Pickard's Manual of Operative Dentistry Professor HM Pickard Pickard's Manual of Operative Dentistry Ninth edition Avijit Banerjee Senior. OXFORD MEDICAL PUBLICATIONS Pickard's Manual of Operative Dentistry MOD8E-PRE(i-xiv) 11/11/03 AM Page ii. Professor HM Pickard – Save this Book to Read pickard manual of operative dentistry 9th edition pdf PDF eBook at our Online Library. Get pickard manual of operative.

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In this Eighth Edition we have retained the objectives and approaches for teach- ing materials science M Data and Computer Communications (Eighth Edition). Presentation describes about rotary instruments in conservative dentistry. Gillmore.4th ed. Pickards manual of operative dentistry lagemahgunste.ml8th ed. Download PDF Pickard's Manual of Operative Dentistry 9th ed. Free PDF Download of Dental Book. Best Dental Library for Dentist. Get all Dental Books.

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Upcoming SlideShare. Like this document? Why not share! An annual anal Embed Size px. Start on. Show related SlideShares at end. WordPress Shortcode. RhondaMcCaskill Follow. Published in: Full Name Comment goes here. The grey-shaded portion of the graph indicates plaque trap often inaccessible to a toothbrush or floss see Figure the min period in which the tooth surface is under threat of 1. In dentine, the critical pH of mineral is 6. These factors can be assessed during history taking and oral exami- nation Chapter 2 and help form the basis of determining the indi- vidual's own risk of developing caries - the caries risk assessment Chapter 3.

The carious process in the normal oral environment will take several weeks to become clinically detectable as lesions with signs and symp- toms. The presence of saliva, with its capacity to buffer acids at the tooth surface causing plaque pH to fall within one to plaque acids and remove food debris and lubricate tooth surfaces also three minutes and initiating demineralization if the pH drops to helps.

The pH can take up to 60 minutes to climb back to normal, aided by the buffering capacity of saliva pH 7. Radiation in the region of other indirect patient factors to ultimately affect the disease pattern the salivary glands, used in the treatment of an orofacial malignant experienced by each individual patient.

These determinants include growth, and Sjogren's syndrome, an autoimmune condition which may the patient's: While the lesion is still within enamel, it can be arrested and possibly reversed in its earliest stages. Once into dentine, the proc- ess can be arrested but if proteolytic destruction of the organic colla- Figure 1.

This section will take the reader through key features of the histological and Q1. What habit may have contributed to this pattern of clinical development of a lesion from its earliest enamel stages through disease? An understanding of the basic histological features of healthy enamel and dentine is a prerequisite to appreciating the changes that occur within the lesion and an outline of these is presented in Table 6.

Further information can be gathered from aids offered in the Appendix. The relationship between lesion his- 1 tology and clinical appearance has been used in a caries detection and assessment system outlined and discussed in Chapter 2 Table 2.

Within enamel Plaque-acid demineralization causes porosities to form within the prism structure, initially beneath the outer surface of enamel: The developing pore volumes through affecting sites not normally associated with caries due to their the depth of the enamel lesion, caused by a longer exposure to reduced accessibility for adequate oral hygiene. It is seen when the oral environment has changed from conditions predisposing to caries to conditions that tend to slow lesion progression.

These lesions often have a dark, hard, shiny exposed den- tine surface see Figure 1. Plaque is evident on a The enamel lesion is shaped as an inverted cone, widest at the portion of a similar lesion on the first premolar indicating that this tooth surface, narrowing towards the enamel-dentine junction, area is likely to be active black circle.

How may this area of the lesion arrested? What ions have contributed to the intact surface zone? The existence of the enamel lesion surface zone may be due to increased extrinsic fluoride ion deposition in this area or as a conse- quence of remineralization metabolism of the biofilm on the tooth sur- face. Histologically, smooth surface lesions have a cross-sectional shape of Figure 1. Fissure lesions take the form of two adjacent smooth surface lesions see Figure 1.

