Clinical Dentistry PDF

Clinical  Week 2 - Principles of Periodontal Instrumentation Instrument Classification Instrument identification Diagnostic instruments - periodontal probe; Naber’s - are used to locate, measure,...

Clinical  Week 2 - Principles of Periodontal Instrumentation Instrument Classification Instrument identification Diagnostic instruments - periodontal probe; Naber’s - are used to locate, measure, and mark pockets, gingival recession, and keratinized mucosa Explorers - used to locate calculus deposits and caries Scaling, root planing, and curettage instruments - used for removal of plaque and calculus deposits Polishing instruments - rubber cups, brushes, and tapes are used to clean and polish tooth surfaces —> air abrasive systems for tooth polishing are also available Schwartz periotrievers - set of two double ended instruments that are highly magnetised —> used to retrieve broken instrument tips from the pocket or furcation areas Sickle scaler - has two cutting edges and is used for supragingival scaling Curettes - used for subgingival scaling, root planing, and removal of gingival wall pocket Universal curettes - can be used in all tooth surfaces of all teeth Area specific curettes - for use in specific area of dentition Ultrasonic and sonic instruments - powered instruments used for scaling and cleaning tooth surfaces and curetting the soft tissue wall of periodontal pocket Basic Design of Instrument  Gracey Curettes Principles of SRP Scaling - is the instrumentation of the crown and/or root surfaces to remove plaque, calculus, and stains Root planing - is the instrumentation of periodontally involved teeth to remove cementum that is rough or contaminated with harmful bacterial products Scaling and root planing is remarkably effective at reducing clinical inflammation and pocket probing depth Principles of SRP: Accessibility Visibility, illumination, and retraction Condition of the instruments Maintaining clean field Instrument stabilisation Instrument activation Operator Positioning Curette Insertion and Activation 1. Curette is inserted into the periodontal pocket 2. Bottom of the periodontal pocket is identified 3. Curettes is turned to a proper cutting position for scaling 4. Blade is moved along the root surface in a scaling stroke removing calculus a too obtuse or acute angulation will result in ineffective calculus removal Strokes:  Week 3 - Prenatal Growth and Development Orthodontics 6-8 Weeks Orthodontics is the branch of Dentistry concerned with facial growth, At 6 1/2 weeks (C), the eyes are nearer the front of the face; the nose is defined, and development of the dentition and occlusion, and the diagnosis, the developing ears appear at the corners of the mouth interception and treatment of occlusal anomalies At 8 weeks (D), the masses comprising the face have fused together to bound the oral cavity, and the forebrain has begun its forward growth, leaving the ears behind Normal Growth and Development Embryology of craniofacial structures Growth and development of the cranium, cranial base, maxilla, and mandible Stages of development of the teeth Ages of dental formation, eruption, and maturation Sequence of tooth eruption Transition from primary to permanent dentition Biology of bone turnover 4 Weeks Face is about as thick as a piece of paper Future face is indicated by the bulging forebrain First 3 branchial arches have formed In the 4th week after conception, 5 tubular swellings appear under the forebrain which are the branchial (pharyngeal) arches Pharyngeal - Brachial Arches  Facial Development The human face is formed between the 4th and 10th week of pregnancy Face is formed by the fusion of five facial swellings - an unpaired frontonasal process, a pair of maxillary swellings, and a pair of mandibular swellings Primary Palate: At around week 6 the medial nasal process and maxillary processes fuse forming lip and primary palate Secondary Palate: During the sixth week of embryogenesis, the secondary palate develops as bilateral outgrowths from the maxillary processes, which grow vertically down the side of the tongue Subsequently, the palatal shelves elevate to a horizontal position above the tongue, contact one another and commence fusion Fusion of the palatal shelves, ultimately divides the oronasal space into separate oral and nasal cavities Facial Clefts Clefts arise due to failure of the facial prominences/ processes to fuse together between weeks 4-10 Cleft Lip: Failure of fusion of the maxillary processes and includes primary palate Involves the lip and alveolus Can be unilateral or bilateral Cleft Palate: Failure of fusion of the secondary palate Aetiology of Clefts: Still a focus of research and precise aetiology unknown Genetic factor - approximately 30 associated genes have been identified but inheritance does not follow a Mendelian pattern (MSX-1) Environmental factors - retinoids (acne/ skin treatments); smoking; alcohol; illicit drugs; drugs (anticonvulsants such as phenytoin, sodium valproate; and antibiotics such as trimethoprim); lack of folic acid/ folate Incidence of Clefts: Normal risk - 1:700 live births 1.9 times higher for Indigenous population (40-50% smoking vs 14% non-indigenous) Differences between population groups American Indians - 1:300 Japanese - 1:400 Chinese - 1:500 Caucasians - 1:700 Afro-Caribbean - 1:2500 Cleft lip incidence - 20-25% Cleft lip and palate - 40-50% Cleft palate - 30-35% 6:3:1 - unilateral left: unilateral right: bilateral Cleft lip and palate (CLP) 2x more common in males Isolated cleft palate more common in females (3:2) Cleft Diagnosis: Ultrasound in week 20 2D detection rate poor (20%) Sensitivity is low and specificity is high 3D ultrasound has much higher success rates at diagnosing (90-100%) Colour Doppler Ultrasound can also visualise abnormal flow of amniotic fluid from mouth to nasal cavity Cleft Treatment: Requires large treatment team - oral and maxilla facial surgeons; plastic surgeons; ENT; orthodontists; restorative dentists; paediatric dentists; dietician; geneticist; paediatric anaesthetist; child health nurses; radiologists; paediatrician; occupational therapists; speech therapist; child psychologist; neurosurgery; craniofacial prosthetist; ophthalmologist 0-1 years - lip repair at 3-6mths and palate repair at 9-12mths —> speech and feeding vs scarring and growth 2-5 years - ENT/ speech therapists assess hearing