comes from submandibular glands, 20-25% from parotids and 2-5% from sublingual glands. During eating the parotids contribute 50% of saliva.
115
How do you measure unstimulated whole saliva rate?
It is measured by spitting into a gradated container for 15 minutes. Less than 1.5ml in 15 minutes suggests decreased function.
116
How do you measure stimulated parotid flow rate?
Carlsson-Crittenden cups are placed over the parotid orifice. Saliva is stimulated by placing 1ml 10% citric acid on the tongue dorsum. Less than 5ml in 5 minutes implies decreased function.
117
What are the functions of saliva?
- Lubricant effect
- Physical cleanser
- Caries control - high HCO3 and PO4 prevent demineralisation
- Pellicle formation - salivary proteins form barrier
- Antimicrobial - Igs/lysozyme/proteins/lactoferrin
- Taste - substances in solution for sense of taste
- Digestion of carbohydrates begin (amylase)
118
What are the effects of long standing xerostomia?
- Difficulties in oral function and wear of dentures
- Increased frequency of caries (particularly cervical caries)
- Acute gingivitis
- Dysarthria
- Dysphagia
- Taste disturbances
- Increased susceptibility to oral candidosis
- Burning tongue/depapillation of tongue - shiny and smooth
- Dry, sore cracked lips
- Salivary gland enlargement
119
What are the causes of dry mouth?
```
Physiological:
- Dehydration
- Mouth breathing
- Anxiety
Congenital:
- Salivary gland hypoplasia/aplasia
Iatrogenic:
- Drugs
- Radiation
- GvHD
Disease:
- Sjogren's syndrome
- Sarcoidosis
- HIV
- HCV
```
120
What is a congenital cause of dry mouth?
It is rare. It can be caused by ectodermal dysplasia which is usually sex linked recessive. There is hypodontia, hypotrichiosis, anhidrosis and it affects salivary and lachrymal glands.
121
What factors are associated with hyposalivation +/- xerostomia?
- Age approximately 30% aged over 65
- Anxiety/depression
- Dehydration
- Drugs
- Radiotherapy/chemotherapy
- Diabetes
122
What drugs can cause xerostomia?
```
It is common:
- Tricyclics
- SSRIs
- Antihistamines
- Diuretics
- Sympathomimetics
- Anticholinergics
- Antipsychotics
- Anti-parkinsonian
- Sedatives
Look at table in notes.
```
123
What other confounding factors must be considered with drug induced xerostomia?
- Age
- Gender
- Smoking
- Psychological factors
- Other diseases causing hyposalivation
- Drug related xerostomia reversible with cessation of drug
124
What is radiation induced salivary dysfunction?
Therapeutic doses of radiation for head and neck cancer can cause a permanent reduction in salivary gland function. The degree of damage is dependent on the number and volume of salivary glands exposed. 26Gy is the threshold below which recovery of 25% stimulated saliva flow rate can occur. There is an acute inflammatory reaction leading to eventual fibrosis, decreased blood flor and loss of acinar cells. There will be scant/sticky saliva leading to increased caries risk/oral candidosis/taste disturbance/dysphagia etc.
125
What is chemotherapy induced salivary dysfunction?
Chemotherapy may also adversely affect salivary function but the extend and underlying mechanism requires further clarification. The effects appears reversible over the following year.
126
What other factors are associated with hyposalivation and/or xerostomia?
```
Autoimmune/immune based:
- Sjogrens syndrome primary or secondary
- Primary biliary cirrhosis
- Autoimmune thyroiditis
- Chronic graft versus host disease
- Sarcoidosis
Infections:
- HIV
- Hepatitis C
- CMV
- EBV
```
127
What are the rare causes of dry mouth?
- Amyloidosis
- Haemochromatotis
- Wegener's disease
- Salivary gland disease
128
What history questions should you ask about xerostomia?
- Does your mouth usually feel dry?
- Does your mouth feel dry when eating?
- Do you have difficulty swallowing food?
- Do you require liquids to sip to swallow foods?
- Do you take water to bed at night because your mouth feels dry at night?
- Have you noticed difficulty wearing your dentures?
- Any soreness of your mouth?