This more developed lesion has a rough surface, acting as a plaque trap. What features of this lesion will help the dentist conclude that it is active, how might these be detected, and how might the patient be managed? Porosities may also be filled with deposited mineral and dietary molecules causing staining e. How might this scenario be managed in a high caries risk may be trapped within the mineral lattice. This creates an arrested, patient?

As the lesion develops over time, Histologically, the carious process may reach dentine before clinical it becomes somewhat chalky, eventually becoming roughened or cavitation is detectable a closed lesion: Defence reactions in the dentine-pulp complex are stimulated at lesion surface.

This can encourage further plaque deposition see Fig- this stage with evidence of translucent dentine at the lesion boundary ure 1. There are no symptoms at this stage, but reactions in the and tertiary dentine deposition at the dentine-pulp interface beneath dentine-pulp complex may be mediated by cytokines and bacterial the advancing lesion see later.

Again, symptoms are unlikely at this breakdown products within the dentine matrix and tubules see later. This zone should be clinically removed when preparing a cavity as it is necrotic, cannot be repaired, and provides a poor quality bonding substrate for adhesive materials to achieve an adequate seal.

Caries-affected dentine zones 2, 3, 4 combined together; Figure 1. The red lines outline the this zone.

The white be described as hypermineralized translucent dentine due to its dotted lines show how the extent of the spread of the dentine glassy appearance in cross-section , one of several reparative reac- lesion subjacent to the EDJ is associated with the same lateral tions of the dentine-pulp complex to the carious process see later.

The aetiology of the colour changes is not clear but a biochem- ical reaction between proteins and carbohydrates in a moist, acidic Within dentine biological environment, the Maillard reaction, may play a part.

Not all Once the lesion has spread histologically approximately into the mid- lesions are uniformly dark brown; some rapidly advancing lesions dle third of dentine, it is often clinically cavitated open on bothocclu- may have a pale discoloration within the caries-infected zone and sal and smooth surfaces with plaque now able to accumulate on the there is no direct link between the colour of dentine and the bacteria exposed dentine surface.

The spread of the lesion will undermine the present within these zones. This may need to be removed during cavity preparation Chapter 7. The patient may experience initial symptoms of acute pulpitis - a 1. The components of carious dentine to in time with appropriate excavation and restoration within the dentine, be considered are the mineral, collagen, bacterial penetration and then the advancing front of the lesion approaches the dentine-pulp tubule structure.

The histological an acute inflammatory response.

Depending on the time scale over changes of the carious dentine biomass through its depth from EDJ to which this has happened, an initial acute pulpitic response poorly pulp are described below, but note that these descriptive zones are localized short, sharp pain on hot, cold or sweet stimuli will evolve into not separate biological entities, but blend into one another without a more chronic response, changing symptoms towards a dull, pro- clear boundaries see Figure 1.

The defence reactions include deposition of translucent dentine, tertiary dentine, and pulpal inflammation. Translucent dentine Sometimes referred to as 'sclerotic' dentine, this glassy zone of dentine zone 4, Figure 1. Its appear- ance is due to the parity of refractive indices of intertubular and intratubular mineral, so allowing light to pass through the sectioned boundaries.

The Whitlockite deposits originate from a combination of a physico- chemical re-precipitation of calcium and phosphate ions diffusing towards the increasing pH environment of the lesion's deepest advanc- ing front and also possibly a vital process of new and rapid mineral deposition from the pulp via the odontoblasts.

Even though hypermin- eralized, this zone of translucent dentine is softer than its deeper, sound counterpart due to the weaker crystalline orientation of Whit- 1 lockite than conventional hydroxyapatite crystals within the tubules Figure 1.

What causes the colour change in dentine caries? It may resemble secondary dentine non-specific in origin Chapter 3. The cavity will probably have histologically, but has an irregular tubular or atubular structure, enlarged due to the undermined enamel having been broken away depending on the speed of its creation.

Reactionary dentine is depos- including marginal ridges of proximal lesions and will be noticeable to ited as a result of a mild irritant where original odontoblasts survive the patient as 'a hole in the tooth'. Reparative dentine is deposited in If the pulp chamber is breached by the lesion, a carious exposure may response to a stronger irritant which compromises the vitality of the be created when excavating very deep caries, and the exposed pulpal original odontoblasts.