and speech; paediatric dentistry assesses preventative care as deciduous teeth erupt, and provide fissure sealing in mixed dentition 7-10 years - alveolar bone grafting —> provide bone for canine to facilitate eruption (root is 1/2 - 2/.3 formed); provide bony support of teeth adjacent to cleft 11-15 years - conventional orthodontic records at age 15 18+ years - orthodontics +/- orthognathic surgery if necessary (restricted maxillary growth); restorative (50% missing lateral incisor); rhinoplasty; revision of cleft repair  Week 4 - Postnatal Growth and Development Ossification Intramembranous: Direct bone formation from osteoblasts Bone can grow from outside Mainly in flatbones Can also occur in long bones to make bones wider Endochondral: Cartilage template forms first; which then gets replaced by bone Bone can grow from within Occurs at epiphyseal plates, usually located just below joints in long bones Makes bones longer Ossification of Craniofacial Skeleton Growth of the Cranial Base Blue - indicates cartilage —> endochondral ossification Pink/ red - indicates osteoids —> intramembranous ossification Growth ceases at intersphenoid (mid-sphenoid) Synchondrosis at age 3 Growth ceases at spheno-ethmoid Synchondrosis at age 7 Growth ceases at spheno-occipital Synchondrosis in late teens Majority of cranial base ossification is endochondral Apposition and resorption occurs mainly to refine the shape of the bone Synchondrosis: Is filled with cartilage A band of proliferating cartilage cells is located in the centre of the Synchondrosis, and a band of maturing cartilage extends in both directions away from the centre Endochondral ossification occurs at both margins Growth at Spheno-occipital Synchondrosis: Temporal bone and glenoid fossa move backward and downward relative to cranial base — > influenced by growth at spheno-occipital synchondrosis Growth of the Cranial Vault 95% of cranial growth completed by age 10 Growth predominantly sutural until about age 4 After 4yrs, cranial growth is mainly by apposition and resorption Bone deposited on outside, whilst bone is resorbed on the inside —> makes cranium larger Brain grows rapidly in infancy thus sutural growth allows this rapid growth to occur —> the sutures and fontanels are spaces for rapid deposition of bone to increase cranium size There is no cartilage at sutures, it is merely a space to allow for rapid bone deposition Sphenoid fontanel - closes 3 months Mastoid fontanel - closes 1 year Frontal fontanel - closes 1-2 years  Synchondrosis Vs Sutures Growth of Maxilla The maxilla articulates with the cranial base so is influenced by the growth changes in this part of the cranial base The maxilla has a significant downwards and forwards movement with reference to cranial base Intramembranous ossification occurs at the sutures posterior and superior to maxilla and also remodelling of the surfaces (resorption anterior to maxilla; apposition at the palate, alveolar ridges, and tuberosity) As the maxilla grows downward and forward, its front surfaces are remodelled, and bone is removed from most of the anterior surface (resorption) —> allows for correct maxilla shape to be created (not too prorated in nasal region) Growth of Mandible Intramembranous ossification occurs lateral to Meckel’s cartilage Meckel’s cartilage is not being replaced, but it is used as a scaffold for the intramembranous ossification to occur in front of it Condylar cartilage develops independently and fuses with mandible at condyle at about 4 months IU Endochondral ossification at the condyle Intramembranous ossification is occurring in most of the mandible (body and ramus) Mandible grows upwards and backwards, and not forwards The effect of the growth is that the mandible comes downwards and forwards —> as Growth Patterns it grows upwards and backwards it pushes against the glenoid fossa which ‘pushes’ it Cephalocaudal direction off resulting in it coming downwards and forwards Structures closer to the cranium grow faster and earlier Body parts further away from the cranium grow later Growth Curves - Scammon: Maxilla follows neural trend Mandible follows general trend Cephalocaudal Maxilla is more influenced by the cranial base (which is more influenced by growth of neural structures) Maxilla matures earlier than mandible Growth Theories Suture Theory: Measuring Individual Growth New bone formed at the sutures, cartilage and synchondroses pushes bone apart and leads to growth Orthodontists need to understand when major growth periods are because All asides act as growth centres under genetic control some of the appliances influence growth and must be implemented during Largely disproven peak/ rapid periods of growth Cartilage Theory: Chronological age; dental age; skeletal age; biologic age Growth of cartilage determines growth of bones, even in areas distant from cartilage Can use hand x-rays to determine when someone is going though a rapid locations growth period —> not common anymore due to radiation protection Cartilage under genetic control and acts as a growth centre measurements Mainly disproven but possible at synchondroses Can also use spine in dental radiographs to determine rate of growth and Functional Matrix Theory - Moss: when individual will be going through a rapid growth period Neither cartilage or bone determines growth Growth is determined by soft tissues adjacent to skeletal units Growth is determined by the functional needs of the soft tissues Also explains why we get atrophy in bone which is not used (broken bone)  Cranial Synostosis Synostosis - early fusion of sutures —> resulting in deformation of cranium Very rare - 1:200,000 live births Can result in blindness —> as eyes continue to grow but there is not growth of the frontal bone and other surrounding bones due to the early suture fusion Sutures can be opened by surgery - devices cut along suture, and then devices are placed to slowly expand the artificially created sutures —> manipulates healing part of bone Crouzon’s syndrome Apert’s syndrome Treacher Collins Syndrome - 1:50,000 live births —> reduction in neural crest cells Hemifacial Microsomia - 1:5000 live births —> disturbance in the development of 1st and 2nd brachial arches  Week 4 - Antimicrobial Therapy in Dentistry Odontogenic Infections Abscesses Localised areas of inflammation with purulent exudate Most orofacial infections are odontogenic Progenitor