Oral Medicine Finals PPT PDF

FINALS ALL IN ONE  ORAL MEDICINE  Spot/Macule – a flat lesion reflecting a change in mucosal colour Patch/Plaque – a thickened lesion (ranges from 1 to a few millimetres) Key Erosions – involves the epi...

FINALS ALL IN ONE  ORAL MEDICINE  Spot/Macule – a flat lesion reflecting a change in mucosal colour Patch/Plaque – a thickened lesion (ranges from 1 to a few millimetres) Key Erosions – involves the epithelium only Definitions Ulceration – whole of the epithelium is breached Bullae – lesions consisting of fluid retention within or under the epithelium; in the oral cavity lesions can burst to leave ersions Vesicles – small pockets of liquid within or under the epithelium found in greater numbers  Type I allergic reaction Transduction of fluid into tissues from capillaries is more than the capacity of the lymphatics to drain it away Triggered when mast cells release histamine into the blood Also triggered by: ACEI Angioedema C1-esterase dysfunction (consequent initiation of complement cascade Latex or LA (rare)  Types of Allergic Reaction / Hypersensitivity Type I Type II Type III Type IV Mediator IgE IgG/IgM IgG/IgM T cells Description Allergic Cytotoxic Immune complex Delayed deposition Examples Contact urticaria (bee RBC destruction post Rheumatoid Allergic contact sting), anaphylaxis, transfusion of arthritis, systemic dermatitis, Type I hayfever, food and mismatched blood lupus erythematous diabetes mellitus, drug allergy type MS  TARGET LESIONS Type 3 allergic reaction May involve nasopharynx, skin and genitals Erythema If all 3 are involved – Stevens-Johnson Syndrome Multiforme Presents orally as haemorrhagic pseudomembrane on lips and oral ulceration Usually self-limiting Manage with fluids and analgesia May be triggered by: Herpes simplex (6 months low dose prophylactic acyclovir) or mycoplasma pneumonia (systemic steroid prednisolone)  K+ channel opener used to treat angina Causes painful, non-healing ulceration Stopping use produces a rapid improvement in symptoms GDP should consult with pt’s physician regarding alternative drug therapy: Beta-blocker – atenolol Nicorandil Calcium channel blocker – amlodipine;** Ulceration isosorbide mononitrate **NB: amlodipine linked with gingival overgrowth ANGINA-RELATED Orofacial Granulomatosis Granulomatous inflammation is chronic inflammation in which the predominant cell is an activated macrophage Consists of an aggregation of macrophages that transform into epithelial- like cells, surrounded by a collar of lymphocytes or plasma cells – these act as a plug preventing transudated tissue fluid passing back into circulation via lymphatics = swelling Presents with: Oedematous lips Infectious: Non-Infectious Cobblestone mucosa Tertiary Syphilis Idiopathic Mucosal tags Tuberculosis Crohn’s Parasite Sarcoidosis Angular cheilitis Mycotic granulomatous infection Wegener’s Diagnosis – biopsy showing granulomatous reaction and negative Ziehl- Melkersson-Rosenthal Neelson stain Foreign body reaction Aetiology – infectious VS. non-infectious SUGGESTIVE OF CROHN’S  Chronic, inflammatory mucocutaneous condition – affects 1-2% of the population Lichen Aetiology- T-cell mediated autoimmune disorder Planus Diagnosis – biopsy with histological confirmation – difficult to distinguish between lichenoid reactions Oral presentation – white papules coalesce to form Wickham’s Histopathological Features: striae; usually posterior buccal mucosa and bilateral Hyperkeratosis Skin lesions – itchy, violaceous macular-papular rash affecting Basal cell liquefaction with flexor surfaces and genitals apoptotic cells (Civatte bodies) When affecting the scalp – planopilaris (can cause scarring T-lymphocyte infiltration alopecia) No epithelial dysplasia 6 subtypes: white (reticular, plaque-like, popular); red (erosive, NO STRIATIONS, NO LICHEN PLANUS atrophic, bullous) Lichenoid Reaction Clinically and histologically similar to lichen planus Aetiology – provoking agent: drugs, food, amalgam etc. Type 4 hypersensitivity reaction Diagnosis – biopsy and histological confirmation + patching testing to identify agent Treatment – remove provoking agent Graft Vs. Host Disease Presents with oral and cutaneous lichenoid appearances as part of a graft vs. host reaction In patients who have received an allo-graft bone marrow transplant GVHD is treated with potent systemic immunosuppressants Intra-oral lesions may respond well to steroids  Recurrent Aphthous Recurrent oral ulceration mainly occurring on non- Stomatitis keratinised mucosa 3 types: minor, major and herpetiform Aetiology – unknown; perhaps Langerhans cells within epithelium activate CD4 and CD8 cells against areas of mucosa resulting in epithelial cell death and ulceration ? Minor: Major: Herpetiform: Systemic causes – iron deficiency, sex hormones 1-5 per crop 1-2 per crop >10 per crop (pregnancy) and drugs (NSAIDs) 2-10mm in diameter ≥1cm in diameter ˂2mm in diameter Local causes – trauma Persist for 10-14 days Persist for >14 days initially Heal without scarring Heal with scarring Persist for 7-21 days Diagnosis – clinical exam and history Heal w/out scarring Peri-ulcer erythema Treatment – explore medical history, CHX mouthwash and topical steroids; clobetasol  Multisystem inflammatory disorder causing: Recurrent oral ulceration, genital ulceration and ocular inflammation (uveitis) Affects young males (20-30’s) Diagnosis – recurrent oral ulceration with two of: genital ulceration, ocular inflammation, Behcet's skin lesions or positive pathergy Syndrome Treatment – immunosuppression; azathioprine, thalidomide, corticosteroids, ciclosporin  Reiter’s Syndrome Asymmetrical Arthritis AKA reactive arthritis Either sexually transmitted (chlamydia) or post GI infection Oral lesions resemble geographic tongue Urethritis, Cervicitis or Diagnosis – synovial aspiration to rule out Conjunctivitis Diarrhoea septic arthritis CAN’T SEE, CAN’T PEE, CAN’T CLIMB A TREE  Most commonly encountered disorder in the dental practice Painful but benign blood filled blisters on buccal mucosa Larger lesions on soft palate Few millimetres in diameter Angina Bullosa More common in elderly Haemorrhagica Causes – minor trauma, post LA injection or steroid inhalers Treatment – reassurance  Mucous Membrane Pemphigoid Autoimmune, chronic, inflammatory condition Occurs mostly in middle-aged, elderly females Loss of adhesion between epithelium and connective tissue along line of basement membrane IgG and IgA deposition Presentation – sub-epithelial blisters that persist for several days before rupturing and leaving ulcers that take weeks to heal Scarring occurs on healing; synechia (scarring of conjunctiva) leads to corneal opacity, refer to ophthalmologist Diagnosis – biopsy with histopathology and direct immunofluorescence Treatment – clinical photographs, graded approach to steroids/immunosuppressants  Least common vesiculobullous disorder Presentation – white areas that can be removed with gauze to leave area of erosion and ulceration Pemphigus Nikolsky’s sign positive; dislodgement of intact superficial Vulgaris epidermis by a shearing force Advanced pemphigus can lead to desquamative and erosive gingivitis and can be fatal due to fluid loss, infection and toxicity Aetiology – thiol drugs with sulfhydryl radical; penicillamine and captopril, non-thiol drugs; NSAIDs and ACEI, stress, diet; garlic, viruses; herpes and radiation Diagnosis – biopsy with histopathology and direct immunofluorescence Treatment – clinical photos, graded approach to steroids/immunosuppressants Wegener’s Granulomatosis AKA Granulomatosis with