Progenitor cells from the subodontoblastic layer tissue will bleed uncontrollably for several minutes before cotton wool then differentiate and are upregulated to produce an atubular defence pledgets can achieve haemostasis. In most cases of a carious pulpal reaction. Inflammation of the pulp pulpitis may, as in any other tissue, the carious process within the depth of the lesion Chapter 5.

In rare be acute or chronic.

In a slowly progressing carious lesion, toxins cases, on late presentation, the pulpal soft tissues undergo a hyperplas- reaching the pulp may provoke chronic inflammation. However, once tic cellular reaction and appear to herniate through the exposure, into the organisms actually reach the pulp a carious exposure , acute the cavity. Inflammatory reactions have vascular and cellular components. In chronic inflammation the cellular compo- 1.

However, in acute inflammation the vascular changes pre- Dentine is a vital tissue containing the cytoplasmic extensions of odon- dominate. The dentine-pulp complex, like ies is the most common microbial source. Dentine caries will result in any other vital tissue in the body, is capable of defending itself. The transparent zone synonymous with the translucent zone is softer than the deeper, less mineralized, sound dentine.

The diagram equates the bacterial content and mineral deposition within the tubule lumen through the progressive zones of carious dentine. From Ogawa et al. Indeed, this infiltration may even be seen in response to initial enamel caries. This chronic inflammatory reaction is mainly due to the movement of bacterial toxins through the dentinal tubules. Secretory immunoglobulins travel in the dentinal fluid up the remain- ing patent tubules.

With increasing carious involvement of enamel and dentine, the area of chronic inflammation increases in size but it is believed to remain localized until pulp exposure. Bacteria may enter the pulp with polymorphonuclear leucocytes predominating and acute inflammation can supervene, spread throughout the pulp and result in pulpal necrosis.

Note the dentine-pulp complex reparative response of LR6 to the distal dentine lesion - the distal pulp horn has been obliterated by deposits of tertiary dentine arrow.

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How many other carious lesions can you detect? As well as con- GORD is a common cause of intrinsic stomach acids entering the oral servative management involving modifying diet, lifestyle and the use cavity on a regular basis and occurs primarily due to transient relaxa- of chewing gum, stomach acids can be neutralized using conven- tion or incompetence of the lower oesophageal sphincter. Certain fac- tional antacids e. Gaviscon or their production limited with oral medications including proton pump inhibitors e.

Losec or H2 antagonists e. Surgical procedures can D Table 1. Stomach hydrochloric acid originates from: Extrinsic, dietary Affects labial surfaces of maxillary anteriors. Drinking habits: Acids include citric, carbonic, acetic, hydrochloric, phosphoric acids. Often associated with a healthy lifestyle - patient understanding required to modify erosive potential of the diet. Rare nowadays due to stringent health environmental and safety regulations in the workplace.

Historically industrial processes where acid was vaporized and inhaled battery manufacturers, tanning factories. Attrition TW caused by occlusal tooth-tooth contact; occlusal facets match with opposing teeth; usually in combination with erosion.

Abfraction contentious Cervical V-shaped enamel-dentine TW lesions with no history of abrasion. GORD, gastro-oesophageal reflux disease. Once this is done, any dental damage can be repaired.

The - Hiatus hernia patient's dentist may often be the first to notice the problem through - Achalasia - a condition associated with a narrowed lower oesopha- the dental manifestations and appropriate referral to medical col- geal sphincter and reduced oesophageal motility leading to stag- leagues may be required.

M - Secondary - gastric irritation, alcohol, aspirin, and other non- ratio, M ratio, Erosion is often a contributory factor in the overall pattern of 1 - pregnancy clinical toothwear. Clinical examples of these are shown in Chapter 2. Trauma to the mouth can produce any combination of the following local injuries: UL2 and LL45 were avulsed in the incident. What might have been the presenting dental complaints for the above patient?