- Dry sore eyes/skin/genital area?
129
What other information do you need in the history of dry mouth?
- Past medical history
- Anxiety/depression
- Drug history
- Social history - smoking alcohol
- Family history - autoimmune diseases
130
What should you do in a clinical examination for dry mouth?
```
General examination:
- Access problems
Extraoral features:
- Stigmata of connective tissue diseases
- Salivary gland swellings
Intraoral findings:
- Lack of pooling saliva on floor of mouth
- Dental mirror sticks to mucosa
- Food retention
- Gingival health
- Caries
- Candidosis
- Depapillation/lobulation of tongue
```
131
What different categories of investigation can be done?
- Clinical
- Radiological
- Laboratory based
132
What clinical investigations can be done?
- Sialometry
- Schirmers test - testing lacrimal gland, filter paper behind eyelids, risk of infection, corneal ulcers
- Rose Bengal staining - better than Schirmer's, dye in eye
133
What radiological investigations can be done?
- USS
- Sialography (will see snowstorm effect - punctate sialectasis
- Salivary scintigraphy
- PET scan
- MRI
- CT
134
What is scintigraphy?
It is a technique which investigates glandular function rather than structure. It measures the active uptake of radio-labelled marker such as technetium-99m after IV infusion.
135
What laboratory based investigations can be done?
- Immunology - ENA/ANA/Rh factor
- Haematology - FBC/CRP/ESR
- SACE
- Liver function
- Thyroid function
- Cryoglobulins
- Other antibodies (anti-mitochondrial, anti-smooth muscle)
136
What biopsy can be done to investigate xerostomia?
A labial gland biopsy to examine at least 5 lobules of minor glands ideally. Histopathological features supportive of Sjogren's syndrome:
- Acinar loss
- Duct dilation
- Periductal fibrosis
- Focal lymphocytic infiltrate
- Focal aggregate of at least 50 lymphocytes
- Over 1 focal aggregate per 4mm2 has high specificity
137
What is the treatment for xerostomia?
Treatment is directed at the underlying cause. Prevention is key due to the lack of efficacy of saliva replacement therapy. Assess patients prior to radio and chemo treatment and manage xerostomia early. Prevent dental complications and stimulation of saliva production A multidisciplinary approach is often required.
- Improve symptoms - salivary substitutes, sialogogues, OH
- Manage candidosis - antifungals, dental hygiene
- Investigate/treat sialadenitis - antibiotics, USS
- Prevent/treat caries, gingivitis - fluoride supplements, antibacterial mouthwash, OH advice, scale and polish, dietary advice
138
What is the role of the dentist in management of dry mouth?
- Caries - diet advice, hygiene advice, fluoride supplements
- Gingivitis - hygiene advice, scale and polish, antibacterial mouthwash
- Restorations/dentures - choice of material, denture retention, implants
- Candidosis - advice (dentures), chlorhexidine mouthwash, topical antifungals
139
What members of a multidisciplinary team work together to treat Sjogrens?
- Rheumatologist
- Ophthalmologist
- Oral medicine specialist
- GDP
- GMP
- Psychologist
140
What diet advice should be given to patients with xerostomia?
- Avoid soft, sticky foods and liquid diets which promote dental plaque development
- Eliminate salty spicy foods – irritant
- Non-cariogenic foods – suggest sugar substitutes
- Limit caffeine – dehydration
- Nutrient deficiencies have been described
141
What hygiene advice should be given to patients with xerostomia?
- Soft electric tooth brush – handle modification
- Accessories – interdental brush/floss
- Use of disclosing tablets
- Children’s toothpaste – mint irritant
- Oranurse toothpaste – bland
142
What microbial control methods can be used in patients with xerostomia?
- High levels of lactobacilli reported
- Chlorhexidine rinse
- Chlorhexidine varnish
- Fluoride rinse has some antimicrobial activity
- Alcohol containing mouthwashes avoided - burn and sore
143
What dental treatment can be done for patients with xerostomia?
- 3-4 monthly visits
- Remember fragility of oral tissues
- Consider fissure sealants
- Glass ionomer choice for provisional restorations
- Dentine of exposed roots - dental bonding resin adhesive systems
- Amalgam more successful than bonded materials
144
Can dentures be provided to patients with xerostomia?
