Oral Pathology PDF

7 020 correction: LARA ALSHARA Lubna Ibrahim Malik Nsour Name Dr. faleh sawair |Page1 I left this space to write a note about the sheet but I couldn’t find suitable description so just enjoy ☺ as you know saliva is very important for the oral health & function, it’s being produced by the 3...

7 020 correction: LARA ALSHARA Lubna Ibrahim Malik Nsour Name Dr. faleh sawair |Page1 I left this space to write a note about the sheet but I couldn’t find suitable description so just enjoy ☺ as you know saliva is very important for the oral health & function, it’s being produced by the 3 major pairs salivary glands: 1- the largest which is the Parotid, located in front of the ear to the lateral ramus, down to the angle of the mandible. It produces 25% of the total daily saliva and it’s mainly serous secretions. 2-Submandibular; which produces 60% of the total daily saliva, it’s mixed serous & mucous gland. 3- Sublingual gland, it’s located in the floor of the mouth, it produces around 5% of the total daily saliva, it’s dominantly a mucous salivary gland. We have also hundreds of minor salivary glands, estimated to be around one thousand, distributed all over the oral cavity but NOT located in the gingiva & the anterior palate ×. Mainly they produce mucous saliva, and they contribute to less than 10% of the total daily saliva. |Page2 = xerostomia Disorders of the salivary glands 1-Developmental anomalies: ▪ Aplasia: no development of one or more major salivary glands. ✓ Is there any association with other abnormalities? And what are the oral manifestations of aplasia?? Answer from google: 1) Example syndromes which have been reported with salivary gland aplasia include hereditary ectodermal dysplasia, mandibulofacial dysostosis and hemifacial microsomia. 2) The main significance of the condition is a lack of saliva, causing xerostomia (dry mouth), with accompanying susceptibility to dental caries (tooth decay) so they typically require regular application of topical fluoride to prevent tooth decay., infections of the mouth, and upper respiratory tract infections (e.g., candidiasis, ascending sialadenitis, laryngitis and pharyngitis). |Page3 ▪ Atresia: blockage or missing part of the secretory or duct system of salivary glands, can be seen in submandibular gland. Usually It manifest clinically as retention cyst as there is blockage. ▪ Salivary gland hypoplasia: Small size of salivary glands. For example; in patients with merkenson-rosenthal syndrome. ▪ Etopic salivary gland tissue: Stafne’s IBC “idiopathic bone cavity”, located medial to the angel of the mandible below the inferior alveolar nerve and it’s continuous with submandibular salivary gland. Ectopic tissue may be found in the Middle ear, and Cervical Lymph nodes. And may develop as a result of lymphoepithelial cyst. ▪ Accessory ducts and lobes: For example; as you see in the diagram, the accessory ducts & lobes of the parotid gland, present in the cheek in the masseter muscle. the salivary glands disorders may present as enlargement of the gland or sometimes with or without redness and signs of infection, most importantly it may result in hyposalivation which will have dramatic effect on the oral health and function; as we can see in the pic below. |Page4 2-Infections of the salivary glands Can be viral or bacterial. ▪ Mumps: - It was common before 1988 (before the MMR vaccine), but nowadays it’s rare to be seen in vaccinated children. - It’s childhood infection and highly infectious that it can spread with airborne droplets or contaminated saliva. - It affects mainly the parotid gland but it can affect the other major SG, also it can affect exocrine glands or tissues particularly in adults. - After incubation period of usually 2 weeks, it starts with fever & malaise and then development of rapid painful swelling in the parotid region that will cause also for example trismus and difficulty in mouth opening and sever pain in the parotid region. - Usually it’s bilateral in 70% of cases. - It lasts for week and it’s self limiting; but if affects adults it may cause inflammation of other organs like the testes (Orchitis (20%)), or ovaries (Oophoritis), or the brain (CNS) (Encephalitis), or the pancreas (Pancreatitis). - Diagnoses: it is usually clinical but if you want with tests: you can find an elevated amylase enzyme in the blood, also with serology you can find IgM against the antigens of the virus. - The immunity after the infection or the vaccine is long lasting. |Page5 ▪ Acute bacterial sialadenitis: (uncommon) - Mainly affect the parotid salivary gland, ✓ the question is why? Answer from 016: 1) The parotid gland is serous secreting gland which will allow the bacteria to enter the duct easily (mucus is more viscous & has higher antimicrobial effect, so it's a hard way for the bacteria). 2) The parotid gland duct is larger, & opens near the upper molars area; which is an area rich of bacteria and plaque. 