Detection and management will be discussed in subsequent chap- ters. Examples of dental trauma can be seen in Figures 1. Can you detect any abnormal clinical findings from the In some cases, untreated traumatic injury can lead to the develop- above picture clue - check the mucosae? Note the large well-demarcated pathological radiolucency originating from the root apex of the fractured and displaced root, post-core and crown complex in the UL2.

The lesion is tracking in the overlying mucosa to the swelling visible in a , d The extracted UL2 root with the post-core and crown removed showing the crack sustained from the impact.

What other findings are evident from the USO? Such teeth are often unsightly or molar-incisor hypomineralization and intrinsic staining fluorosis and prone to excessive toothwear or loss of clinical crowns, and thus they tetracycline as well as the hereditary conditions of hypodontia, amelo- may require restoration to improve appearance or function or to pro- genesis imperfecta, and dentinogenesis imperfecta. These defects, their aetiology, and 1. What habit may have contributed to this pattern of disease?

This child was allowed to suck a bottle of sweet drink frequently. Not conclusive, but may be due to the Maillard reaction, a biochem- 1 ical reaction between proteins and carbohydrates in a moist, acidic Q1. Improved oral hygiene would have arrested this active part of the lesion. Fluoride, calcium, and phosphate ions in particular help to form a more acid-resistant fluoride-substituted hydroxyapatite.

How might this scenario be managed in a high caries risk patient? Can you detect any abnormal clinical findings from the Q1. What features of this lesion will help the dentist conclude above picture? Difficult, but did you notice the mucosal swelling level with the patient be managed? The lesion has surface roughness detectable as vibrations in the handle of the ball-ended explorer as it is gently run across the lesion Ql.

The near complete obliteration of the pulp chamber and root canal agent. This patient was under preventive therapy including modifica- spaces in the UL1. Diagnosis and risk assessment Chapter 3: Both aspects followed see Figure 2.

Detecting clinical problems and their aetiology Chapter 2: Prognosis Chapter 3: Formulating an individualized care plan treatment plan Chapters 5. Recall Chapter 8: H Figure 2.

Adapted from Domejean el al.

Pickard's manual of operative dentistry

JMin Intervent Dent Information gathering9 This aspect of patient management involves gathering the relevant It is critical that detailed notes are made for all stages of the patient information based on which sound clinical judgements can be made as management pathway, at every visit. This can be done through compu- to the best course of treatment for the individual patient.

Clinical ter software packages or hand-written notes. Each patient will have detection works on two levels: The answers to a carefully and with experience can be adjusted to specific needs and conditions planned series of questions will help to shed light on the nature and and modified to assess aetiological factors of the presenting disease severity of the problem presented.

A generic structured 'interview' see later. Table 2. History of presenting complaint s Commencement: HPC Location: Avoid putting words in the patient's mouth. Are they getting better, staying the same or deteriorating? Answers to the above will often provide the clues to help make the correct diagnosis. How regularly do they visit the dentist? Medical history MH Most dentists use a printed checklist, which should include information regarding: Check medication in the Dental Formulary or equivalent.

Medications causing dry mouth, gingival overgrowth, or vomiting should be noted. Relevant when considering appointment logistics for the care plan for the individual. Relevant when planning care, preventive advice.

Helps to ascertain the possible aetiology of the problem.

It is better to have a system that encompasses all aspects of follows, divided into a general and oral examination. When examining the oral mucosae, learn a sys- tem which ensures that all aspects of the oral cavity are included, i.

The demean- around the oral cavity. Chapter 5. Oral examination Table 2. Intra-oral Mucosae All internal buccal, labial, alveolar mucosae including vermilion border of lips, tongue dorsum, lateral borders and ventral surfaces , retromolar areas, hard and soft palate, floor of mouth.

Palpation of the pterygoid muscles. Tenderness in the pterygoids muscles -? Dry mucosae and frothy saliva indicative of dry mouth. Relevant to assess periodontal status, which will affect the overall restorative status of the mouth and of the individual tooth. Prostheses Crowns, removable dentures, fixed bridges, implant-retained crown and bridge work, orthodontic appliances fixed and removable.

