Crafting A Companys Strategy Business Essay

Crafting A Companys Strategy Business Essay To compete in the globalized business, company requires strategic planning and strategic thinking and by crafting good corporate strategic they can become strategically competitive. A companys strategy is a master plan of the company which entails that how the company would able to achieve its vision and objective. Strategy is a significant planning as it is universal with respect to the whole organization (Chapter 2: leading the Process of Crafting and Executing Strategy). Strategies involve managers at all organization level in which senior executives plays a vital role in the strategic- making process. The CEO (chief executive officers) is responsible for the chief strategy maker, chief strategy implementer and the chief direction setter and holds the responsibility of leading the strategy -making, strategy- executing process. In some organization, the owner of the organization or CEO personally decides the key elements of the strategy and performs function as a strategic visionary and other managers may assist with the help of collecting and analyzing the companys data. At the same time, CEO may also inquire advice from the senior managers and tenure and important employees in order to design overall strategy. Steve Job, CEO of Apple is an apt example of the corporate CEO who plays major role in the shaping their companys strategy. In most of the company, other senior executives and managers have influential role in strategic decision making such as the chief financial officers, the vice president for the respective departments i.e. the marking, production, finance, human resources etc. Strategy making process enrolls by different approaches the delegation approach, the chief architect approach, the corporate entrepreneur approach and the team approach (Chapter 2: leading the Process of Crafting and Executing Strategy). Crafting strategy functions is very vital for the company because it incorporates changing competitive environment, minimizes competitive disadvantage and also provides better understanding of the external environment. It focuses on the objectives, goal, vision and mission of the company. It enhances the process of motivation and strength of decision making. It provides a base so that the actions can be implemented properly and accurately. Therefore, crafting a companys strategy is really job for senior executive and the companys board of director (Chapter 2: leading the Process of Crafting and Executing Strategy). Question: 2 What would your reaction be if your employer required you to sign a statement annually certifying that you have complied with the companys code of ethics? Code of Ethics is standard guidelines which are designed to set up the acceptable behaviors from the employees. To enforce high standard of ethical behavior, employers approaches many practices such as provides mandatory training, encourage compliance and establish tough consequences for unethical behavior, appointing committee of senior employees or the employees who are champions of high ethical standard in order to work for heading up companys ethics enforcement process or signing up of the declaration statement. In which, signing up the declaration statement is very effective and highly implemented practice used in the organization with respect to the ethical codes. In this process, employers asked to employees to sign a statement which certifies that employees are complied with the companys code of ethics. Different employee has different reaction toward the code of ethics or toward this process in accordance to their perception, their view, their priority of the work and their understanding about the code of ethics (Chapter 2: leading the Process of Crafting and Executing Strategy). Code of ethics follows the policy with respect to internally and externally environment of the company and hence delivers more values to the company as well as to the employees. If I would ask to sign up the declaration statement which inbounded with the code of ethics of the company I would try to have better understanding of every code and their needs in my work. I would try that business code of ethics does not contradicts with my personal values and ethics and would try to enhance my skills and work based on the ethics. After getting deep understanding of the ethics I would signed up the ethics annually and try to implements in my professional and personal life (Chapter 2: leading the Process of Crafting and Executing Strategy). Code of ethics is very beneficial not only for the organization but also for the personal life therefore, signing up is not important but implementation is also important (Chapter 2: leading the Process of Crafting and Executing Strategy). Short note on five phase of Strategy Executing Process The managerial process of crafting and executing a companys strategy consisits of five integrated and interrelated phase consists of developing a strategic vision, setting of objectives, crafting a strategy in order to achieve the vision and objective of the company, executing and implementing the strategy in the organization and monitoring developments, evaluating performances and making corrective adjustments. All five stages are interrelated and interconnected and very vital for any organization to achieve the vision of the company (figure 1) (Chapter 2: leading the Process of Crafting and Executing Strategy). Figure : Five phases of strategy executing strategy Source: (Chapter 2: leading the Process of Crafting and Executing Strategy) Developing a strategic vision: The initial phase of executing strategy phase is to develop a strategic vision in which company required to set vision of the company that what will be the future in terms of market, product, technology or customer. This steps provides long term direction to work with a sense of action to be executed and it also communicates management aspirants to the stakeholders. Setting objectives: The second stage proceeds with setting of the objective, the strategic objectives and the financial objectives. Setting objectives entails that how much, when and by what kind of performance is expected for the company. For measuring the company performance a balance scorecard approach is used. Crafting a strategy to achieve the objectives and vision: After setting the vision and objective of the company the important step is to crafting a strategy in order to achieve the set vision and objective. Crafting strategy deals with the internal and external environment of the organization. This process is a part of the team work while in some organization this is a job of senior executives and CEO of the company. The strategy is a collection of the strategic actions, principles and business approach of the organization. Implementing and executing the strategy: Crafting a strategy is an important step to move forward for achieving the vision of the company but its not effective without the implementation and execution in every department respectively. It consists of several processes to make employee to implement the strategy for this exerts the effective leadership to keep the process forward and enhancing. Monitoring developments, evaluating performances and making corrective adjustments. Crafting and implementing the strategy is not one time process. It should continues and adjustable in accordance with the changing market and competitive environment. To capture the new opportunity and to compete globally strategy required modifying and enhancing the performance. Therefore, put constructive pressure on company to achieve fruitful results, make approaches to promoting innovation, stimulate corporate interpreneruship, push corrective actions to improve the process od strategy making and strategy execution process. Display ethical leadership and lead social responsibility initiatives.