3) Opening area of submandibular gland is rich of saliva (more protection from bacteria). - The usual predisposing factor is decreased salivary flow rate, so the bacteria will ascend through the duct to infect the gland; so they call this infection ascending parotitis. The xerostomia is caused by: disease of the salivary gland such as; Sjogren’s syndrome, or Radiation, or some drugs like tricyclic antidepressants, or in immunocompromised patients like HIV, or it could be secondary to obstructed ducts which increase the susceptibility to infections usually chronic but sometimes can increase in severity to present as acute infection. - Microbiology: Usually the disease is mixed bacterial infection, caused mainly by staph. aureus and strep. Pyogenes; so there is a need usually of broad spectrum antibiotics to treat it. |Page6 - Clinically how to recognize the acute bacterial sialadenitis, there is swelling of rapid onset, painful causes trismus (difficulty in mouth opening), redness of the skin, and as it is an acute infection he would have fever, malaise, lymphadenopathy. In blood tests you would find increase in the erythrocytes sedimentation rate “ESR” & increase in the white blood cell count (leucocytosis). - To confirm that it’s a bacterial rather than viral infection, you can do milking of the parotid gland you will find puss coming out from the stensen’s duct as seen in the pic.  It’s NOT recommended to take biopsy from the parotid gland, or to do sialography in the acute bacterial sialadenitis. ✓ Why?? Answer from 015 Biopsy is contraindicated from parotid gland because it could cause 1- damage to the nerve and paralysis. 2- scar formation and obstruction. 3- Fistula. 4- Infection for the parotid. " Sialography: '' (injection of radiopaque substance then we take X-ray) The gland has inflammation so increase vascularity > that lead to weakness for the lining of the ductal system, when you apply injection with pressure in that area (during sialography) it could cause rupture of the acini and spreading of the infection. So it’s not permitted to do sialography for any patient with acute bacterial or viral sialadenitis. - Histologically: (done for educational purposes) o Intense AICI in acini, periductal tissue & within ducts. o Ductal dilatation. o Abscess formation → healing by fibrosis. |Page7 ▪ Chronic bacterial sialadenitis - This means the cause of the infection is persistent and it’s usually secondary to duct obstruction. - Mainly seen in the submandibular gland as duct obstruction is commonly seen there. Sometimes when there is chronic hyposalivation they will develop chronic bacterial sialadenitis as well. - It’s usually unilateral. - Clinically: a) Recurrent tender swelling of the submandibular region. b) Inflamed orifice of wharthon’s duct. c) Pus coming out from the duct. - Histologically: As it’s persistent and long lasting you will see more destruction to the SG tissue; so you find atrophy of the acini, replacement with interstitial fibrosis, CICI in the gland, dilated ducts and mucous (squamous) metaplasia, stones within the ductal system. |Page8 ▪ Recurrent Parotitis: - Inflammation of the parotid gland, mainly seen in children, usually the enlargement is bilateral. It’s painful swelling with redness and fluctuation is not a feature of recurrent parotitis. - Mostly these cases resorb spontaneously; but some may persist to the adult life causing recurrent parotitis of the adults. - The etiology is unknown, it could be congenital defect of the secretory system of the gland or chronic hyposalivation. o P.S: in the slides there is a question about pus presence but the dr didn’t mention it. 3- Obstructive & traumatic lesions: Common & important disease of the major & minor salivary glands. - could be the result of a disease in or around the lumen of the duct, usually because of stones or mucous plugs within the duct, but could be also caused by disease of the lining of the duct or tumour around it, or because of trauma or surgery to the gland which cause blockage or fibrosis. - In the parotid papilla region (which is located in the buccal mucosa opposite to the upper molars) it may be exposed to trauma by various causes like: appliances, sharp teeth or restoration, surgery in the region. Chronic trauma to parotid papilla, RAS (I guess it means recurrent aphthous stomatitis) Ulceration around a stone From slides not mentioned by the dr. |Page9 ▪ Sialolithiasis: (or development of stones in the SG) - 50% of major salivary gland diseases which means it’s common. - The stone can develop in the gland itself or in the duct. - ~ 90% of cases is seen in SMG “submandibular gland” mostly at the duct bend and distal third. -2nd most common site is the parotid but it is rare. And 2% of cases is seen in Sublingual & minor SGs. ✓ Is there is Any association with gallstones or kidney stones?? Some studies say yes & some no; I couldn’t find a specific answer. ▪ Clinically: Usually seen in Adults, mainly males (2M: 1F). Unilateral. Can be multiple within the same gland. Most cause symptoms: pain & swelling usually at meal time (and will disappear with time but in some patients may develop infection and chronic bacterial sialadenitis), sometimes may develop retrograde infection. ▪ How to confirm the diagnosis? 