Relevant regarding oral hygiene procedures, plaque-retentive margins, aesthetics, status of abutment teeth. Intercuspal position ICP , retruded contact position RCP , protrusive, retrusive, lateral excursive movements -working and non-working side contacts. Skeletal discrepancies. Can you spot an error in the above charting? Which tooth, side, position - e. Presence of existing restoration s - location mesio-occlusal, buc- In the UK, the most commonly used notations are the Palmer system cal, cervical, etc.

Both are shown in Figure 2. A drawback of the Palmer notation is that this can be difficult to 4. Presence of carious lesion s - location, mICDAS classification see input into electronic notes although current software packages are later , lesion activity. Presence of toothwear - location buccal, occlusal, incisal and extent in enamel or dentine, exposing pulp 6. Presence of other abnormalities, e. With practice, this can be done with a series of abbreviated responses, and good teamwork with the nurse can expedite this process.

Figure 2. In both on the relevant tooth in the chart. It is important to check all five systems the deciduous dentition is labelled a-e from the midline. Users tend to credit these systems for crossing language boundaries but confusion Figure 2.

Pickard's Manual of Operative Dentistry, Eighth edition

FDI 16 see quadrant prefixed by a number Courtesy of Dental Update. What is the name given to the overlying segment of gingivae on the distal aspect of the occlusal surface in both examples above? The clinical manifestation of the carious dis- ease process is the progressive lesion it creates within the dental hard tissues. A dentist must be able to link the visual clinical appearance of the lesion with the underlying histological damage that has occurred in the tooth, at a particular moment in time.

In this way, the dentist can then decide how to manage the lesion and the disease process in that individual patient. In an attempt to do this, several visual indices have been described overthe years. In , the ICDAS International Caries Detection and Assessment System Foundation was convened to pro- duce an evidence-based clinical caries assessment system to be used primarily for epidemiological and research studies, as well as for use in Figure 2. A simpler, modified version is presented in enamel fissure showing the damage inflicted to the intact enamel Table 2.

Then, depending on the Q2. What hand instrument should be used instead? This index requires that points listed and discussed Table 2. Images show teeth sectioned longitudinally through occlusal lesions, representative clinical examples of each mICDAS score.

No enamel demineralization or a narrow surface zone of opacity. No clinical cavitation detectable. Demineralization involving the middle to inner third of dentine. Demineralization involving the inner third of dentine towards pulp.

What treatment may be required for this tooth? They can easily be missed clinically unless the surfaces are clean and vision aided by the use of magnification. FOTI, fibreoptic transillumination.

From Pitts NB Diagnostic tools and measurements - impact on appropriate care. Community Dent Oral Epidemiol Note that careful selection ment of the particular lesion over time. The 'caries ice- threshold bias when interpreting data for caries prevalence in a popula- berg', developed in collaboration with cariologists and epidemiologists, tion. This permits the development of of caries, patients with early stage lesions within enamel, cavitated or strategies to manage caries at a population level as well as at a patient not, will not be included in the final data, thus incorrectly reducing the level.

The iceberg can be seen in Figure 2. The site and distribution of lesions in a patient's mouth might cannot be cleaned effectively with a tooth brush.

These areas on give an indication to underlying aetiological factors. For example, newly erupting, partially erupted or submerged molars are particu- patients with xerostomia dry mouth due to salivary gland disease or larly susceptible to carious attack.

The and lesions that circumvent the neck of the crown at the gingival mar- surfaces of particularly imbricated crowded teeth can be more sus- gin. Patients with eating disorders may have lesions on the lingual- ceptible due to the lack of access to oral hygiene aids.

Therefore, a lesion H To aid the process of clinical information gathering, other tests may be requested, the results of which must help verify or make the final diag- radiographically restricted to enamel will probably have spread his- tologically across the enamel-dentine junction EDJ into the outer nosis of the problem and possibly its aetiology.