bacteria e.g. streptococci Abscesses and cellulitis Resist phagocytosis —> capsule bacteria Leading cause is dental pulp infection —> anaerobic bacteria Fibroblasts ‘wall it off’ Periapical abscesses Untreated Abscesses: Can also be periodontal tissues and operculum (flap of gum tissue over a partially Macrophage enzymes breakdown hard and soft tissues erupted tooth) Treat surgically - drain pus by extraction or root canal; incision to drain soft tissues Relevance to Dentistry: Cellulitis - inflammation of connective tissue —> can develop if infection not resolved Significant portion of clinical work will involve dealing with impact of infection —> caries, periodontal disease, dental abscesses, maxillary sinusitis of endodontic origin, candidiasis Primary approach is surgical —> restorations, root scaling, root canal therapy, properly fitting dentures Antimicrobials are a useful adjunct therapy, but must be a clear need for them such as spreading infections, fever, risk group Maxillary Sinusitis Endodontic origin - spread from maxillary posterior teeth Can be atypical infections When to Use Antibiotics Often unilateral Antibiotics are appropriate when infection is spreading —> cellulitis; lymph node Apical periodontitis —> periapical mucositis involvement; signs of inflammation (LA ineffective); systemic involvement (fever, malaise) Oral Candidiasis - Thrush Periodontal Disease: Inflammation of gingiva and periodontal tissues from bacteria in plaque Endogenous infection Surgical approach is scaling and root planing (SRP) Overgrowth of the yeast Candida albicans (C. Glabrata; C. Tropicalis less Chlorhexidine mouthwash common) Moderate-to-severe periodontitis - SRP + amoxicillin/ metronidazole Opportunistic pathogen Prophylaxis: Risk factors - very old or very young; in poor health; overuse of antibiotics; HIV Used to be commonly used to reduce risk of infective endocarditis infection or AIDS; chemotherapy or immunosuppressive drugs; taking steroid Side effects and risk of resistance medication; diabetic with high blood sugar; poorly fitting dentures Prescribe for patients with cardiac conditions with high risk of adverse outcomes Artificial heart valves, history of infective endocarditis, congenital heart conditions, transplant with problem in valve Common Dental Prescriptions Around 1.17 million dental prescriptions in 2022 Top 15 drugs - 7 antibiotics and 1 antifungal Infective Endocarditis Repeated Group A Strep infections Strep throat, impetigo, scabies Acute rheumatic fever —> autoimmune response damages heart valves Leads to rheumatic heard disease Bacteraemia following dental procedure Prophylactic Therapy Recommended dose is 2g amoxicillin orally 1 hour before procedure —> clindamycin for patients with immediate hypersensitivity to penicillin or cephalexin for non- immediate hypersensitivities Not required for all procedures Ones with high incidence of bacteraemia —> extraction, scaling and root planing Oral health of patient —> full mouth probing on patient with periodontitis Not restoration, LA administration, or probing healthy teeth Prescribe for patients with cardiac conditions with high risk of adverse outcomes Artificial heart valves, history of infective endocarditis, congenital heart conditions, transplant with problem in valve  Choice of Antibiotics Adverse Reactions Narrow spectrum - Penicillin V, amoxicillin Broad spectrum - Co-amoxyclav (Augmentin); azithromycin, metronidazole, clindamycin Unexpected or unintended effect - range from headaches, Bactericidal - Metronidazole, penicillin vomiting, liver or kidney injury Bacteriostatic - Trimethaprim, sulfonamides, tetracycline, azithromycin Dose-related - extension effects or side effects Antibiotics for Odontogenic Infections: Allergic reaction - requires sensitisation —> e.g. penicillin First line antibiotics - amoxicillin or penicillin —> active against gram-positive and gram-negative Idiosyncratic - not really understood, may have genetic (amoxicillin is better absorbed) causes If penicillin allergy - clindamycin can be used —> active against gram-positive bacteria Risks and Side Effects: Second line only if necessary - e.g. patient allergic to penicillin (needs clindamycin); unresponsive Gastrointestinal upsets are common - nausea, vomiting, infection; or cellulitis diarrhoea —> colitis Routine use contributes to resistance —> broad spectrum antibiotics increase risk of resistance Clostridium difficult infections - broad spectrum antibiotic use For unresponsive infection - metronidazole plus amoxicillin or penicillin V; Co-AmoxyClav (clindamycin, co-amoxyclav) —> health care associated (Augmentin) infection; vulnerable people (elderly, history of GI disease Other Situations: Other infections - fungal infections —> on the increase Maxillary sinusitis - Co-amoxiclav Hypersensitivity reactions Pericoronitits - partially erupted wisdom teeth —> metronidazole, amoxicillin or erythromycin Known issue with beta lactams and sulphonamides - penicillin (allergies) (1:50,000 patients have drug-induced anaphylaxis) —> Candidiasis - amphotericin B, miconazole (Daktarin) medical history important Patients on bicillin - long term use (repeated strep throat) —> amoxicillin Immediate - anaphylaxis (trouble breathing, low blood pressure, swelling of tongue, throat) —> adrenaline needed Delayed - rashes —> antihistamines Interactions with other medications - warfarin, clotting factors; oral contraceptives, enterohepatic cycling Tetracyclines - dental staining, enamel hypoplasia, bone deformation —> not for under 12yrs old or pregnant women Metronidazole - causes DNA strand damage to anaerobic bacteria —> “disulifrium-like” reactions (nausea, vomiting, flushing of the skin, tachycardia, shortness of breath) —> avoid alcohol Selective Toxicity Drugs work by disrupting metabolic processes Need drugs that kill or inhibit the microorganism without damaging the host cells —> side effects are from the drug damaging host cells Exploit the differences between microorganisms and host cells - bacteria being prokaryotes; fungi, Protozoa, and helminths being eukaryotic; and viruses being obligate intracellular  Antimicrobial Resistance Mode of Action of Antimicrobials Defined as strain of microorganism is not inhibited or killed by that antimicrobial —> failure of a treatment to manage a patient’s infection Antibacterials derived from fungi and can be semi-synthetic Important