Developmental Defects of Teeth

developmental defects of teeth with recent genetic concepts INTRODUCTION: Disorders of development of teeth may be prenatal or postnatal in origin and may be inherited or acquired. Their recognition and evaluation requires a thorough knowledge and evaluation of the normal chronology of the human dentition and of the normal development and structure of the teeth.Disorders of development of teeth of teeth may be due to abnormalities in the differentiation of the dental lamina and the tooth germs, causing anomalies in the number, size and form of teeth (abnormalities of morphodifferentiation) or to abnormalities in the formation of the dental hard tissues resulting in disturbances in tooth structure (abnormalities of histodifferentiation). Abnormalities of histodifferentiation occur at a later stage in development than abnormalities of morphodifferentiation; in some disorders both stages are abnormal. Histophysiology of tooth development:A number of physiologic growth processes particip ate in the progressive development of the teeth. These are – 1. Initiation The dental lamina and associated tooth buds represent those parts of the oral epithelium that have the potential for tooth development. Different teeth are initiated at different times. Initiation induction requires ectomesenchymal epithelial interaction. A lack of initiation results in the absence of either a single or multiple teeth or complete lack of teeth. Abnormal initiation may result in the development of single or multiple supernumerary teeth. 2. ProliferationEnhanced proliferative activity after initiation results successively in the bud, cap and bell stages of the odontogenic organ. Proliferative growth causes regular changes in the size and proportions of the growing tooth germ. A disturbance has entirely different effects according to the time of occurrence and the stage of development that it affects. Tooth anomalies may include disturbances in the size, proportion or number of teeth 3. H istodifferentiation It succeeds the proliferative stage. The formative cells of the tooth germ developing during the proliferative stage undergo definite morphologic as well as functional assignment.Differentiation of odontoblasts and ameloblasts takes place resulting the formation and apposition of enamel and dentin. Disturbance is the stage results in defects in the structure of tooth like amelogensis imperfecta type 1 and 4. 4. Morphodifferentiation The morphologic pattern or basic form and relative size of the future tooth are established by morphodifferentiation that is by differential growth. Dentinoenamel junction and dentinocemental junctions are established. Disturbances in morphodifferentiation may affect the form and size of the tooth without impairing the function of the ameloblasts or odontoblasts. 5. ApppositionIt is the deposition of the matrix of the hard dental structures. Defects in apposition results in anomalies like amelogenesis imperfecta type 2, dentin dysplas ia. 6. Mineralization and Maturation After matrix formation full mineralization and dental hard tissue maturation. Anomalies like amelogensis imperfecta type 3, fluorosis and interglobular dentin. CLASSIFICATION OF DEVELOPMENTAL DEFECTS OF TEETH 1. Anomalies of initiation and proliferation – anomalies of number hypodontia and anodontia hyperdontia – anomalies of size Microdontia Macrodontia – anomalies of shape Germination Fusion Concrescence 2. Anomalies of morphodifferentiation anomalies of size and shape Dilacerations Dens invaginatus Dens evaginatus Taurodontism Talon cusp 3. Anomalies of histodifferentiation – enamel defect Amelogensis imperfecta type I – dentin defect Dentinogensis impefecta type I,II,III 4. Anomalies of apposition – enamel defects Amelogensis imperfecta type II, IV Enamel hypoplasia Enamel pearl – dentin defects Dentin dysplasia Regional odontodysplasia – cementum defects Hypercementosis Hypophophatasia 5. Anomalies of mineralization – enamel defects Amelogenesis imperfecta type III Enamel fluorosis Anomalies of initiation and proliferation Development disturbances in number a. ypodontia and anodontia True anodontia or congential absence of teeth may be of two types Total anodontia – in which all teeth are missing. It may involve both deciduous and permanent teeth. It is a rare condition when it occurs it is frequently associated with generalized disturbances, hereditary ectodermal dysplasia. Partial anodontia (hypodontia or oligodontia) Hypodontia when there is lack of development of one or more teeth Oligodontia is a subdivision of hypodontia indicating the lack of development of six or more teeth. An incidence of 1. 5 – 10% is seen excluding 3rd molars in permanent dentition and . 