Investigations have a third of dentine. Examples of lesions investigations must not be interpreted individually, but in conjunction detected from bitewing radiographs of a high caries risk patient are with all the other methods described in this chapter to help formulate shown in Figure 2.

Once experience has been gained in interpret- the diagnosis for the patient. All investigations are prone to false-posi- ing radiographs, other clues can often be found to help with the diag- tive and false-negative outcomes. Analysing the relative proportions of nosis and potential activity status of the lesion s. These might include these outcomes, statistical measures of sensitivity the measure of how the outline of the pulp horns - often tertiary dentine has been laid effective an investigation is at detecting true disease and specificity down in response to the disease process and this can be seen by the the measure of how effective an investigation is at detecting true relative shrinkage of the pulp horn subjacent to the spreading lesion.

For caries detection, lucency is a clue that, at the time when the film was taken, the lesion these include radiographs and pulp vitality sensibility and percussion was in a state of relative activity causing demineralization.

If the den- tests. Radiographs It is vital that a report of all radiographic findings is duly noted in the patient's notes for long-term scrutiny, monitoring, and medicolegal Horizontal bitewing radiographs should be used to aid lesion detection reasons. A film holder and beam- aiming device should be used routinely in order to obtain the optimal Table 2. Enamel Lesion miCDAS Incipient occlusal lesions are difficult to detect and only later stage El Outer half of enamel 0,1 occlusal lesions are clearly visible on radiographs.

Periapical radio- E2 Inner half of enamel 1 graphs may be used to assess the depth of proximal lesions in ante- rior teeth. Dental panoramic tomograms should not be routinely Dentine Lesion miCDAS used for caries detection due to their limited resolution and increased D1 Outer third of dentine 2 radiation dose when compared with small intraoral films.

Can you find more lesions and radiographically classify them? Can you comment on the radiographic changes of the pulp chambers in those teeth? Pulp vitality sensibility tests The status of pulp innervation sensibility can be assessed to ascer- H Technically, the term vitality implies the status of the pulpal blood flow. Clinical signs of a non-vital, cotton wool pledgets soaked in ethyl chloride or ice sticks may be necrotic pulp may include: Check equivalent teeth on the contralateral side products of haemoglobin in the pulp chamber.

Greying and reduced to the tooth in question and then the adjacent teeth acting as an translucency might also be noticed.

Ask the patient to raise ration covering it. A fine gutta percha point inserted into the tion into the periodontal membrane. The patient's hand must be in contact with the metal Figure 2. The UL6 is vital with no symptoms. Avoid restorations and the gingival margin as false-positive readings may ensue.

The posterior multirooted teeth, a mixture of vital and non-vital pulp tis- probe is placed on a clean, sound tooth surface contralateral and sue may confound the interpretation of the reading. If the patient feels pain then at least Figure 2. The current is gradually increased by the dentist until partial innervation of the pulp remains. At this point they are instructed to let go of the handpiece and the circuit is broken. It is important to note in the above cases, a positive response from The numerical value can be recorded and is useful for monitoring the pulp does not necessarily mean all is well.

There is no clinical purposes for a particular tooth but is not equivocal as the readings way of knowing if there is partial necrosis or denervation in a dental can vary from the same patient. False-positive responses may be elic- pulp and multirooted teeth can present with partially diseased pul- ited through stimulation of nerve fibres in the periodontium and in pal tissue.

They should let go to break the circuit when a sensation is felt in the tooth. The bacterial population and the cari- apical tissues and periodontal membrane, not the pulp directly. If peri- ogenicity of the biofilm develops in a structured manner in correla- apical periodontitis is present, the piston-like effect of the tooth being tion with its age - the older the plaque, the more anaerobic and pushed into the inflamed periapical tissues will elicit acute tenderness.

These The inflammation in the periodontal tissues might be caused by the proprietary kits neither assess the direct activity of lesions nor patient toxins from a non-vital pulp.

They also can be helpful as strong motivators for patients to improve their own Once a carious lesion is detected, it would also be useful to ascertain oral health with better oral hygiene procedures.