1- Usually you can do it with bimanual palpation of the ductal system at the site if the submandibular gland duct. Also in the pic it can be seen clinically by inspection. Usually we treat them by surgical exposure and removal. | P a g e 10 2- By radiographs, but not all stones are sufficiently calcified to be seen; there is 40% of parotid stones and 20% of the submandibular can’t be seen radiographically. 3- Sialography: by injecting a radio opaque material then take a radiograph, as seen in the pic we can see the ductal system, but there is a partial obstruction caused by the stone in the parotid gland. Stone | P a g e 11 4- Sialoendoscopy: new technique where we insert an endoscope inside the ductal system, we can see the stones and sometimes it can help in the removal of the stone. Pathogenesis: There is altered mucous with subsequent deposition of calcium salts, which will get collected with desquamated cells & microorganisms. - The stone: Is composed of calcium, phosphate, and to a lesser degree bicarbonate. It can be variable in size, usually they are round or oval in shape, the surface can be smooth or rough. and there usually yellowish or white in colour. - ✓ Why they (stones) develop more commonly in the submandibular gland?? Answer from 015: 1- Because of the irregularity (tortuous) & length of the duct. 2-Mucus gland (if any disturbance happened the mucus can be calcified easily). 3-Gravity. | P a g e 12 - Gland changes: As it’s chronic disease and there is susceptibility to infection, it has the same histology as in chronic bacterial sialadenitis: a) Duct dilatation, squameuos & mucous metaplasia. b) Acinar atrophy & replacement fibrosis. c) Periductal CICI & fibrosis. d) CICI of lobules. ▪ Radiation induced sialadenitis - SG are sensitive but more particularly the serous acini are more sensitive like in the parotid gland than the sublingual gland radiation. - The patient will develop immediately after radiation (within 24 hours “from slides, not mentioned”); xerostomia and tender swelling. But if the radiation dose is high it can cause irreversible fibrosis & squamous metaplasia; which will lead to persistent xerostomia, so we can expect the complication of permanent xerostomia… | P a g e 13 ▪ Sialadenitis (inflammation) of minor salivary glands Can be seen in mucous extravasation cyst and in nicotinic stomatitis and in sarcoidosis and in Sjogren’s syndrome. ▪ Necrotizing sialometaplasia A disease with unknown etiology, that affects the minor salivary glands particularly in the palate (hard or soft). sometimes it may follow infiltration anesthesia in the palate; particularly that use vasoconstrictor, so they think it could be as a result of ischemia to the area leading to necrosis to the tissue. The patient develops spontaneous necrosis; so there is development of deep ulcer around 2 cm in diameter, it’s painless ulcer, and persist around 2 months (long duration!). and because of deep, painless and chronic lesion, the patient may mix it with oral cancer. It’s self limited even after this long duration, the palate will heal but some fibrosis may develop in the region. | P a g e 14 - Histologically: In the surface epithelium you would find there is Pseudoepitheliomatous hyperplasia and deep in the tissue you will find proliferation of the ductal system (squamous metaplasia), and there is atrophy of the acini & necrosis of the salivary glands lobules, mucous excavation outside in the tissue, with the development of CICI. ➢ The histological findings can be mixed with SCC because of the surface epithelium, and sometimes with malignant salivary gland tumor like mucoepidermoid carcinoma. ▪ Sialadenosis (Sialosis) - Non inflammatory, non-neoplastic enlargement, bilateral usually, of the salivary gland; particularly the parotid gland. - Unknown etiology, it could be defect in neurosecretory control. Seen associated with alcoholism or some endocrine disorders like diabetes mellitus or hypothyroidism or acromegaly, sometimes seen in pregnancy or nutritional disorders like bulimia nervosa or patient taking antipsychotic drugs (Clozapine) or malnutrition or liver cirrhosis and chronic renal failure. | P a g e 15 - Histology: hypertrophy of acini & edema of CT, but there is NO damage to the salivary gland tissue & NO effect in the salivary secretion rate. - Sialochemistry: ↑ K+ & Ca++ ▪ Sjogren’s syndrome: important disease - it’s immune mediated chronic inflammatory disease (cell mediated) mainly damage to the salivary gland & other exocrine glands. - It’s considered as non-organ specific AID. - So there is inflammatory damage to the salivary and lacrimal glands and other exocrine glands; leading mainly to Xerostomia & Xerophthalmia (dryness of the eyes). - Lymphocytic infiltrate & replacement of glandular parenchyma; So there is irreversible damage to the execratory components of the glands. | P a g e 16 - Clinically: ~ less than 1% of population, can be seen in our region. Usually affect Middle aged. Females: ~ 90% . - We have types of sojgern’s syndrome: 1) Primary SS (Sicca syndrome); the patient only has xerostomia & Xerophthalmia. 