multi-drug resistant strains (MDR) - pseudomonas aeruginosa, erythromycin- Antibacterials target sites - cell wall synthesis, protein synthesis, resistant Group A strep. (S. Pyogenes), clindamycin-resistant Group B strep. (Bone nucleic acid synthesis, and cell membrane function infections) Drugs that Affect Cell Wall Synthesis: Dentistry - Prevotella resistant to penicillin (Russia, Romania, Europe) Beta lactams and cephalosporins - penicillin and flucoxacillin Dentists second largest prescriber of antibiotics Glycopeptides - vancomycin (only works on gram+) Increase in use and misuse of antibiotics —> antibiotics used as feed additive in agriculture; Target peptidoglycan antibiotic-resistant genes as markers in GMO crops Allergies WHO have declared it one of the top 10 global public health threats to humanity —> 70% of Drugs that Affect Protein Synthesis: HCAI are resistant to one common antibiotic; increase in resistance in community-acquired Prokaryote ribosomes are different to humans and thus interfere with infections; contributes to 700,000 deaths per year binding of mRNA to ribosome for translation Innate Resistance: E.g. aminoglycosides, tetracyclines, macrolides, chloramphenicol, No mechanism to transport drug into cell clindamycin Do not contain or rely on the antibiotic’s target process or protein Drugs that Affect Nucleic Acid Synthesis: E.g. gram- bacteria are naturally resistant to beta-lactams Structure of DNA is same in prokaryotes an eukaryotes Acquired Resistance: Targets enzymes that aren’t present in eukaryotes Microorganisms develop genetic mutations that allow them to resist antibiotics E.g. sulfonamides, trimethoprim (bacteriostatic) Develops with repeated exposure Drugs that Affect Cell Membrane Function: Can arise by spontaneous chromosomal mutation providing selective advantage (altered Bind to lipopolysaccharides and interact with phospholipids in the protein) or via horizontal gene transfer from another immune bacteria cell (acquiring pieces of outer and inner membranes (cationic detergents) DNA) Effective against MDR gram- (Pseudomonas aeruginosa, Immunity cause - altered target; inhibition of uptake (decreased permeability of drug), Acinetobacter baumanii, Klebsiella) modifying pathway; or acquisition of plasmids (degradative enzymes e.g. Beta-lactamases; or E.g. polymixins (colistin) effluent pumps) Resistant strains can become dominant Altered target - target enzyme may change sufficiently e.g. by mutation to cause a lowered affinity for the antimicrobial drug e.g. mutations in DNA gyrase and quinilones Alteration in access to the target site (altered uptake) - decreased permeability (Vancomycin and gram- bacteria); active transport (E.coli and tetracycline; P.falciparum and chloroquine; C.albicans and azoles) Drug inactivation - production of enzymes that inactivate the antibacterial agent e.g. beta- lactamases inactivate beta-lactams Horizontal gene transfer - plasmids containing resistant genes are passed on from immune Metronidazole: bacteria to new bacteria which now inherits the immunity Nitroimidazole Used for anaerobic bacteria (e.g. fusobacterium), and protozoan infections (Trichomonas) Appears to cause microbe DNA strand damage Side effects Anti-fungal Drugs: Only small number availed Target - cell membrane; and beta-glucan synthesis Anti-fungal Resistance: Emerging as a threat WHO - fungal priority pathogens list Eukaryotes - 4 classes Mechanisms similar to bacteria Immunity causes - efflux pumps; decreased permeability; altered drug targets; degradative enzymes; overproduction of target Solutions to Developing Resistance: Develop new drugs - $5 billion to develop new antibiotic; 80% of candidates fail; 2000-2018 there has been approval for 15 new drugs; 1980-2000 had 63 Better management - using appropriate drug for the infection (not taking antibacterial for vial infection); directed therapy if possible; combinations when necessary; alternative if first one is not effective  Week 4 - Pharmacology of Local Anaesthetic Local Anaesthetics Local anaesthetics consist of a lipophilic aromatic ring linked by an ester or amide to a basic side chain (or tertiary amine) Amide linkage give some longevity to the compound —> majority used have amide bonds rather than ester bonds (cocaine, procaine) Amides are more stable and have longer plasma half-lives thus LA’s used in dental (lignocaine and articaine) are amides Terminal amine can exist in tertiary form (non-ionised = lipid soluble) or quaternary (ionised = water soluble) Most LA’s are weak bases and are mostly ionised at physiological pH —> usually exist as salts The LA needs to be non-ionised in tertiary form to cross the membrane However, non-ionised (tertiary amine) has weak channel blocking activity; needs to switch to ionised (quaternary amine) form once inside the cell LA blocks voltage gated Na+ channels in post-synaptic nerve cells (excitable tissues) to prevent action potentials from being transmitted LA binds most strongly to the open and inactive states of the channel —> act on cytolytic side on S6 transmembrane domain Act on voltage gated NA+ channels Time of onset - dependent on solubility —> those that are high lipid soluble cross interstitial spaces slowly and may be sequestered in myelin and adipose tissue Mostly water soluble when injected —> switches to tertiary form to be able to cross the membrane, and once inside cell switches back to quaternary form which has stronger channel blocking activity Inflammation and infections in tissues leads to acidotic tissues which favours the water soluble (ionised, quaternary) configuration of the LA thus reducing the numbers of unionised molecules that can penetrate the axolemma (cross the membrane) and elicit an action. Addition of adrenaline to a local anaesthetic solution reduces the plasma concentration of the drug and thus decreases its potential toxicity —> Also creates a slower rate of absorption allows a greater uptake of local anaesthetic drug by nerves, enhancing the degree of block and prolonging effect Afferent Fibre Modalities  Week 6 - Special Needs Dentistry Special Needs Dentistry Disability Almost 18% of Australians have a disability (4.4 million people) “The branch of dentistry that is concerned with the oral health care of people with an intellectual 1.4 million people have a profound disability (1 SND : 78,000) disability, medical, physical, or psychiatric