The absence of saliva or the presence of a reduced difficult to measure objectively intraorally, but certain intraoral clues quality of saliva is an important aetiological factor in the increased can be gleaned from the: If plaque can be found on non-retentive sites, 2. The surfaces of the as a biofilm will remain on their surfaces. The other main aetiological factor that have produced two- or even three-tone plaque disclosing solutions, can be assessed during this detection phase of patient management, is Figure 2.

How could you manage this case? This is done by asking the patient to fill out a diet analysis sheet see Figure 2. They should 2. Examples of some of these are shown in Table 2. Many detection No indication of the relevance of the diet analysis should be given at technologies work on four basic physical principles affecting mineral- the first appointment so as not to bias the patient or allow them to ized dental tissues: It is important to what they are actually doing!

The results should then be analysed by understand how a particular technology works to be able to interpret the dentist and an appointment made to discuss them. Issues to look accurately the information it is giving. An example of such an ambigu- out for are frequency of meals, hidden sugar content e. It is imperative ries, optical light scattering and fluorescent characteristics, as research that the dentist works with the patient to modify their existing dietary has shown the unit is affected by both properties to a varying degree.

Chastising the patient and ordering them to change may have Therefore the interpretation of results, that is whether to cut a cavity the opposite effect! Work with positive reinforcement, offering sugges- or not, must be used with caution in the clinical environment, again in tions or allowing the patient to make sensible suggestions to lower conjunction with all the other information gathered for the particular B their sugar intake, frequency, and duration.

Remember, positive patient. What stands out as the main problem regarding this patient's sugar intake? The four columns indicate the basic physical principle on which each technology relies. In this way, the overall clinical problem can Relating to attrition: Relating to abrasion: Work place..

Interests, hobbies, sport activities. Medication Illness present Illness past. Has the illness been treated By a doctor. In hospital. Alcohol Figure 2. However, these are often com- bined as the cause and, therefore, the clinical manifestations, of tooth- wear lesions are multifactorial see Figure 2. Note the smooth surfaces and peripheral rims of enamel on UL3 to UR3 as well as the amalgam restorations in the premolars standing proud of the tooth surfaces. There was no evidence of gastro- oesophageal reflux from the history.

Enamel loses surface characterization and becomes smooth see Figures 2. Can cause smooth-cupped lesions on pos- 2 terior occlusal surfaces. Can also affect the occlusal surfaces of the Figure 2. What would be the obvious cause of the buccal cervical aspect of mainly anterior teeth. Can you guess the cause of the abrasion? Note the reflective, smooth, featureless labial enamel surfaces of UR2 to UL2.

Pickard's Manual of Operative Dentistry, Eighth edition

There are early signs of incisal attrition abrasion lesions. What is the cause? What might be the presenting complaint of this patient? However, without the aetiological factor s of toothwear being tip of the tongue due to the roughness and poor aesthetics.

Toothwear also needs careful monitor- sible darkening of teeth due to the change in the optical qualities of ing over a prolonged period to be able to assess its relative progress the remaining mineralized tissues, again affecting overall aesthetics.

Type of dental fracture to and causing the trauma. Any suspicions of a head injury including sustained see Figure 2. Depending patient compliance issues. Check patient's tetanus status.

Have any teeth been care plan see later. From Andreasen et al. Blackwell Munksgaard. These defects have to be detected and diagnosed from the intraoral Table 2. Hypoplastic- -I matrix, normal maturation: Hypomineralized - normal matrix, J. Molar-incisor hypomineralization Systemic illness high fever, respiratory illness from 0 to 2 years Figure 2. Hypomineralized - white-yellow or yellow-brown opacities, easily chipped, T sensitivity exposed dentine, plaque stagnation.

Intrinsic dental fluorosis Excessive fluoride ion intake water, toothpaste, tablets poisons Figure 2. Chalky-white flecks, confluent blotches, brown discoloration, pitted enamel. Intrinsic tetracycline stain Figure 2. Nowadays rare. Dark, grey horizontal bands affecting all teeth. Third molars, second premolars, upper lateral incisors most affected.