2) Secondary SS where we have xerostomia & Xerophthalmia and connective tissue disease which could be rheumatoid arthritis or systemic lupus erythematosus. Diseases associated with secondary SS: o RA (15%) o SLE (30%) o Systemic sclerosis o Primary biliary cirrhosis o Dermatomyositis o Mixed CT disease | P a g e 17 - Because of the xerostomia there would be a lot of clinical signs and symptoms: 1- mouth o Discomfort o Difficulties in eating, swallowing & speech o Disturbed taste sensation; (metallic taste). o Dry, red & shiny mucosa painful wed o Burning sensation no o Susceptibility to infections: Candidiasis, ascending sialadenitis, root (rampant) caries o Red, atrophic, lobulated (cobble-stone) tongue + 2- Eyes: Keratoconjunctivitis Sicca o Corneal keratotic lesions o Failure of tear secretion: the patient will feel burning sensation of the eye, and will say as there is sand in the eyes o Conjunctivitis To confirm that there is dryness they usually do Schirmer test; where they put filter paper in the internal corner of the eye and see how much of the paper will be wetted with time; if it’s less than 5ml within 5min then is considered xerophthalmia. | P a g e 18 - Other complications: o Severe tiredness & Arthralgia o Xeroderma (skin dryness), nasal dryness, vaginal dryness o Sinusitis, tracheitis, dysphagia o Atrophic gastritis, pancreatitis, purpura o Anemia, leukopenia, thrombocytopenia o SG enlargement; can be seen up to 30% of cases, and in other reports around 15%. *SG enlargement on SS can be caused by: • secondary to ascending Sialadenitis. • Lymphoma in the parotid gland. • And because of the disease itself, as it’s an inflammation in the gland, so it Causes enlargement. So you have to be careful… - Histology: o Lymphocytic infiltrate, mainly T lymphocytes that cause acinar destruction so they will replace the acini; but the ductal system there will proliferation of epithelium & myoepthelial forming the ducts, so at the end the patient will have islands of epithelial and myoepithelial cells located in background of T lymphocytes in a sea of lymphocytes these structures are Epimyoepithelial islands; which can help in SS diagnosis. | P a g e 19 o Inflammation usually starts around the intralobular ducts, and this inflammation doesn’t cross the interlobular septa and the interlobular capsules; where in lymphoma we can see inflammation in the interlobular capsules & septa. - To test for xerostomia, we should do sialometry 1 which is measurement of mixed unstimulated salivary flow rate. There is graduated tube which allow the patient to spit the saliva for 10 minutes, if it’s less than 0.1 ml/min then it’s considered diagnostic for xerostomia. - In the eye the ophthalmologist should do the Schirmer test, to diagnose the xerophthalmia. 5 mm - For diagnosis it’s not recommended to take biopsy 2 of the parotid gland for example, so we take from the labial minor SGs. To confirm sjogren’s we should find these lymphocytic cells or inflammation which is usually seen around the ducts, we should confirm the presence of more than focus of these inflammatory cells in 4 mm2, and each focus should be composed of more than 50 lymphocytes to consider the case positive. | P a g e 20 2 4 mm - Also we can do sialography 3, they will find the dilatation sialectasis of the glandular system, and can usually be seen as snow storm appearance or cherry blossom appearance; so these appearances are suggestive for sjogren’s syndrome. “Snowstorm” Cherry blossom | P a g e 21 - We can also do salivary scintscanning 4, where they inject [99Tm] pertechnetate, normally this material will be taken by the SG & will be execrated in the saliva with time. But in sjogren’s syndrome there is decrease in the material uptake and any amounts taken will take longer time to be secreted in the saliva. - We can do antibody screening 5, in these patients there is multiple AB can be seen: o SS-A (seen in 75%) or sometimes called RO. o SS-B (seen in 40%) or sometimes called LA. o RF = rheumatoid factor o ANA = antinuclear antibody - In serology 6, we can see increase in the erythrocyte sedimentation rate (ESR) and Hypergammaglobulinaemia caused by the autoantibodies. - To confirm the diagnosis of sjogren’s, 4 of the following 6 criteria should be present: 1) At least 1 specified ocular symptom; 2) At least 1 oral symptom; 3) Abnormal findings on Schirmer's test; 4) Abnormal results on salivary gland biopsy; 5) At least 1 abnormal result for unstimulated salivary flow rate, sialography, or scintigraphy. 6) Presence of at least 1 of the following antibodies: RF, ANA, SS-A or SS-B. | P a g e 22 - The etiology: o is unknown for sjogren’s syndrome, it could be autoimmune disease but the antigen is unknown. o There is genetic susceptibility. o They incriminate some viruses particularly EBV. Other viruses from slides CMV, HHV-6, Retrovirus. - Complications: Other than xerostomia & xerophthalmia and their complications. These patients can develop B cell lymphoma (non-Hodgkin lymphoma), the relative risk is 14 times greater than patients without sjogren’s syndrome. ✓ Does the lymphoma develop more in primary or secondary sjogren’s syndrome??. | P a g e 23