conditions that require special methods or techniques to 8.2% of Aboriginal and Torres Strait Islander people identified prevent or treat oral health” - AHPRA requiring assistance with core activities “That part of dentistry concerned with the oral health of people adversely affected by intellectual 76.6% of people identifying as requiring assistance live with family disability, medical, physical, or psychiatric issues” - RACDS and 19.4% live alone Specialty since 2003 20 practicing Specialists in Australia (major cities) Principles Professional Organisations: ANZASND - The Australia and New Zealand Academy of Special Needs Dentistry —> is the All individuals have a right to equal standards of health and care peak body representing registered specialists All individuals have a right to autonomy, as far as possible, in relation ASSCID - Australian Society of Special Care in Dentistry —> for anyone who has an interest to decisions made about them IADH - International Association for Disability and Oral Health Good oral health has positive benefits for health, dignity and self- esteem, social integration, and general nutrition —> the impact of Barriers poor oral health can be profound Categories of Special The majority of people with a disability have disabilities that are mild Needs Affordability - high cost of dental treatment or moderate and do not require specialist dental care Acceptability - dentists refuse to accept Most people with mild or moderate disability could, and should receive Physical disability patients dental care in mainstream primary dental services Cognitive impairment Availability - lack of trained dentists Sensory impairment Accomodation - the need for haematological Infectious diseases cover Access Audit Endocrine diseases Accessibility - difficulty in finding a suitable Parking, kerbs, lighting Hepatorenal diseases dental clinic Entrance - ramp, proximity, ground floor Bone diseases Patient: Reception and waiting room - clear signage, non-slip flooring, Cardiovascular diseases Lack of perceived need communication aids Respiratory disease Anxiety or fear Appropriate seating, space for wheelchairs Bleeding disorders Financial constraints Corridors - width and space to manoeuvre, no obstructions Blood dyscrasias Access difficulties/ mobility Surgery - design, and space to manoeuvre Immunosuppression Dental Profession: Toilet facilities - space, transfer bars, raised seat, alarm in place Head and neck cancer Inappropriate manpower resources Means of escape - visual alarm, exits accessible by all, signage, Neurological disorders Uneven geographical distribution Disability awareness training for staff Psychiatric disorders Training and experience Other special considerations Insufficient sensitivity to patient needs and communication skills Referrals Society: When to Refer: Implications for Dentists Insufficient public support Significant communication difficulties - not simply non-verbal Inadequate facilities Uncooperative Access Inadequate manpower planning Medical status - may require multidisciplinary team Don’t assume Insufficient support for research Physical access - can’t transfer and weight bearing Care with language Government: What to Include: Consider what the patient can maintain Lack of political will Reason for referral Acknowledge carers Inadequate resources Information gathering - from GP; current medications; past Consent/ capacity Low priority medications; specialist reports and results of investigations Restraint Waiting lists Pain; swelling; or trauma Who treats? Capacity When Meeting a Person with a Disability: Care Environments Radiography - especially OPG Don’t make assumptions - always ask Care environments can increase Inappropriate Referrals: Be patient - allow time for questions to be behavioural challenges including those with: Mild communication difficulties - e.g. ASD, mild dementia, answered limited social interaction; excessive noise; augmented communication aids Listen - use an active non-judgemental crowded accomodation; neglect and Mild cooperation challenges technique abuse; physical health needs not Mild medical complications - e.g. diabetes, blood thinners, bone- Believe what you tell them recognised; pain not recognised or sparing medications —> may need investigations first e.g. INR, Respect the person for who they are managed FBC Gather additional information if required Can ask advice from SND specialist When talking to a carer, include the person These patients may take extra time but we don’t have to make a with disability in the conversation profit on every patient  Capacity Neurological Conditions Principle of autonomy Presume capacity Cerebral palsy and other acquired disorders Need the correct environment for consent e.g. sensory issues in ASD Down syndrome Capacity - decision specific; temporal (e.g. may fluctuate in psychiatric conditions); the right Multiple sclerosis to make ‘bad decisions’; substitute decision maker is a last resort Parkinson’s disease Motor neurone disease Huntington’s disease Consent Epilepsy Must be Valid: Dementia and other cognitive impairments Voluntary and unconditional Cerebral Palsy: Patient informed of all pertinent information Intellectual disability - 30-50% Patient understands the information and the consequences of treatment and NO treatment Epilepsy - 40% Two Aspects: Speech difficulties Patient consent Vision Clinician consent Hearing Discussion must be documented: Severe disability in 20% The ‘consent form’ is not the consent Down Syndrome: Commonest cause of intellectual disability Trisomy 21 (over 90%) Pain Assessment in SND Epilepsy (up to 13%) Challenging if communication is limited e.g. cognitive impairment Sleep apnoea Pain may become chronic before it is recognised Bradycephalic Treatment is ineffective unless the aetiology is understood Cardiac problems (ToF, PDA, valvular disease) The usual assessment tools may not be applicable Delayed speech Changed behaviour may be the only clue - aggression, refusal to cooperate, excessive drooling, Ophthalmic disturbed sleep, pulling at face, altered eating habits, changed communication Hearing Rely on carers to interpret Dementia Atlanto-axial instability Patients With Challenging Behaviours Behavioural techniques Multiple Sclerosis Oral sedatives - Temazepam or Oxazepam (short half-life) —> ask GP to prescribe and take supervised Autoimmune disease affecting the