polyangiitis Multisystem autoimmune disease of unknown aetiology Non-infectious cause of oro-facial granulomatosis Causes inflammation of the blood vessels in your nose, sinuses, throat, lungs and kidneys Strawberry gingivae or palatal tissues Refer for specialist care Fatal if left untreated Kawasaki Disease Usually seen in children Presentation – desquamation of lips, fingers and toes, mucosal erythema and strawberry tongue Involvement of the coronary artery increases aneurysm STRAWBERRY TONGUE and infarction risk If suspected, refer to paediatric cardiologist immediately Treatment – aspirin** and immunoglobin **NB – one of the only times you’d prescribe aspirin to children due to link with Reye’s Syndrome  Systemic Lupus Erythematous Autoimmune disease of connective tissue Usually affects women of child-bearing age Presentation – oral ulceration, honeycomb plaque, raised keratotic plaque, nonspecific erythema, purpura, petechiae, and cheilitis with butterfly rash Diagnosis – biopsy, blood tests or autoantibodies ANA and LE cells Treatment – systemic corticosteroids with other CAN PRESENT LIKE LICHEN PLANUS / immunosuppressants LICHENOID REACTIONS Erythematous Candidiasis Most common type of candidiasis Often in denture / removable prostheses wearers May also occur in prolonged broad-spectrum Abx use, corticosteroids and HIV patients Causes burning sensation and metallic taste Presentation – flat, red patches of varying size on palate and dorsal surface of tongue, loss of filiform papillae Treatment – local oral and appliance hygiene Pseudomembranous Candidiasis AKA Thrush Presentation – white plaques on oral mucosa that can be removed with gauze to leave a red base/sots of blood Commonly seen in immunocompromised patients; poorly controlled diabetes, corticosteroid inhaler use or HIV Treatment – manage underlying problem e.g. correct use of steroid inhalers using spacers and rinsing mouth after use  AKA Candida leukoplakia Presentation – white and hyperplastic lesions, Hyperplastic not removable with gauze due to hyperkeratosis Candidiasis Higher pre-malignant potential than other leukoplakias Aetiology – unknown; but predisposed by smoking Diagnosis – biopsy Treatment – antifungals, smoking cessation, removal; excision, laser or cryotherapy  AKA Chronic Atrophic Candidiasis Presentation – diffuse erythema of denture-bearing area with occasional petechiae, mainly on upper jaw Aetiology – candida albicans, constant denture wear, poor denture hygiene and high carb diet Diagnosis – usually clear cut Denture Treatment – leave dentures out at night in solution; CHX or hypochlorite, and topical antifungals Induced Can be seen following placement of hard lining Stomatitis material as they are porous due to air inclusions during mixing, creating voids where candida albicans can colonise  Angular Cheilitis Inflammation of one of both corners of the mouth, can be itchy or painful Presentation – corners of mouth are red and crusting Aetiology – candida albicans, staph aureus or streptococci Diagnosis – clinical examination Treatment – eliminate predisposing factors; iron deficiency, Crohn’s, correct increased OVD, improve oral and denture hygiene and topical antifungals; miconazole  Presentation - rhomboid shaped, smooth, red surface located in midline of the dorsum of the tongue, anterior to circumvallate papillae Seen in corticosteroid and inhaler users, HIV, diabetes and chronic atrophic candidiasis Aetiology – possibly related to persistence of Median embryonic midline tongue structure; tuberculum impar Rhomboid Glossitis Diagnosis – clinical appearance and location Treatment - none  Impetigo Highly contagious skin infection Affects infants and children Presentation – red sores on face, burst and develop honey coloured crusts Aetiology – staph aureus or beta-haemolytic streptococci Often mistaken for recurrent herpes simplex Treatment – oral and topical Abx; amoxicillin/clindamycin  PRIMARY CHANCRE Syphilis Sexually transmitted bacterial infection with 4 stages – primary, secondary, latent and tertiary Presentation – firm, painless, non-itchy skin ulcers orally and on genitals Oral features have 3 stages: GUMMA Primary chancre Snail-track ulcers Gumma Aetiology – treponema pallidum SNAIL-LIKE ULCER Treatment – Abx; penicillin  Human Herpes Virus 1 & 2 Produce acute herpetic gingivostomatitis and recurrent herpes simplex (cold sores) HSV1 – causes lesions above the belt; oral and oropharyngeal HSV2 – causes lesions below the belt; anogenital Acute herpetic gingivostomatitis is always accompanied by systemic malaise, fever and cervical lymphadenopathy Usually a trigger for recurrent herpes simplex; systemic illness, UV, stress, menstruation Treatment - acyclovir Human Herpes Virus 3 Varicella Zoster Responsible for chicken pox and shingles; recurrent varicella zoster Shingles usually only affects one dermatome and is associated with significant neuropathic nerve damage and pain Presentation – intra-oral ulceration, red rash, fluid- filled blisters that burst and crust Treatment – systemic antiviral; acyclovir 800mg If pain persists after zoster has cleared, tricyclic drugs can be prescribed Human Herpes Virus 4 Epstein Barr Responsible for infectious mononucleosis; glandular fever Contracted from saliva through kissing Presentations – sore throat, facial swelling and ulceration with creamy exudate and palatal petechiae Treatment – fluid and analgesics, metronidazole may relieve sore throat No antiviral drug is effective at managing EBV  Associated with Kaposi’s Sarcoma – in itself Human associated with HIV Herpes Virus 8 Presentation – oral lesions on palate which are: Red or purple in early stages Blue / black in later stages Diagnosis – biopsy Treatment – manage underlying condition; HIV or HHV8  Kaposi’s sarcoma HIV Oral Hairy Leukoplakia vertical corrugation on the lateral boarder of the tongue Pseudomembranous Candidiasis  Mild, contagious viral infection common in young children Presentation – red, fluid-filled lesions in the mouth that burst to leave ulceration with red base, rash on hands and feet Aetiology – Coxsackie virus A5, A10 and A16 Hand, Foot and Mouth Diagnosis – clinical examination Disease Treatment – soft diet, antipyretics and analgesics  Herpangina Painful enterovirus infection – affect GI tract Presentation – sore throat, red spots become raised into vesicles that form honey ulcers with red outline Usually 1-2mm in diameter Aetiology – Coxsackie virus A7, A9, A16, B2-5 Diagnosis – clinical examination Treatment – treat if symptomatic  Aetiology – ectopic sebaceous glands Diagnosis – clinical examination Treatment – reassurance or cosmetic Fordyce surgery using CO2 laser Granules Geographic Tongue AKA Glossitis Migrans Presentation – irregular depapilated patches of the filiform papillae Usually asymptomatic Aetiology – unknown; associated with pustular psoriasis Diagnosis – clinical examination; review in 2 weeks to assess migration of patches Treatment – reassurance and zinc phosphate mouthwash TDS Fissured Tongue Aetiology – unknown; associated with Down’s and Melkersson-Rosenthal Syndrome Diagnosis- clinical examination Treatment - reassurance  White Sponge Naevus Presentation – bilateral, symmetric, white, ‘spongy’ thick plaques on buccal mucosa, FoM, ventral tongue, soft palate Affects middle-aged women and smokers, linked with psoriasis Aetiology – mutations of keratin 4 and 13 Diagnosis – clinical examination Treatment – reassurance (make pt aware may affect other areas of body – larynx and genitalia), topical tetracycline may be beneficial in some cases DD- hairy leukoplakia Nicotinic Stomatitis AKA Smoker’s Keratosis Smoker’s can develop hyperkeratotic changes on their oral mucosa in response to chemical and thermal irritation Usually found on palate May cause minor salivary glands to become blocked / inflamed Smoker’s Melanosis Melanocytes are stimulated as a result of irritation from: Chemicals Thermal In tobacco smoke Presentation – brown / grey / black pigmentation on buccal and labial mucosa  Black Hairy Tongue Elongation of filiform papillae located on dorsum of the tongue and subsequent discolouration from chromogenic (colour- producing) bacteria Aetiology – response to infection, fever, xerostomia or tobacco Diagnosis – clinical examination Treatment – eliminate causative agent, tongue scraper, keratinolytic drugs – podophyllin 25% in tincture of benzoin Amalgam Tattoo Aetiology – amalgam debris implanted into soft tissues subsequently breaking down to release silver salts that cause staining Diagnosis – clinical examination; found adjacent to restored teeth Treatment – none; replace amalgam with composite ?  