09 – . % for primary dentition. Most frequently affected teeth are 3rd molars, mandibular 2nd premolar, maxillary lateral incisor and maxillary 2nd premolar. In case of deci duous dentition usually maxillary lateral incisor are missing. According to Grahen and Granath there is a close correlation between congenitally missing deciduous teeth and their permanent successors suggesting a genetic factor. A familial tendency for this defect is noted. Graber reported enough evidence that it is actually the result of one or more point mutations most often transmitted in an autosomal dominant pattern with incomplete penetrance and variable expressivity.Some investigators implied that hypodontia is a normal variant suggesting that humans are in an intermediate stage of dentitional evolution. A proposed future dentition would include one incisor, one canine, one premolar and two molars per quadrant. Hypodontia correlates with the absence of appropriate dental lamina. Mostly this is due to genetic alteration. However, environmental factors like trauma, infection, radiation and endocrine disturbance may also result in loss of developing tooth bud. Hypodontia is asso ciated positively with microdontia, reduced alveolar development, increase free way space and retained primary teeth.Pax 9 gene maps to chromosome 14, it encodes a transcription function that is important in the development of pharyngeal pouches. Its mutation may lead to congenitally missing teeth. Syndromes associated with hypodontia: – cleft lip/palate – crouzon syndrome – down syndrome – hyphidrotic ectodermal dysplasia – ellis van crevald syndrome – oro facial digital syndrome b. hyperdontia it is the development of an increase number of teeth. Genetics of hyperdontia suggests an autosomal dominant pattern of inheritance with incomplete penetrance. The variable expression and penetrance of the gene may be affected by the environmental factors.The development of hyperdontia is development of excess dental lamina which leads to formation of additional teeth. An incidence of . 3-3% and a male to female ratio of 2:1 is noted. It occurs most frequently in permanent dentition and approximately 90% of cases present in maxilla with a strong predilection for the anterior region. Terms used to describe supernumerary tooth depending on their location i. Mesiodens is located in the maxillary incisor resion. It is the most common supernumerary. ii. Distodens/ distomloar is the accessory fourth molar iii.Paramolar is a posterior supernumerary tooth situated lingually or buccally to a molar tooth. Classification based on morphology In the primary dentition morphology is usually normal or conical. Greater variety is seen in case of permanent dentition Conical is a small peg shaped conical tooth and is the most common supernumerary. It develops with root formation ahead or at an equivalent stage to that of permanent incisor. It can result in rotation or displacement of the permanent incisor but rarely delays eruption. Tuberculate possess more than one cusp or tubercle and is barrel shaped.Root formation is delayed as compared to pe rmanent incisors. They are often paired and are commonly located on the palatal aspect of the central incisors. It results in delayed eruption of the incisors. Supplemental refers to a duplication of teeth on the normal series and is usually found at the end of the tooth series. Most commonly permanent maxillary lateral incisor is the supplemental supernumerary. Majority of the deciduous supernumeraries are of this type. Odontome is listed as the fourth category by Howard. It is a hamartomoatous malformation nd is composed of more than one type of tissue called composite odontoma. Mainly two types are there complex and compound. Syndromes associated with hyperdontia 1. cleft lip/palate 2. cleidocranial dysplasia 3. gardner syndrome 4. oro facial digital syndrome Developmental disturbances in size of tooth a. microdontia – teeth which are smaller than normal. Females demonstrates a higher a frequency of microdontia and hypodontia. Three types are – True generalized micr odontia in this all the teeth are smaller than normal. It is seen in cases of piutatry dwarfism, Down syndrome, congenital heart diseases. Relative generalized microdontia normal slightly smaller teeth present in the jaws larger than normal producing an illusion of microdontia. Role of hereditary as jaws are inherited from one aren’t and tooth size from other parent. – Microdontia involving single tooth is common condition affects maxillary lateral incisors and 3rd molar most commonly. b. macrodontia – teeth that are larger than normal. Three types similar to that microdontia – True generalized macrodontia all teeth are large. Seen in cases of pituitary gigantism and pineal hyperplasia with hyperinulinism. Relative generalized macrodontia presence of normal teeth in similar jaw giving an illusion of macrodontia – Macrodontia of single tooth relatively uncommon. Occasionally seen in cases of hemihypertrophy of the face. Should not be confused with f usion of teeth. Development disturbances of shape of teeth a. germination – anomalies which arise from an attempt at division of single tooth germ by an invagination with resultant incomplete or complete formation of teeth. Incidence of . 