Amelogenesis imperfecta Figure 2. Thin enamel, yellowish teeth dentine showing through. Or granular, pitted, stained thin enamel. Soft, friable, stained or chalky-white enamel, frequently lost due to weakness at the enamel-dentine junction EDJ. Dentinogenesis imperfecta Odontoblast defect affecting dentine matrix formation and mineralization. Short roots, bulbous crowns, pulps obliterated.

Note the pattern of teeth affected - maxillary central incisors and tips of maxillary canines and all mandibular incisors approximately a third of the length from the incisal edges and tips of the mandibular canines too. The patient presented with two poor quality acrylic crowns on the upper central incisors and buccal cervical caries on the lower incisors.

The disto-palatal fissure shows marked enamel breakdown and demarcated border opacities. Courtesy of K Weerheijm. This patient resided in a Sudanese village with natural fluoride levels in the drinking water exceeding ppm F. The maxillary central incisors have been polished by a dentist using a fine grit bur, so removing the superficial weakened fluorotic enamel. The number of episodes per day and their frequency throughout A: In the lower left second premolar, there is no MO charted in 'existing each hour period.

This would ensure that the patient's teeth were restorations' but one has been included in 'treatment to be done'. Well bathed in plaque with a pH below 5. I also feel that this book can have considerable value to new postgraduates involved with any aspect of operative dentistry as a simple refresher text. British Dental Journal, I am in my first year of study of dental hygiene and therapy and I have found this book very useful.

There are some great photographs to illustrate the conditions described in the text and the content is not too complex. I would recommend it! Avijt Banerjee: It is vital for modern dentists to appreciate the effects of disease on the dental tissues and the science underpinning the materials that they use in order to maximize restoration success and longevity. Their interaction in this book catalyses the development of the operative skills required to prepare and restore teeth effectively.

The 9th edition of this classic dental textbook has been extensively re-worked, re-styled, and updated to keep abreast of current knowledge, principles, and the modern practice of operative dentistry. The book describes, in a clear and structured manner, the causes of dental disease, methods of identifying the disease process in our patients, and the development and execution of patient-centred management strategies based on disease control and lesion prevention.

Common operative procedures and techniques are explained in concise bulleted points, tables, and flowcharts and illustrated in full colour. The authors are world-renowned experts in the field of Cariology, Minimally Invasive Dentistry, and Dental Biomaterials. New chapters on patient management, disease diagnosis, and risk assessment, with the correlation of dental histology and the material chemistry, combine in this new edition to provide a unique insight into the contemporary world of Operative Dentistry.

This book is the ideal support, at all undergraduate levels, for dental undergraduates and dental care professionals e. For registered adopters of the book: Read more Read less. Representative Credit offered by NewDay Ltd, over 18s only, subject to status. Terms apply. Learn more. Customers who viewed this item also viewed. Page 1 of 1 Start over Page 1 of 1. Avijit Banerjee. Essential Skills for Dentists. Paediatric Dentistry. Advanced Operative Dentistry: A Practical Approach, 1e.

David Ricketts BDS. Essentials of Dental Caries. Customers who bought this item also bought. David A. Dental Morphology: An Illustrated Guide, 1e.With practice, this can be done with a series of abbreviated responses, and good teamwork with the nurse can expedite this process.

Customers who viewed this item also viewed. Not tender to Usually not tender Not tender. Note also that the upper and lower teeth are worn by approximately the same amount. Tenderness in the pterygoids muscles -?

Salivary flow Salivary flow should be measured because a feeling of a dry mouth may be subjective rather than actual. Enamel Lesion miCDAS Incipient occlusal lesions are difficult to detect and only later stage El Outer half of enamel 0,1 occlusal lesions are clearly visible on radiographs.

Dark, grey horizontal bands affecting all teeth. Published in: The Whitlockite deposits originate from a combination of a physico- chemical re-precipitation of calcium and phosphate ions diffusing towards the increasing pH environment of the lesion's deepest advanc- ing front and also possibly a vital process of new and rapid mineral deposition from the pulp via the odontoblasts.