Racial Pigmentation Most common cause of oral pigmentation Presentation – often affects gingivae and mucosal surfaces, diffuse deep purple / brown / black discolouration in the form of patches, striates or strands Aetiology – melanin granules produced by melanoblasts Treatment – none; reassurance Melanotic Macules AKA Freckles Aetiology – generated or intensified by sun exposure; freckles darken from sun exposure, melanotic macules do not Intra-oral lesions do not usually appear before 40 years Diagnosis – clinical examination Treatment – none; reassurance Nevi Melanocytic nevi are benign proliferations of nevus cells in epithelial, submucosal layer or both Light brown and dome shaped Aetiology – congenital Diagnosis – biopsy to differentiate from melanoma Treatment - excisional biopsy Addison’s Disease Presentation – hyperpigmentation of palate and depapillation of tongue Aetiology – following adrenocortical damage caused by autoimmune system, TB or carcinomatosis (dissemination of carcinoma in the body) – causing overproduction of ACTH which stimulates melanocytes producing generalised hyperpigmentation Diagnosis – adrenal hypofunction is determined by hypotension, reduced plasma cortisol levels and low response to synthetic ACTH Treatment – corticosteroid replacement therapy  Melanoma Aggressive malignant tumours of melanocytes Presentation – asymptomatic brown, dark blue or black macule sometimes with erythema or ulceration, may become nodular, irregular and asymmetric Rarely present intra-orally – 1% of case Most likely I/O site – palate Melanomas on tongue or buccal mucosa are usually metastatic Prognosis is very poor – 5 year survival rate = 15% Diagnosis – biopsy Treatment – surgical removal  Presentation - small, slow-growing, benign lesion that resembles a small cauliflower Affecting tongue, lips and buccal mucosa Squamous Aetiology – Human Papilloma Virus Cell Treatment – surgical incision Papilloma Heck’s Disease AKA Focal Epithelial Hyperplasia Asymptomatic, benign, neoplastic white / pink papules in oral cavity Caused by HPV  Sjogren’s Syndrome Xerophthalmia (dry eyes) and xerostomia due to autoimmune, chronic, inflammatory damage to lacrimal and salivary glands If these features occur alone – Primary Sjogren’s If they are accompanied by another connective tissue disorders (rheumatoid arthritis / CREST ) = Secondary Sjogren’s Sicca Syndrome – symptoms of Sjogren’s but negative labial gland Histopathology: biopsy Salivary glands infiltrated by lymphocytes resulting in Affects mostly middle-aged women acinar destruction with fibrosis and myoepithelial cell proliferation Increased risk of caries, Diagnosis – labial gland biopsy with histological confirmation; PD and candida sialography shows ‘snow-storm’ appearance due to sialectasia CREST Syndrome: (cystic dilatation of ducts) Calcinosis infection Raynaud’s Phenomenon Treatment – methylcellulose eye drops, saliva substitutes and Esophageal Dysmotility preventative dental care Sclerodactyly Telangiectasia  Mucocele Presentation – dome-shaped, translucent swelling, commonly on lower lip or FoM Aetiology – damage to the duct of a minor salivary gland leading to extravasation of mucus Ranula – mucocele in FoM associated with sublingual Diagnosis – clinical examination gland, may extend under Treatment – superficial mucoceles may resolve mylohyoid muscle and spontaneously or bust; deeper mucoceles may present as submandibular swelling – plunging ranula require surgical removal / cryotherapy Salivary Gland Neoplasm Pleomorphic Adenoma – most common Malignant: Benign: Mucoepidermoid Carcinoma Pleomorphic Adenoma (poorly encapsulated) salivary gland neoplasm, commonly Adenoid Cystic Carcinoma Warthin’s Tumour (encapsulated) Acinic Cell Carcinoma found in parotid gland or palate Carcinoma ex Pleomorphic Adenoma With the exception of “Adenoid Cystic Carcinoma”, lesions are relatively asymptomatic; this means they can reach considerable size before Histopathology – pleomorphic being diagnosed appearance with epithelial and myoepithelial cells; poorly encapsulated Diagnosis – needle biopsy Treatment – surgical removal  Haemangioma Presentation - red or blue, soft and painless fluctuant swellings on tongue, buccal mucosa and vermillion border Usually blanch, unlike purpura or petechiae Sturge-Weber Syndrome Benign tumour of blood vessels often Congenital condition resulting in a combination of haemangiomatous lesions affecting the face forming a red birth-mark These patients commonly suffer from epilepsy Treatment – cryotherapy, laser ablation or blocking the feeder vessels  Lymphangioma Lymphatic malformations, benign, fluid-filled cysts in lymphatic vessels Congenital; usually apparent at birth or by the age of 2 Diagnosis – prenatal ultrasound, postnatal MRI, CT or ultrasound Treatment – surgical removal, sclerotherapy (shrink swelling via injection), radiofrequency ablation (high frequency via needle)  Presentation - ‘Lump’ of granulation tissue with ulcerated surface and covered in a yellowish fibrinous exudate Can occur anywhere in oral mucosa or on skin If on gingivae – vascular epulis (can also occur during pregnancy – pregnancy Pyogenic epulis) Granuloma Aetiology – trauma Treatment – remove any overhanging restorations, calculus or foreign body  Peripheral Giant Cell Granuloma AKA Giant Cell Epulis Presentation- red / purple gingival swelling Aetiology – chronic irritation or trauma Diagnosis – biopsy and histological confirmation Treatment – surgical excision with stripping of the periosteum and curettage of underlying bone  Central Giant Cell Granuloma Benign, non-neoplastic lesion of the bone that erupts out onto the gingivae Aetiology – unknown Effects – root divergence, destruction of surrounding bone and cortical expansion Differential diagnoses – Brown tumour (hyperparathyroidism), ameloblastoma and odontogenic keratocyst Treatment – surgical curettage Brown Tumour (Hyperparathyroidism) AKA Osteitis fibrosa cystica Occurs secondary to hyperparathyroidism Abnormal bone metabolism, extensive bone resorption replaced by fibrovascular tissue and giant cells with deposits haemorrhage and hemosiderin (brown in colour) Distinguished from a giant cell granuloma through bone chemistry – increased PTH Treatment – treat the hyperparathyroidism; removal of offending glands and the tumour should regress  Development of benign exostoses (bony outgrowths) that can occur in the palate or mandible Torus manidbularis – found on lingual aspect of mandible, below canine/premolar teeth, often