CNS Nitrous oxide sedation Chronic inflammatory neurodegenerative disease IV sedation Demyelination of the nerves of the CNS GA - morbidity e.g. post anaesthetic delirium Progressive but may relapse and remit Peak age of onset is 30yrs Cause unknown —> maybe genetic predisposition Toothbrush Adaptations Risk factors - EBV, smoking, vitamin D deficiency, reduced sunlight, geographical latitude Dental Management of MS Patients: Office accessibility Mobility impairment - getting to appointments; transfers Fatigue - self-care; getting to appointments Weakness/ incoordination - self-care Possible cognitive impairment - self-care; remembering appointments; remembering instructions Possible mood changes - self-care Possible facial pain Autism Spectrum Disorder Medication side effects - xerostomia Orofacial Manifestations: Developmental - multiple genes + environmental implicated —> early signs usually apparent Intermittent facial numbness around 2yrs Facial palsy or spasm Highly heritable Paroxysmal pain syndromes (neuropathic) - high frequency Spectrum disorder episodes of shock-like or lancinating pain; trigeminal neuralgia Sensory problems (1-5% of patients) Epilepsy in 30% Mild dysarthria Intellectual disability (32%) Lhermitte sign 40% are non-verbal Monocular visual disturbances Triad - decreased social interaction; poor communication skills; specific behaviours (rituals, routine)  Drugs Osteonecrosis of the Jaw Blood thinners Prevention: Antimicrobials If patient on Denosumab, consider timing of treatment (close to next injection) Analgesics Minimise surgical trauma Gastrointestinal Ensure good haemostasis - sutures, haemostatic agents Hormonal Avoidance of smoking Respiratory Appropriate post op review Bone sparing medications - oral or injected Risk Factors: Psychotropic Treatment from malignancy is a greater risk than osteoporosis Recreational/ social drugs Recent dental surgery, mainly tooth extraction (~65% of patients) OTC/ complementary medicines Risk seems to be higher for cancer than osteoporosis patients Tropical medicines If a patient is to be started on high-dose/ IV bisphosphonate treatment, then ideally any Antiresorptives: planned dental work should be done prior to this to minimise risk Alendronate (Fosamax) IV bisphosphonate use Risedronate (Actonel) Dual pharmacy - risk higher if on a bisphosphonate and antiangiogenic therapy Zoledronic acid (Reclast) simultaneously Denosumab (Prolia) Concurrent bone metastases or multiple myeloma Dental or periodontal disease Antithrombotics Injury from poorly fitting dentures Additional possible risk factors in those with cancer, HIV, anaemia, diabetes mellitus Medications: Anticoagulants - Warfarin (Coumadin); Heparin (injectable); Dabigitran (Pradaxa); Rivaroxiban (Xarelto) Management of Prolonged Bleeding Antiplatelet drugs - Aspirin; Clopidogrel (Plavix) Avoid other drugs causing bleeding - e.g. NSAIDs; Sit patient upright complementary medications Direct pressure with gauze for 15 minutes Reasons for Prescribing: If no improvement, irrigate to identify source of bleeding and apply further direct pressure Atrial fibrillation If still no resolution, infiltration of LA, absorbing dressing, Tranexamic acid DVT Transfer to hospital Pulmonary embolism Immobility Recent surgery  Week 8 - Dental Pain Intraoral Pain Craniofacial Pain Odontogenic pain - associated with the teeth and periodontium Mucogingival and tongue pain - may be localised or generalised Can include musculoskeletal disorders like whiplash, Salivary gland disease and dysfunction e.g. mumps temperomandibular disorders and masticatory muscle disorders Systemic disorders and treatments may also contribute to orofacial pain e.g. HIV infection, Other conditions that can give rise to orofacial pain include - chemotherapy, and radiation therapy primary headaches; neuropathies (e.g. trigeminal neuralgia); Odontogenic Pain: intracranial disorders (tumours, haemorrhage), sinusitis Tooth pain (odontalgia) includes pulpitis and pulpal necrosis - pain may be referred to other areas of the head, neck, and mandible Pain conditions associated with the supporting tissues includes acute apical periodontitis, acute apical abscesses etc. Mechanisms of Tooth Pain Odontogenic Pain Changes in Response to Pulpitis Teeth, particularly the dental pulp are richly innervated by myelinated and Axon sprouting in pulp, thus increasing innervation —> sensitisation unmyelinated afferents Altered ion channel expression These fibres may be activated by temperature, chemical, or mechanical stimulation Blood flow (vasodilation) and plasma extravasation increased in inflamed Pulp is innervated by a high proportion of large diameter, myelinated A-beta fibres pulp —> leading to increases in local delivery of protein bound drugs such In the tooth there is a very distinct distribution of the nociceptive afferents as NSAIDs Myelinated afferents typically innervate dentinal tubules - dentinal hypersensitivity Also central changes - central sensitisation due to exposed dentinal tubules results in the chief complaints of pain with sharp, bright, and stabbing sensations —> these relate to the characteristics of myelinated nociceptors Unmyelinated afferents terminal on the perivascular regions of the pulp - inflammation of the pulp (such as pulpitis) results in chief complaints of dull aching Dentinal Hypersensitivity and throbbing type pain —> these relate to the properties of unmyelinated Five mechanisms have been proposed nociceptors 1. Hydrodynamic theory - relies on the proximity of mechanosensitive neurons in close proximity to movement of fluid within dentinal tubules 2. Direct innervation - hydrodynamic theory doesn’t cover the full range of Pulp activation seen in odontogenic pain 3. Neuroplasticity - relies on peripheral sensitisation and plasma extravasation Pulpal inflammation is primarily localised infection by microorganisms, with the 4. Odontoblasts mechanoreceptors - odontoblasts acts as mechanoreceptors; potential for bacterial infection to indirectly activate nociceptors resulting in the odontoblasts express a range of TRP channels and also release signals like release of inflammatory mediators ATP Example - increased levels of prostaglandin E2 (PGE2) are associated with pain 5. Algoneurons - low threshold mechanoreceptors contribute to tactile allodynia reports in patients ATP released binds to ATP receptors which is expressed