Some patients use dentures successfully. The tongue adheres to and dislodges the denture. Mucosal irritation and ulceration is common. There can be dentures with reservoirs for artificial saliva. Implants are good due to increased comfort and function of prostheses.
145
What different products can be used to manage a dry mouth?
- Oral moisturisers
- Gustatory and mechanical stimulation of salivation
- Special toothpastes and mouthwashes
- Saliva substitutes
- Lip creams and ointments
- Systemic therapy
146
What are oral moisturisers?
Often patients take frequent sips of water, they can have saline solutions of water plus sodium bicarbonate. Overuse removes small amounts of mucous saliva from oral tissues and increases dry mouth sensation.
147
What are gustatory and mechanical stimulants?
There can be acidic stimulation which is uncomfortable and increases enamel demineralisation. There can be use of sugarless chewing gum, lozenges (salivix pastilles, SST tablets).
Other stimulatory methods:
- Acupuncture is used when mainly stimulated salivary function is affected, it is the result of neuropeptide release (VIP and calcitonin gene related peptide), in recent systematic review inconclusive evidence to confirm efficacy
- Electrostimulation
148
What are the saliva substitutes?
- Carboxymethyl cellulose, mucin, polyacrylic acid
- Oils and glycerine
- Majority of patients prefer water
- The relief is insignificant and short lived, patients can find them unpalatable, they are impractical to handle and expensive
- Choice based on personal preference
- Mucin may have better patient acceptance
- PH >6 dentate patients – saliva orthana (comes from pigs, contains fluoride)
- Ph <6 edentulous subjects – glandosane
- Other options are milk, glycerine, olive oil, margarine, Anhydrous crystalline maltose
149
When is pilocarpine used in Sjogrens syndrome and what is it?
When residual secretory capacity in salivary glands exists we may use cholinergic agents such as Pilocarpine. It is a tablet which stimulates all exocrine glands including mouth, eyes, sweat glands, increases secretion in lungs. It is a parasympathomimetic with mild B-adrenergic stimulating properties and non-specific. The increased salivary output is transient dose related and consistent. Animal studies show caries reduction. There is a lack of correlation between improved salivary flow and quality of life scores which may be related to coexistence of comorbidities. It is approved for treatment of radiation induced xerostomia. 5mg orally 3 times daily with titration up to 10mg. From present evidence it is advisable to prescribe pilocarpine after completion of radiotherapy for a 3 month trial if no contraindications.
150
What are the side effects and contraindications of pilocarpine?
Adverse effects are flushing, sweating, urinary frequency. Contraindication in uncontrolled asthmatics, narrow angle glaucoma, acute iritis.
151
What is the systemic therapy for Sjogren's syndrome?
- Interferon alpha - can be given as lozenge, improvement of salivary gland histopathology
- Infliximab - TNF blocker which increases salivary flow rate and gives improved symptoms of oral dryness, increased risk lymphoma
- Hydroxychloroquine - flow rate increased in 82% patients, improved oral discomfort, 40% decrease in number of oral infections, few adverse effects
- Corticosteroid irrigation parotid gland - increased flow rate, relief of symptoms, risk of infection and pain
152
How can oral candiosis be prevented?
- Optimise denture hygiene
- Remove dentures at night
- Use chlorhexidine mouthrinses 3 times weekly
- Acrylic dentures soaked in Milton solution diluted to 50% with water
- Metal dentures soaked in 0.2% chlorhexidine
153
How can oral candidosis be treated?
- Nystatin sugar free suspension 1ml qds
- Miconazole gel
- Systemic fluconazole in recalcitrant cases
- Consider 1st week of month chlorhexidine prophylaxis 10ml twice daily and dilute to 50% with water if irritating to mucosa and use alternate days
154
What is the first line therapy for ascending parotitis?
Amoxicillin
155
What is the treatment of ulcerative mucosal disease in dental practice?
- Benzydamine hydrochloride
- Chlorhexidine
- Lidocaine gel
- Topical corticosteroids