bilateral Torus palatinus – may form in midline of Tori palate Treatment – none; may be surgically removed if causing interference with Triple lamination – combining 3 materials to fabricate a denture base that utilises the retentive aspects of denture fitting the torus  Osteoma Benign neoplasm of bone in which new bone grows on another piece of bone 2 types: compact and cancellous Treatment – excision if they become large and problematic or interfere with denture fitting Multiple osteomas in Gardner’s Syndrome (comprises of intestinal polyps with high malignancy potential) Oral osteomas should prompt referral for bowl radiography +/- endoscopy  Fibrous Dysplasia Self-limiting condition in which an area of bone is replaced by fibrous tissue leading to local swelling Monostotis – affecting a single bone Polyostotis – affecting multiple bones Ground glass Aetiology – mutation in GNAS-1 gene appearance Does not cause displacement of teeth Treatment – none Albright Syndrome A variation of polyostotic fibrous dysplasia causes café au lait spots and precocious puberty in females  Cherubism Rare, autosomal dominant condition Presentation – symmetrical, painless swelling of the jaw, failure of teeth to erupt (mandibular molars) Onset at 3-4 years old, symptoms abate (becomes less severe) by 30 years old Histology – multinucleate giant cells in fibrous tissue Treatment – maintain dental health and facial re- contouring after age 30  Homogenous Leukoplakia Dysplasia Erythroplakia Usually higher malignancy potential than leuoplakias Disordered tissue architecture Due to increased cell growth Speckled Leukoplakia; Usually severely dysplastic And altered cellular differentiation Non-Homogenous Degree of dysplasia indicates likelihood of malignant Leukoplakia transformation Lesions where the dysplastic features extend the full thickness of epithelium but do not breach the basement membrane are called “carcinoma in situ” and once the basement membrane is breached become “invasive carcinoma”  Primary Herpetic Gingivostomatitis HSV1 predominantly, occasionally HSV2 Most commonly affects young children Presentation: Widespread oral ulceration – intra epithelial vesicles Blood crusted lips Pyrexia Management: Acyclovir elixir – 200mg 5X daily for 5 days Antiseptic MW Fluids, don’t touch ANOMALIES OF TOOTH FORMAT ION AND ERUPT ION  Maxillary Second Mandibular Third molars lateral incisors premolars central incisors Hypodontia Genetic Mutations: § MSX1 (associated with missing 8’s and 5’s) § PAX9 (associated with missing molars) Arises due to abnormality in induction of § SHH (associated with solitary median maxillay oral ectoderm by ectomesenchyme incisor syndrome) Presence of conical teeth may be associated with Syndromes: the absence of the same tooth on the opposite Crouzon Syndrome side Down’s Syndrome Hypodontia = missing 1-6 teeth X-Linked Hypohidrotic Ectodermal Dysplasia Oligodontia = missing >6 teeth Anodontia = total lack of teeth Incidence: Treatment – paeds, ortho, prostho 0.1-0.9% in primary, ratio unknown Anodontia patients may require new dentures 3.5-6.5% in permanent (third molars – 9-37%) every 6 months to mimic developing dentition Permanent anomalies occur in 30-50% of those with hypodontia in primary dentition  Inherited disorder involving ectodermally derived structures – hair, nails, skin and teeth Presentation: Sparse hair Anhidrosis – Lack of sweating Hypodontia Dry skin X-linked Aetiology – mutation in ED1 gene Hypohidrotic Due to lack of sweating, patients at risk of hyperthermia if Ectodermal not diagnosed early Dysplasia Teeth are often small and conical, large anterior diastema often seen  Solitary Very rare Median Presents with a midline symmetrical Maxillary maxillary central incisor Central Incisor May be associated with CLP, choanal Syndrome stenosis, umbilical hernia Hypoplasia of Sella turcica, pituitary dysfunction, growth hormone deficiency Often managed by moving to one side for prosthodontic replacement  Autosomal dominant or X-linked trait, occurring by budding of dental lamina Super- Can resemble normal series (incisiform, caniniform, numerary molariform) – supplemental Teeth Can be conical or tuberculate Often bilateral – if on one side, suspicions raised on other side Supernumerary primary teeth are more likely to have supernumerary permanent teeth Incidence: 2:1 male:female in pemanent 98% occur in maxilla, anterior palate – mesiodens (75%) Associated with cleidocranial dysplasia and Gardner’s Syndrome  Cleidocranial Dysplasia Autosomal dominant congenital disorder Mutation to RUNX gene Presentation: Underdeveloped or absent clavicles Retained deciduous teeth Supernumerary teeth High vaulted, narrow palatal arch Delayed eruption of permanent teeth  Can arise due to fusion of adjacent tooth germs or separation of a single tooth Megadont germ to form 2 separate teeth; Teeth germination Germination can cause caries at interface between the 2 crown segments so should be fissure sealed Commonly affects maxillary central incisors Treatment – acceptance, remodelling, XTN plus ortho and bridge or implant Microdontia Any tooth that is smaller than normal Affects females > males Commonly affects maxillary lateral incisors and third molars Associated with Cleft Lip Palate and Ehlers-Danlos Syndrome Treatment – addition of composite  Most commonly affects molars Talon cusps – affect cingulum of maxillary incisors Caries can develop between the grooves of accessory cusp and tooth surface Treatment – selective grinding over time Accessory to reduce occlusal interference and Cusps promote deposition of tertiary dentine OR sectioning cusp and partial pulpotomy  Evaginated Tooth AKA Dens Evaginatus Presentation – small tubercle projection on occlusal surface Most commonly affecting premolars and bilateral Pulp can extend into evagination so if they # in function – pulp exposure Treatment - selective grinding over time to reduce occlusal interference and promote deposition of reactionary dentine or removal and pulpotomy  Invaginated Teeth AKA Dens in dente Presentation – invagination in the crown of a tooth Aetiology – invagination of enamel epithelium into dental papilla during tooth development Pulp necrosis may Most commonly affects maxillary lateral incisors, followed by maxillary central incisors and canines cause facial cellulitis Treatment – placement of resin sealant/restoration to minimise risk of caries, RCT if morphology favourable Taurdontism AKA Bull-like tooth Enlarged pulp chamber Aetiology – forms due to failed/late invagination of Hertwig’s root sheath Furcation is displaced apically Associated with amelogenesis imperfecta and ectodermal dysplasia Regional Odontodysplasia AKA Ghost Teeth Presentation – abscesses prior to eruption, poorly developed crowns, delayed/failed eruption and open apices, hypoplastic/hypocalcified enamel and dentine Permanent teeth usually less severely affected than primary Treatment – XTN of affected teeth Enamel Defects Hypoplasia – less enamel matrix is produced than normal but the enamel present is healthy; may see pitting and grooving Hypomineralisation – defect in mineralisation of enamel matrix proteins; enamel is more porous and susceptible to caries and wear, further divided into: Hypocalcification – dull, lustreless enamel, opaque white (chalky) or honey coloured Hypomaturation – similar to hypocalcification, less severe Amelogenesis Classified according to: Imperfecta Phenotype Inheritance Type I – Hypoplastic Autosomal dominance Type II – Hypomaturation Autosomal recessive Generalised enamel defects affecting most/all Type III – Hypocalcified