by unmyelinated In addition, steroids and NSAIDs have been shown to reduce PGE2 levels in the fibres —> receptors are activated and signals are sent to CNS tissues of patients with pulpitis Bacteria have also been shown to directly activate nociceptors —> lipopolysaccharide (LPS) can activate toll-like receptors (TLR4 shown to be on pulpal afferents)  Week 8 - Dental Pharmacology Refresh COX Inhibitors Allosteric Modulation Side effects = gastro-intestinal Allosteric modulators are a group of substances that bind to a receptor to Can be thought of as constitutive (COX-1) and inducible (COX-2) forms of the enzyme change that receptor's response to stimuli COX-1 appears to have “housekeeping” role and is expressed by many different cell Shifts curve types COX-2 is induced in inflammatory cells when activated by pro-inflammatory cytokines (for example). EP3 inhibit Gastric acid secretion, increase gastric mucus secretion —> COX inhibitors counter this. Some attempt at selective COX inhibitors, e.g. celecoxib shows some selectivity for COX-2 over COX-1 Other Unwanted Effects: Cardiovascular – hypertension (related to inhibition of COX-2 in kidney) Reversible renal insufficiency - in those with compromised renal activity —> Blocks the PGE2/I2 mediated vasodilation. Bronchospasm – seen in “aspirin-sensitive” asthmatics Prostanoids in Inflammation PGE2 and PGI2 are generated by local tissues and blood vessels during inflammation and PGD2 mainly released by mast cells These three are also powerful vasodilators, but also work in concert with other inflammatory vasodilators, thus contributing to redness and increase in blood flow to inflamed tissues Prostanoids don’t directly cause increase in permeability from capillaries, but potentiate the effects of bradykinins and histamine Prostanoids also contribute to peripheral sensitisation of nociceptors (sensitise terminals to effects of other stimuli like bradykinins). NSAIDs anti-inflammatory and analgesic effects are due to blocking these actions (above) Protaglandins (especially E- produced in the hypothalamus) induce fever and NSAIDs block this production Benzodiazepines NSAIDs Can be shorter (6hrs, naproxen, Benzodiazepines are allosteric modulators on GABA-A channels meloxicam, celecoxib) acting. Agonist of drug binds to protein Generally well absorbed from GIT and highly bound to plasma proteins (mainly Agonist GABA binds to protein where benzodiazepines alters opening of channels = albumin), thus have limited distribution to extracellular spaces altered function —> greater response to same amount of drug However, plasma extravasation may increase delivery to the inflamed tissues. Reduce muscle tone - central spinal cord action Since highly plasma bound, may compete for the same binding sites with other Reduce anxiety highly bound drugs, which may include warfarin, phenytoin, furosemide, Contribute to sedation propranalol, verapamil, diazepam Anterograde amnesia - e.g. flunitrazepam (Rohypnol) Longer term use can cause tolerance Sometimes used to treat insomnia Paracetamol If used recreationally it is a synergistic with alcohol Paracetamol is a COX inhibitor is an excellent antipyretic with weak anti- inflammatory action Paracetamol objectively reduced soft tissue swelling after 3rd molar surgery —> better result than with ibuprofen. Metabolised in the liver (with a half-life of 2-4hrs). Toxic doses cause nausea and vomiting and afer 24-48hrs potentially fatal liver damage TGA suggest less than 4g /24hrs, other jurisdictions (UK) 3g unless small ( diabetes and obesity 20-200x sweeter than sugar Sugar substitutes either non-nutritive - low or no calories; minimal Anti-cariogenic nutrition or nutritive - contain calories; minimal nutrition Sugar Alcohols: Examples - Sorbitol, Maltitol, Mannitol, Erythritol, Xylitol Obesity Classified as nutritive sweeteners with 1/3 to 2/3 the caloric content of sucrose Most are not well absorbed in the GIT Obesity in children has more than tripled since 1970 Occur naturally in certain fruits and vegetables 1 in 4 Australian children and adolescents are overweight Are poorly fermented by oral acidogenic bacteria 64% of Australian adults are overweight Are low or non-cariogenic Dietary sugars and carbohydrates contribute to the obesity No after-taste ‘epidemic’ Xylitol and erythritol protect against tooth decay by decreasing levels of Strep mutans in saliva Sucrose, fructose, maltose - ‘average’ consumption of 40-60kg and plaque per year per person Xylitol is well studied, but the latest research shoes that erythritol has the most anti-cariogenic Dentists need to actively counsel patient about the effect of sugar effect compared to xylitol and sorbitol consumption on their oral and systemic health (similar to smoking Sorbitol: intervention) Naturally occurring, mostly sourced from corn syrup Chewing gum, diabetic lollies, toothpaste, and mouthwash Oral Mutans Streptococci 1/2 as sweet as sugar Strep mutans and Strep sobrinus are implicated in dental caries Low/ non-cariogenic - ferments slowly formation Not easily digested or absorbed Thrive in an acid environment Diarrhea if consumed in large quantities Thrive on fermentable carbohydrates (sugar) Erythritol: Produce lactic acid as a metabolite creating an acidic environment Occurs naturally Produce extracellular polysaccharides that promote adhesion to 70% as sweet as sugar tooth structure Heat stable - used in baking The lactic acid production may tip the mineralisation- Lollies, soft drink, chewing gum demineralisation balance within the oral environment to promote Absorbed in GIT but excreted unmetabolised in urine with minimal effect on insulin levels cavitation of tooth structure Used as sugar substitute in ketogenic diets Lactic acid pH = 2.4 - compared to hydrochloric acid pH = 2.0 Reduces Strep mutans levels Xylitol: Artificial Non-Nutritive Sweeteners Occurs naturally in plants and animals Saccharin: Produced commercially from birch and corn 300x sweeter than sugar 60% of the calories and sweetness of sugar Bitter aftertaste First used as a sugar replacement for diabetics Increased risk of side effects including cancer formation (carcinogenic) Sugar shortage during WW2 —> mass production of xylitol Aspartame (Nutrasweet/ Equal): Anti-cariogenic effect 160-220x sweeter than sugar Fatal to dogs and cats Increased risk of multiple cancers in animals and brain tumours in Extensively studied humans Not fermentable by Strep mutans Sucralose (Splenda): Anti-cariogenic - Strep mutans will metabolise xylitol before sucrose —> bacteria expend energy 600x sweeter than sugar attempting to metabolise xylitol to no avail (futile cycle) —> decreases replication and adhesion to Acesulfame Potassium (ACE-K): teeth 200x sweeter than sugar Decreases pathogenic effect of P. Gingivalis Cyclamate: May aggravate GIT issues (approx. 