5% is seen and it more common in primary dentition. Higher frequency in maxillary anterior region.It may retard eruption of permanent successor. Usually appear as one with two completely or incompletely separated crowns that have a single root and root canals. Twining production of equivalent structure by divisions resulting in one normal and one supernumerary tooth. Etiology is unknown although a genetic basis has been suggested. b. fusion – union of two normally separated tooth germs. Depending upon the stage of development of the teeth at the time of the union. More common in the deciduous than in the permanent dentition. Union by dentin, separate pulp chambers/ canals. May retard eruption of permanent successor. . concrescence â⠂¬â€œ form of fusion which occurs after root formation. Teeth are united by cementum only. As a result of traumatic injury or crownding of teeth with resorption of the interdental bone. More frequently in the posterior and maxillary region. Anomalies of morphodiferentiation Anomalies of size and shape a. dilaceration: An angulation or a sharp bend or curve in the root or crown of a formed tooth. Due to trauma during the period in which the tooth is forming, with the result that the position of the calcified portion of the tooth is changed and the remainder of the tooth is formed at an angle.Syndrome associated with dilaceration. Lamellar ichthyosis. Present difficulty at the time of extraction. b. dens invaginatus: dens in dente It is a deep surface invagination of the crown or root that is lined enamel. Results due to invagination in the surface of tooth crown before calcification has occurred. This can be due to increased localized external pressure focal growth retardation and fo cal growth stimulation in certain areas of the tooth buds. The permanent maxillary lateral incisors are the teeth most frequently involved. Two forms are usually seen as Coronal dens in dente – more frequent prevalence varies from . 4% to 10%. Depth of iinvagination varies from a slight enlargement of the cingulum pit to deep infolding that extends to the apex. Radicular dens in dente – rare and thought to arise secondary to proliferation of hertwig’s root sheath with the formation of a strip of enamel that extends along the surface of the root. Radiographiclaly the affected tooth demonstrates an enlargement of the tooth. It chances of caries and pulp infection. c. dens evaginatus – Leong’s premolar it is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps.Unilaterally or bilaterally with an increased mandibular predominance. Pathogenesis is the p roliferation and evagination of an area of the inner enamel epithelium and subjacent odontogenic mesenchyme in to the dental organ during early tooth development. If seen in association with another varaiton of coronal anatomy. Shovel shaped incisors affected incisors demonstrate prominent lateral margins, creating a hollowed lingual surface. Maxillary incisor is the most commonly affected. This extra cusp may contribute to incomplete eruption, displacement of teeth and/or pulp exposure with subsequent infection following occlusal wear or fracture. . taurodontism – it is an enlargement of the body and pulp chamber of multirooted tooth with apical displacement of the pulpal floor and bifurcation of the roots. Overall shape of the taurodont resembles that of the molar teeth of cud chewing animals â€Å"bull like† Shaw classified taurodont teeth into 3 division according to the degree of apical displacement of pulpal floor – hypotaurodont (mild) – mesotaurod ont (moderate) – hypertaurodont (severe) may occur as an isolated trait or as a component of specific conditions like 1. klinfilter’s syndrome . amelogenesis imperfecta 3. orofacial digital syndrome 4. hypohydrotic ectodermal dysplasia 5. tricho dento osseous syndrome 6. down syndrome It is seen that taurodontism may develop in presence of any one of a large number of different genetic alterations. These findings suggest that chromosomal abnormalities may disrupt the development of the tooth form and that taurodontism is not the result of any specific genetic abnormality e. talon’s cusp – Is also known as dens evginatus of the anterior teeth. It is a well delineated cusp that is located on the surface of an anterior tooth.Predominantly affects permanent dentition esp maxillary lateral incisors. It projects from the lingual surface of the affected tooth and forms a three pronged pattern that resembles an eagle’s talon. The cusp blends smoothly with the tooth except that there is a deep development groove where the cusp blends with the sloping lingual tooth surface. It is associated with other dental abnormalities like supernumearary teeth, odontomas, impacted teeth; peg shaped lateral incisors and dens invaginatus. It is also associated with other syndromes like Rubinstein Tyabi syndrome & Sturge Weber syndrome.Complications like interference with occlusion, comprised esthetics, displacement of teeth, caries, periodontal problems and irritation of the adjacent soft tissue may occur. ANOMALIES OF HISTODIFFERENTIATION Enamel defects a. Amelogenesis imperfecta type I AI is a heritable enamel defect in the absence of