X-linked recessive primary and permanent teeth Type IV – Sporadic Hypomaturation/hypoplasia/taurodontism Aetiology – mutation in AMELX, ENAM and MMP20 genes Causes poor aesthetic, sensitivity, wear and increased caries risk Treatment – prevention, GIC and SSCs can reduce sensitivity, composite veneers to improve anterior aesthetic and cast metal onlays to protect occlusal surfaces of posterior teeth Molar-Incisor Hypomineralisation Aetiology – childhood infections, Beta-lactam antibiotics or repeated fevers at time of development (7-8 months in utero for molars, 3-4 months after birth for incisors) Usually very sensitive – toothbrushing and achieving anaesthesia difficult Treatment – FV or tooth mousse for sensitivity XTN or retention of molars: If XTN – do so between 8-10 years as roots of 7’s bifurcating If retaining – restore with GIC/PFMC, retain until adulthood and reassess; bridge, denture or implant provision as necessary Incisors treated with micro-abrasion or composite veneers to improve aesthetics  Fluorosis Excessive intake of fluoride can cause enamel mottling Permanent hypomineralisaton of enamel characterised by greater surface porosity than normal Chronological distribution of fluorosis distinguishes it from other enamel defects  Dentinogenesis Imperfecta Autosomal dominant condition with 3 variants: D.I. with osteogenesis imperfecta D.I. associated with teeth alone ‘Brandy-Wine Isolate’ seen in Eastern USA Radiographically: Pulps are usually obliterated so pulp exposure and PAP rarely occur Roots are short and thin Teeth appear opalescent and blue / brown in colour Radicular Dentinal Dysplasia AKA Rootless Teeth Both dentitions affected Microscopically coronal dentine may appear normal but roots are composed of dysplastic dentine leading to pulp obliteration Roots are short leading to tooth mobility (often point of diagnosis)  Natal - teeth present at birth Neonatal – erupt within 30 days of birth Mandibular central incisors most common May be familial or associated with a syndrome Natal / Can be problematic during breastfeeding Neonatal and pose inhalation risk Treatment – smooth sharp edges or XLA Teeth if mobile  T RAUMA GUIDELINES 2020  P R I M A R Y D E N T I T I O N  ENAMEL FRACTURE Clinical Findings Fracture into enamel only Radiographic Findings None Treatment Smooth sharp edges Follow up None required  ENAMEL-DENTINE FRACTURE Clinical Findings Fracture into enamel and dentine Check for missing fragments, suspect aspiration or soft tissue imbedding Radiographic Findings None Treatment Cover with GIC or composite as required Follow up 6-8 weeks  ENAMEL-DENTINE-PULP FRACTURE Clinical Findings Fracture into enamel and dentine + pulpal exposure Radiographic Findings Confirm stage of root development – LCPA or occlusal Treatment Partial pulpotomy with non-setting Ca(OH)2, GIC, composite cap XLA Follow up 1 week, 6-8 weeks, 1 year (RAD)  CROWN-ROOT FRACTURE (NO PULPAL INVOLVEMENT) Clinical Findings Fracture into enamel, dentine and root Loose fragments of tooth may present Radiographic Findings Extent of fracture confirmed Extension into pulp may be confirmed Treatment Remove loose fragment and assess If restorable – GIC restoration If unrestorable - XLA Follow up 1 week, 6-8 weeks, 1 year  CROWN-ROOT FRACTURE (WITH PULPAL INVOLVEMENT) Clinical Findings Fracture into enamel, dentine and root – pulp exposed Loose fragments of tooth may present Radiographic Findings Extent of fracture confirmed Extension into pulp may be confirmed Treatment Remove loose fragment and assess If restorable – pulpotomy / RCT, restore with GIC If unrestorable - XLA Follow up 1 week, 6-8 weeks, 1 year (with RADS)  ROOT FRACTURE Clinical Findings Loose/displaced coronal aspect of tooth Occlusal interference Radiographic Findings Location of fracture confirmed Typically mid or apical third of root Treatment If not excessively mobile – monitor (if displaced, will spontaneously reposition) If excessively mobile – XLA, leave apical third to resorb, reposition and splint in 4 weeks Follow up 1 week, 4 weeks (splint removal) 6-8 weeks, 1 year (with RADS)  ALVEOLAR FRACTURE Clinical Findings Mobility/dislocation of several teeth Occlusal interference Radiographic Findings Location of fracture confirmed Relationship of maxillary and mandibular dentition Treatment Reposition under LA Stabilise against unaffected dentition with splint (4wks) Monitor Follow up 1 week, 4 weeks (splint removal) 6-8 weeks, 1 year (with RADS)  CONCUSSION Clinical Findings TTP No displacement / mobility Radiographic Findings None Treatment None Monitor Follow up 1 week 6-8 weeks  SUBLUXATION Clinical Findings TTP Some mobility, no displacement Radiographic Findings Slightly widened PDL Treatment None Monitor Follow up 1 week 6-8 weeks  EXTRUSIVE LUXATION Clinical Findings Tooth appears elongated Excessive mobility Occlusal interference Radiographic Findings Very widened PDL Treatment If no occlusal interference – leave If excessive mobility or extruded >3mm - XLA Follow up 1 week, 6-8 weeks, 1 year  LATERAL LUXATION Clinical Findings Tooth displaced (lingual/palatal) Immobile Occlusal interference Radiographic Findings Widened apical PDL – occlusal radiograph Treatment If no occlusal interference – leave If excessively displaced – XLA, reposition and stabilise with splint (4 wks) Follow up 1 week, 4 weeks (splint removal), 6-8 weeks, 1 year  INTRUSIVE LUXATION Clinical Findings Tooth displaced – through labial bone plate or permanent tooth bud Crown disappeared into socket Palpable labially Radiographic Findings If displaced through bone plate – apex visible, tooth shorter If displaced into perm tooth bud – apex not visible, tooth elongated Treatment Allow to spontaneously reposition – 6-12 months Follow up 1 week, 6-8 weeks, 6 months, 1 year  AVULSION Clinical Findings Completely out of socket Radiographic Findings To assess baseline and any displacement of permanent tooth Confirms tooth has not been intruded Treatment DO NOT REPLANT PRIMARY TEETH Follow up 6-8 weeks  Discolouration of tooth TTP Mobility Things to Position Remember: Displacement Tetanus jab status – may recommend booster Pulp sensibility tests are UNRELIABLE in primary and NOT USED P E R M A N E N T D E N T I T I O N  Clinical findings: Incomplete fracture (crack) of enamel TTP -ve Normal mobility Pulp sensibility +ve Radiographic findings: 1x Periapical recommended Nothing abnormal Enamel Treatment: infraction If severe can seal with bonding resin Otherwise do nothing Follow up: None required  Clinical findings: Loss of enamel No visible dentine TTP -ve Normal mobility Pulp sensibility +ve Radiographic findings: 1x Periapical recommended Enamel loss visible Treatment: Enamel If available, lost tooth fragment can be rebonded fracture Otherwise restore with composite Follow up: 6-8 weeks (clinical + radiographic) 1 year (clinical + radiographic)  Clinical findings: Loss of enamel and dentine No visible pulp TTP -ve Normal mobility Pulp sensibility +ve Radiographic findings: 1x Periapical recommended Enamel and dentine loss visible Enamel- Treatment: dentine If available, lost tooth fragment can be rebonded Fragment should be rehydrated by soaking in water/saline for 20 mins fracture Otherwise restore with composite Follow up: 6-8 weeks (clinical + radiographic) 1 year (clinical + radiographic)  Clinical findings: Loss of enamel and dentine No visible pulp TTP -ve Normal mobility Pulp sensitive to air, cold, sweets, etc Radiographic findings: 1x Periapical recommended Enamel and dentine loss visible Treatment: Enamel- Partial pulpotomy/pulp capping dentine-pulp