50g/day) 30x sweeter than sugar Can assist remineralisation by interfering with acid production by bacteria —> if used in chewing Increased cancer risk gum saliva is stimulated, raising pH, buffering acids, and promoting remineralisation Neotame (Nutrasweet): Oral Hygiene Products - xylitol tooth wipes for babies, xylitol mouthwash, xylitol floss, xylitol gel 7000x sweeter than sugar —> most have not been tested for efficacy Safer than aspartame Xylitol toothpaste is a great alternative for individuals who are anti-fluoride Approved food additive - generally recognised as safe by US FDA  Week 9 - Prevention of Common Oral Diseases Plaque Induced Diseases Interproximal Cleaning For tight contacts use floss string or sticks Teeth with gingival inflammation have a 45x higher risk of extraction vs teeth with Only use interdental brushes if there is enough space healthy gingiva Xmas tree shape interdental brushed not recommended Dental plaque = biofilm Interdental brushes remove more plaque and reduce gingivitis more effectively Microbial exotoxins and endotoxins initiate inflammation of gingival tissue than floss —> they remove plaque 2-2.5mm below gingival margin Signs of plaque induced gingivitis - red, swollen, bleeding on brushing or probing, usually painless —> probing depths = repeat with each tooth, including the distal of the back teeth Oral Hygiene Instruction: If the floss becomes shredded or stuck between the teeth - find out why and Educate patient about the disease process (Simple words) fix it (sign of potential overhang, catch, calculus) Tooth brushing technique Interproximal cleaning Hygiene products (chemotherapeutics) Chlorhexidine Professional Cleaning Includes: Removal of calculus and plaque - supragingival and subgingival cleaning/ Anti-microbial scaling Reduces plaque Flossing and prophylaxis (polishing) Bacteriostatic at low concentration - 0.02-0.06% Ultrasonic —> hand-scaling instruments —> prophylaxis paste —> Bacteriocidal at high concentrations - 0.12-0.2% flossing (LA if needed) Stains teeth, but stains can be removed with ultrasonic scaler Alcohol and water versions available —> alcohol can dry mouth Savacol Basic Toothbrushing Curasept - non staining version of chlorhexidine (not as effective?) Soft bristles, correct size and shape to fit tight areas Bristles at 45 degree angle Ensure to brush gingival margins - where the tooth meets gums Essential Oils Anti-microbial Circular motions Ingredients - methyl salicylate, eucalyptol, thymol, menthol, ethanol Twice daily for 2 mins Good for reducing gingivitis Electric toothbrush is better —> rotational oscillation removes plaque more Chlorhexidine is better for plaque control effectively with less pressure No staining Effective toothbrushing is dependent on the motivation and skill of the brusher Reduces calculus amounts compared to chlorhexidine 1. Brush the outer tooth surface, then the inner tooth surface, then the chewing Disadvantages - non-alcohol versions do not work well surface 2. Inner areas - tip the brush long ways and use the tip up and down 3. Don’t forget the tongue (try not to get gag reflex) Water Flossers Alternative to flossing for those with limited manual dexterity or with oral appliances Toothpaste Unclear effectiveness at plaque control Fluoride Low abrasion Spit don’t rinse Difficulties in Maintaining Oral Hygiene Can treat sensitive teeth or bleach teeth Oral hygiene instruction may or may not be accepted Non-fluoride alternatives - tea tree, bicarbonate, xylitol Depends upon personal motivation Any behaviour changes are usually short term Tongue Cleaning Variation in attitude, ability, life situations, and priorities Patient history and examination will reveal information about oral hygiene skill, knowledge, manual dexterity, motivation, and self-esteem Reduces the number of organisms, tongue coating, and halitosis Tooth anatomical factors - crowding, tooth surface/ position in jaw (posterior teeth), proximity to frenum, recession, deep grooves, plaque retentive anatomy Crowding - misaligned teeth are more plaque retentive and more challenging to clean  Partial Dentures Periodontitis Prevention Removable partial dentures need thorough cleaning, especially abutment All periodontitis is preceded by gingivitis, but not all gingivitis teeth and clasps progresses to periodontitis If worn at night, can result in gingival inflammation In some more susceptible individuals, subgingival plaque stimulates a Refer to therapeutics guideline for denture hygiene advice destructive immune response Diabetes - both type 1 and 2 are major risk factors for the development of periodontal disease Smokers - the most important controllable environmental risk factor Iatrogenic Dental Disease in periodontitis —> the more a patient smokes, the greater degree of periodontal disease Open contacts Smoking cessation - patients who stop smoking eventually decrease Over or under contouring restorations their risk to levels of non-smokers Crowns and Bridges: Early Detection: Margins should be seamless with no gaps or overhangs to retain plaque Gingival bleeding during toothbrushing Subgingival margins are harder to clean Any change in gingival colour (redness) or shape (swelling) Restoration Overhangs: Persistant halitosis (bad breath) or bad taste Need to be removed or replaced Receding gums Plaque retentive Tooth mobility or movement Avoid overhangs with effective wedging Bleeding gums are usually the earliest sign and should not be ignored  Week 9 - Introduction to Endodontics Pulp Innervation Introduction to Endodontics Pulp cavity - pulp chamber and root canal Three types of trigeminal sensory nerve fibres - The dental pulp is classified as soft connective tissue - it is composed of A-beta, A-delta, and C fibres cells; odontoblasts, fibroblasts, and other cells A-beta (5%) and A-delta (15%) - are myelinated Vessels: with very fast conduction speed and a low The pulp is a richly vascularised organ excitability threshold —