Restore with non-setting Ca(OH)2 + composite/GIC Complete RCT may be required fracture Follow up: (complicated) 6-8 weeks (clinical + radiographic) 3 months (clinical + radiographic) 6 months (clinical + radiographic) 1 year (clinical + radiographic)  Clinical findings: Mobile fragments TTP +ve Pulp sensibility +ve (normally) Radiographic findings: Recommended radiographs 1x periapical 1x occlusal 2x additional radiographs at different horizontal/vertical angulations CBCT can be considered Apical extension of fracture not visible Crown-root Treatment: fracture Removal of mobile fragment Cover exposed dentine with GIC/composite (without Follow up: 1 week (clinical + radiographic) pulpal 6-8 weeks (clinical + radiographic) 3 months (clinical + radiographic) involvement) 6 months (clinical + radiographic) 1 year (clinical + radiographic) 1/year for 5 years  Clinical findings: Mobile fragments TTP +ve Pulp sensibility +ve (normally) Radiographic findings: Recommended radiographs 1x periapical 1x occlusal 2x additional radiographs at different horizontal/vertical angulations CBCT can be considered Apical extension of fracture not visible Crown-root Treatment: Removal of mobile fragment fracture If incomplete root formation, partial pulpotomy If complete root formation, RCT (with pulpal Follow up: 1 week (clinical + radiographic) involvement) 6-8 weeks (clinical + radiographic) 3 months (clinical + radiographic) 6 months (clinical + radiographic) 1 year (clinical + radiographic) 1/year for 5 years  Clinical findings: Mobile coronal section Displaced coronal section TTP +ve Pulp sensibility -ve Radiographic findings: Recommended radiographs 1x periapical 1x occlusal 2x additional radiographs at different horizontal/vertical angulations CBCT can be considered Apical extension of fracture not visible Treatment: Replacement of coronal fragment if displaced Check repositioning with radiographs Stabilise with flexible splint for 4 weeks (up to 4 months) Root Monitor for 1 year (cervical fractures may heal) RCT coronal segment if infected and not mobile If mobile coronal segment, remove and RCT retained root for post-crown fracture Follow up: 4 weeks (splint removal) 6-8 weeks (clinical + radiographic) 4 months (splint removal) 6 months (clinical + radiographic) 1 year (clinical + radiographic) 1/year for 5 years  Clinical findings: Mobile segment of multiple teeth which move together Occlusal disturbance Pulp sensibility -ve (likely) Radiographic findings: Recommended radiographs 1x periapical 1x occlusal 2x additional radiographs at different horizontal/vertical angulations CBCT can be considered Fracture lines in bone Treatment: Reposition and stabilise with flexible splint for 4 weeks Alveolar Monitor pulp condition of teeth Consider RCT if -ve sensibility for >1yr (can be false negative) fracture Follow up: 4 weeks (splint removal) 6-8 weeks (clinical + radiographic) 4 months (clinical + radiographic) 6 months (clinical + radiographic) 1 year (clinical + radiographic) 1/year for 5 years  Clinical findings: Normal mobility TTP Pulp sensibility +ve Radiographic findings: Recommended radiographs 1x periapical No abnormalities Treatment: Concussion None Monitor pulp condition for >1 yr Follow up: 4 weeks (clinical + radiographic) 1 year (clinical + radiographic)  Clinical findings: Increased mobility TTP Bleeding from gingival crevice Pulp sensibility may be -ve Radiographic findings: Recommended radiographs 1x periapical 1x occlusal 2x additional radiographs at different horizontal/vertical angulations No abnormalities Treatment: None Subluxation If excessive mobility, flexible splint for 2 weeks Monitor pulp condition for >1 yr Follow up: 2 weeks (splint removal) 12 weeks (clinical + radiographic) 6 months (clinical + radiographic) 1 year (clinical + radiographic)  Clinical findings: Increased mobility Appears elongated Pulp sensibility -ve Radiographic findings: Recommended radiographs 1x periapical 1x occlusal 2x additional radiographs at different horizontal/vertical angulations Increased PDL space apically Tooth not fully seated in socket Treatment: Extrusive Reposition and splint for 2-4 weeks Monitor pulp condition luxation Follow up: 2 weeks (splint removal) 4 weeks (clinical + radiographic) 8 weeks (clinical + radiographic) 12 weeks (clinical + radiographic) 6 months (clinical + radiographic) 1 year (clinical + radiographic) 1/year for 5 yrs  Clinical findings: Tooth displace (palatal/labial) Associated fracture of alveolar bone Immobile Percussion gives a high metallic (ankylotic) sound Pulp sensibility -ve Radiographic findings: Recommended radiographs 1x periapical 1x occlusal 2x additional radiographs at different horizontal/vertical angulations Widened PDL space apically Treatment: Lateral Reposition and splint for 4 weeks Monitor pulp condition and make endodontic evaluation at 2 weeks luxation Follow up: 2 weeks (clinical + radiographic) 4 weeks (splint removal) 8 weeks (clinical + radiographic) 12 weeks (clinical + radiographic) 6 months (clinical + radiographic) 1 year (clinical + radiographic) 1/year for 5 yrs  Clinical findings: Tooth displaced into socket Immobile Percussion gives a high metallic (ankylotic) sound Pulp sensibility -ve Intrusive Radiographic findings: luxation 1x periapical 1x occlusal Recommended radiographs 2x additional radiographs at different horizontal/vertical angulations No PDL space apically  Treatment: If incomplete root formation Allow to reposition spontaneously Orthodontic repositioning if no change in 4 weeks Monitor pulp and begin RCT immediately if indicated If complete root formation 7mm intrusion = Surgical repositioning If pulp necrotic, begin RCT at 2 weeks Follow up: Intrusive 2 weeks (clinical + radiographic) luxation 4 weeks (splint removal) 8 weeks (clinical + radiographic) 12 weeks (clinical + radiographic) 6 months (clinical + radiographic) 1 year (clinical + radiographic) 1/year for 5 yrs  Prognosis Splinting Endodontics Systemic Check Follow-up (Clinical + antibiotics tetanus Radiographic) Closed apex - Good 2 weeks RCT at 2 weeks Amoxicillin Yes 2 weeks, 4 weeks, 12 immediate weeks, 6 months, 1 year, replantation 1/year for 5 yrs Closed apex - extra- Average 2 weeks RCT at 2 weeks Amoxicillin Yes 2 weeks, 4 weeks, 12 oral 60 mins weeks, 6 months, 1 year, 1/year for 5 yrs N Open apex - Very good 2 weeks RCT if Amoxicillin Yes 2 weeks, 4 weeks, 12 immediate necrosis/infection weeks, 6 months, 1 year, replantation 1/year for 5 yrs Open apex - extra- Good 2 weeks RCT if Amoxicillin Yes 2 weeks, 4 weeks, 12 oral 60 mins necrosis/infection weeks, 6 months, 1 year, 1/year for 5 yrs  T R A U M A C O M P L I C A T I O N S  Trauma cause: Luxation with displacement Pulp canal (typically) obliterations Management: May be identified through yellow discolouration Monitor radiographically RCT if required  Trauma cause: Luxation injuries Pulp necrosis disrupting blood supply, more common in closed apex Management: Closed apex = RCT Open apex = MTA plug + RCT  Features: PDL damage from trauma propagated by necrotic External pulp Causes lateral root resorption inflammatory Radiographic findings: resorption Chance finding Radiolucency on lateral surface of root Treatment: Mechanical/chemical irrigation root canal and dress with non-setting Ca(OH)2 Monitor radiographically Obturate if stabilised  Diagnosis: Pink discolouration of tooth Internal Chance radiographic finding inflammatory Rounded symmetrical radiolucency centred resorption over the root canal Treatment: Mechanical and chemical irrigation of root canal Dress with non-setting Ca(OH)2 Monitor radiographically for stability Obturate if stable  Features: Typically caused by severe PDL damage Ankylosis Dentine fuses to bone and is resorbed in bony remodelling Diagnosis: Infra-occluded tooth Metallic tone on percussion PDL not present on radiograph Treatment: Composite buildups to reach occlusal plane Decoronation/extraction for implants Monitor R E L E VA N T HUMAN DISEASES KIDNEYS Control of the Acid-Base Endocrine Activity RBC Production BP Control (Renin-Angiotensin-Aldosterone Balance System Filter the blood – remove waste, control fluid Metabolism produces hydrogen ions that must be Kidneys are essential for bone maintenance Kidneys produce erythropoietin which acts When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert balance and regulate electrolytes buffered to maintain constant pH Synthesise calcitriol (active metabolite of Vit D) which on the bone marrow to maintain red cell production pro-renin already present in blood into renin and secrete it directly into circulation. Renin Bicarb buffer system (HCO3- acts on the gut to increase and thus haemoglobin converts angiotensinogen released by the Only urea and creatinine should be filtered; ) accepts hydrogen ions and forms CO2 and H2O calcium and phosphate uptake concentration liver into angiotensin I. Angiotensin I is converted into angiotensin II by angiotensin- blood and proteins are too large – their Bicarbonate is regenerated as well as resorbing filtered This suppresses parathyroid hormone release from the converting-enzyme in the lungs. Angiotensin II causes vasoconstriction (increasing blood presence indicates endothelial damage bicarb from the urine (via proximal tubule) parathyroid glands, reducing osteoclast activity pressure) and stimulates the secretion of aldosterone from the adrenal cortex, which causes an increase in the reabsorption of sodium and water into the blood and loss of potassium (electrochemical balance) and so increasing the volume of extracellular fluid in the body, increasing blood pressure.  Dental Relevance of Kidney Disease Normochromic normocytic anaemia due to a failure in production of erythropoietin Impaired haemostasis (increased urea in the blood due to decreased GFR causes acidosis which results in poor platelet aggregation, decreased excretion of salt and water can lead to an increase in blood pressure which can lead to poor haemostasis, decreased vWF, decreased thromboxane and increased prostacyclin) Decreased calcitrol production can lead to hyperparathyroidism, resulting in increased osteoclast activity which can affect XLAs and periodontal disease Excretion of drugs can be prohibited and doses may need to be modified (consult the BNF) If a patient has had a renal transplant they will likely be taking an immunosuppressant to prevent rejection, which predisposes to oral infections (e.g. pseudomembranous candidiasis) Liver Disease What is raised in Gilbert’s syndrome? Unconjugated hyperbilirubinaema Implications for drug metabolism and bleeding What is haemachromatosis? Liver produces vitamin K dependant clotting factors – II, VII, IX and X and prothrombin (helps stabilise clots) Increase absorption of iron leading to increased deposition on organs including Consider local measures – surgical or tranexamic acid to aid haemostasis the liver Causes of liver disease: 1. Infection – hepatitis Primary biliary cirrhosis A genetic disease that affects females 2. Excess alcohol (90% of patients) and the peak age 40-60 3. Drugs – paracetamol overdose years. It is characterised by damage to the 4. Vascular – Budd-Chiari syndrome – hepatic vein obstruction, portal hypertension, ascites and jaundice biliary ducts due to chronic granulomatous inflammatory process that 5. Alpha 1-antitrypsin deficiency – most common congenital liver disease in kids leads to cholestasis, cirrhosis and portal 6. Wilson’s disease – accumulation of copper in liver and brain hypertension. 7. Malignancy Clinical features of Liver Disease Jaundice – yellow pigmentation of Foetor hepaticus – distinctive Dupuytren’s contracture – knots Liver flap – tremor of the hand skin, sclera and mucosa caused by smell of breath; late sign of of tissue form under the skin, when the wrist is extended raised plasma bilirubin levels disease pulling fingers into bent position Leukonychia – white lines or dots Palmar erythema Finger clubbing Spider naevi on finger nails/toenails Bruising – due to vitamin K Parotid enlargement Ascites/ankle oedema clotting factors  Jaundice Pre-hepatic Hepatocellular Obstructive Caused by Caused by viral Caused by haemolysis infection (Hep gallstones, Resulting in A, B, C), EBV, pancreatic reduced uptake cirrhosis, Budd- cancer and PBC of bilirubin, and Chiari Resulting in reduced syndrome, increased conjugation Wilson’s disease conjugated and alpha-1- bilirubin – dark antitrypsin urine and pale deficiency stools E N D O C R I N E D I S O R D E R S Cushing’s Disease Excess glucocorticoid production Most common cause – pituitary adenoma secreting ACTH Cushingoid features may follow long term steroid use Clinical features: Moon face Buffalo hump – deposition of fat at top of back Abdominal obesity Wasting of proximal limbs Hirsutism – male type hair growth due to excess androgen  Thyroid gland secretes two iodine-containing hormones – thyroxine (T4) and tri-iodothyronine (T3) Graves disease is a form of this – antibody binds to thyroid Hyper- stimulating hormone receptor on thyroid cells and stimulates it thyroidism Clinical features (related to increase in metabolic rate and stimulation of sympathetic nerve system): Weight loss Increased appetite Feeling hot – even in cold weather Increased bowel activity – with loose motions Goitre Exophthalmos (in Graves) Treatment – surgical removal of abnormal tissue  Caused by autoimmune destruction of the thyroid or removal of thyroid Hypo- Clinical features: thyroidism Weight gain – despite modest diet Feeling cold – even in warm weather Lethargic – mentally and physically Constipated Bradycardia Myxoedema – deposition of mucinous material in subcutaneous tissues Treatment – thyroxine replacement by single, daily tablet  May occur due to autoimmune destruction of the glands but more commonly surgical removal – total thyroidectomy for thyroid cancer Hypopara- Symptoms resemble hypocalcaemia: thyroidism Paraesthesia Numbness and tingling – in extremities Muscle cramps Trousseau’s sign Chvostek’s sign Diagnosis – hypocalcaemia with low PTH levels Treatment – active metabolites of vitamin D; calcitriol Bisphosphonates Alendronate and risedronate Taken in osteoporosis, Paget’s or multiple myeloma (to prevent progression of cancer into bone) When ingested by osteoclasts they cause apoptosis inhibiting Pts taking bisphosphonates need special care when undergoing dental bone resorption XTN. The altered bone metabolism can lead to osteonecrosis. XTN should be avoided where possible and ideally carried out before Poor GI bioavailability bisphosphonate therapy is started. Absorption impaired b presence of calcium in intestine – take on empty stomach Established osteonecrosis is rarely treated surgically as trimming/removal of bone usually induces necrosis further. Use of a Side effects – oesophagitis caused by direct mucosal contact topical chlorhexidine gel to keep the necrotic bone clean has been reported with tablet  Haemostasis is the natural arrest of haemorrhage Factors brought about in 3 ways; affecting Contraction of the blood vessels blood Platelet aggregation Formation of the platelet plug to plug small deficiencies clotting and the clotting cascade (the extrinsic pathway is activated by damaged tissue whilst the intrinsic pathway is activated by blood contacting a surface other than endothelium) Thrombin, produced by the clotting cascade, converts fibrinogen to fibrin, which forms a fibrous meshwork enabling a clot to form  Haemophilia A If severe, give IV factor VIIII injection, if mild give DDAVP – stimulates release of factor VIII and vWF from endothelial cells Anticoagulants – warfarin inhibits vitamin K clotting factors – II, VII, Haemophilia B – IX, X, heparin activates anti- thrombin III which inactivates Give IV Factor thrombin and factor Xa, NOACs inhibit factor Xa IX injection Blood clotting Antiplatelet Von Willebrand’s Disease – vWF prolongs the life of drugs – aspirin factor VIII and helps stabilise the platelet plug, give IV and clopidogrel Factor VIII or DDAVP Thrombocytopaenia – average platelet count is 150-400 x10 9/l – it’s significant if falls below 100x10 9/l  Warfarin Omeprazole Inhibits the production of vitamin K clotting factors (II, VII, IX and X) Indications – atrial fibrillation, prophylaxis after inserting prosthetic Alcohol Miconazole heart valve and prophylaxis of embolism in RHD Drugs that increase INR should be checked 72 hours before surgery – preferably day of the anticoagulant Must be between 1.9-4.0 effect of warfarin Teeth can be safely extracted using haemostatic agents – sutures, Ibuprofen Metronidazole surgical, tranexamic acid INR does not need to be check in non-invasive surgery – pros, Erythromycin scaling, fillings, crown Check the BNF before completing prescription New Oral Anticoagulants (NOACs) Rivaroxaban Dabigatran Apixaban Thrombin inhibitor Factor Xa inhibitor 12 hour half-life, taken 12-14 hour half-life, taken 2X daily once daily in the evening 5-9 hour half-life, taken Skip morning dose once in mornings Only NOAC to have an antagonist - No change to routine daclizumab necessary Delay morning dose until after Tx Factor Xa inhibitors Indicators- atrial fibrillation and stroke prevention Short half-life and less interactions with drugs than warfarin – however more expensive  Sutures DDAVP (desmopressin) – stimulates the release of factor VIII and vWF from endothelial cells, vWF prolongs the life of factor VIII and stabilises the platelet plug Controlling Tranexamic acid – anti-fibrinolytic Post-op Haemorrhage Surgicel – oxidised cellulose; serves as a scaffold for platelet adhesion and aggregation leading to faster clot formation Local anaesthesia – if containing vasoconstrictor it can help haemostasis Silver nitrate – chemical cauteriser; nitric acid synthesis  A pharmacokinetic reaction occurs when the presence of one drug affects the concentration of another drug at its site of action (e.g. aspirin displaces warfarin from protein-binding sites and therefore increases the effective warfarin concentration) A pharmacodynamic reaction is one where the drug effect is modified due to the presence of another drug. When interacting in this way, the Drug drugs may act as agonists or antagonists and the effects may be beneficial or adverse. For example, flumazenil antagonises the effects of midazolam (beneficial antagonist) whilst β-blockers antagonise the effect of interactions salbutamol (adverse antagonist). The clinical relevance of drug interactions can be classified using the “ACT” system: A = Avoid (this combination should be avoided as the adverse interaction is clinically important) C = Caution (be cautious as an adverse interaction may occur) T = Theoretical (an interaction is theoretically possible but unlikely to occur at the doses used in clinical dentistry)  Important interactions Entacapone, Amphetamin used to treat Parkinson’s es, cannabis Sedation of β-blockers disease, is a and cocaine patients The can interact catechol-O- can increase Aspirin taking other Anti- The use of anticoagulant with methyltransfera adrenaline displaces CNS muscarinic aspirin with effects of NSAIDs can β-blockers adrenaline, se (COMT) toxicity (limit warfarin The depressants drugs inhibitor (the Omeprazole Aspirin other NSAIDs warfarin are reduce the increase L.A. causing an the amount from protein prolonged (including (decrease initial enzyme increases the increases the or increased by excretion of toxicity due increase in of adrenaline binding sites, use of alcohol) acetylcholine involved in the sedative sedative corticosteroid omeprazole, methotrexate, to reduction systolic blood metabolism of containing therefore paracetamol should be levels and effects of effects of s increases midazolam, increasing in hepatic pressure and adrenaline) and L.A. in increasing can cause avoided as used to treat midazolam midazolam the risk of miconazole, the risk of blood flow increasing so it may be patients who the effective liver damage over- Parkinson’s) gastric erythromycin toxicity the risk of a wise to limit have abused warfarin sedation can cause dry the amount of irritation , ibuprofen cerebrovascul such drugs concentration lead to mouth adrenaline and alcohol ar accident administered to within the respiratory patients taking previous 24 depression entacapone hours) Leukaemia Lethargy Malignant progressive disease Thrombocytopaenia Recurrent infections leads to petechiae Increased numbers of immature or abnormal leucocytes are produced Suppress production of normal blood cells Leading to anaemia and other symptoms Gingival hypertrophy Presentation Mouth ulcers (due to neutropenia) All forms of leukaemia are C/I in any form of surgery without consulting haematologist Mucosal Bruising Two types of acute leukaemias: Haemorrhage Gingival bleeding 1. Acute myeloid leukaemia 2. Acute lymphoblastic leukaemia  Reduction in haemoglobin concentration in blood 10 days: signs of more serious Facial pain localised over the affected sinus that can Symptoms 25 breaths/min) - IV Antibiotics - Decreased O2 sats - Supplemental O2 (maintain 94-98%) - Increased heart rate (130 bpm) - Increased lactate (>2) 3 out - Systolic BP 1 year ago c. There is deviation from normal sequelae of eruption – options later incisors erupting prior to centrals Maxillary centrals require 9mm of space to erupt into If the maxillary Exposure and closed eruption technique – flap raised, bracket Maxillary laterals require 7mm of space to erupt into incisor is missing attached to a gold chain consider auto- bonded to the palatal aspect of Requests DPT and anterior occlusal to assess developing transplantation – tooth to avoid unfavourable gingival contour – ortho dentition – horizontal parallax can be used to assess usually lower 5s traction applied 2 weeks later position CARIES  Tooth Structure Dentine Pulp Enamel 70% mineral, 20% organic material and Becomes smaller with age due to continuous 96% is composed of mineral; 10% water deposition of dentine hydroxyapatite Softer than enamel – decays more rapidly Radicular pulp is continuous with periapical tissues through the apical foramen Ca10(PO4)6OH2 - critical pH = Elastic – prevents brittle enamel from # Derived from dental papilla of the tooth germ 5.5 Dentinal tubules give degree of Function – form dentine, supply tooth with permeability which can lead to sensitivity moisture and nutrients and sensory function Thickest over the cusps (2.5mm) 3 forms – primary, secondary, tertiary Plexus of Raschkow contains Aδ-fibres and C and thinnest over CEJ fibres Secondary – forms once root formation is complete and tertiary - forms in Ameloblasts initiate formation response to a stimuli – reactionary dentine forms from pre-existing Nerve supply is from trigeminal nerve (V2 upper teeth and V3 for lower teeth) of enamel