any systemic disease. Reported incidence varies from 1:14000 to 1:4000. Multiple inheritance patterns are noted. It may differentiated into 4 main groups depending on the clinical presentation and the likely stage of enamel formation that is primarily affectes. – hypoplatic hypocalcified – hypomature â⠂¬â€œ hypomature hypoplastic with taurodontism Each group is further subdivided into several subgroups depending on the mode of inheritance as well as the clinical appearance of the defective enamel. Genetic studies – have shown that etiology of AI is related to the alteration of genes involved in the process of formation and maturation of the enamel. X linked AI has shown the defective gene is closely linked to the locus DXS85 at Xp22. this site has been identified as the general location of the human gene amelogenin the principal protein in the developing enamel.In the case of autosomal dominant type of AI the locus of the defective gene is on the ch 4q21 to which enamel protein enamelin maps. AI type I Hypoplatic The basic alteration centers an inadequate deposition of enamel matrix. Any matrix present is mineralized appropriately. Subgroups (Witkop 1989) I A – hypoplastic, pitted AD I B – hypoplastic, local AD I C – hypoplastic, local AR I D – hypoplastic, smooth AD I E – hypoplastic, smooth XR I F – hypoplastic, rough Ad I G – enamel agenesis, AR Clinical feature: – In the generalized pattern pinpoint to pinhead sized pits are scattered across the surface of the teeth. Buccal surfaces of the teeth are affected and staining of these pits may occur – In the localized pattern, the affected demonstrate horizontal rows of pits a linear depression. The altered area is located in the middle third of the buccal surface of teeth. – The type IC is more severe and typically demonstrate involvement of all teeth in both dentitions – In type ID the enamel of all teeth exhibits a smooth surface and is thin hard and glossy – Anterior open bite is seen and teeth exhibit a thin peripheral outline of radiopaque enamel on radiograph – In type IE this is a lesion showing lionization effect. In females the teeth would exhibit alternating zones of normal and abnormal enamel. Males exhibit diffuse thin, smooth and shiny enamel in both dentitions. The teeth have the shape of crown formation with open contacts. – In the rough pattern, the enamel is thin, hard and rough surfaces. An anterior open bite is common. – In enamel agenesis demonstrate total lack of enamel. The teeth are the shape and color of the dentin. The surface is rough. Dentin defects b. Dentinogenesis imprfecta A hereditary developmental disturbance of the denitn in the absence of any systemic disorder.This is an autosomal dominant condition affecting both deciduous and permanent teeth. Affected teeth are gray to yellowish brown and are tulip shaped. Genetic studies show that the gene defective maps to chromosome 4 in case of type II. It encodes a protein called dentin sialophosphoprotein and constitutes about 50% of the noncolllagenous component of dentin matrix. DI type I is due to mutational changes in gene coding pro alpha 1, pro alpha 2 chains of type I collagen, major protein of organic matrix in bone and dentin.Recent studies report that type II and type III arise from a single mutation of DSPP gene and that these are not separate disease but rather phenotypic variation of a single disease. Acc. to Sheild’s classification DI type I – osteogenesis imperfecta with opalescent teeth DI type II – isolated opalescent teeth DI type III – isolated opalescent teeth Brandywine Extensive studies have proven that DI is a disorder distinct from Osteogenesis imperfects so a revised classification is proposed DI type I corresponds to type II of Sheild’s Type II corresponds to type III of Sheild’sThere is no substitute for type I of Sheild’s classification Clinical and radiographic features – deciduous teeth are affected most severely followed by the permanent incisors and first molars – enamel is normal but separates easily from dentin because of defective dentinoenamel junction – once exposed the d entin often demonstrates significantly accelerated attrition – radiographically, the teeth have bulbous crowns cervical constriction thin roots and early obliteration of the root canals and pulp chambers. Type III has shell teeth demonstrating normal thickness enamel in association with extremely thin dentin and dramatically enlarged pulps Histologic features – The dentin adjacent to the enamel junction appears similar to normal dentin but the remainder is distinctly abnormal – Short tubules course through an atypical granular dentin matrix which often demonstrates interglobular calcificaiton. – Cells can be seen entrapped within the defective dentin Anomalies of apposition Enamel defects a. amelogenesis imperfecta type II & IVAI type II – hypomaturation the enamel matrix is laid down appropriately and begins to mineralize however there is a defect in the maturation of the enamel crystal structure Classified into Type IIA – hypomaturation, p igmented AR Type IIB – hypomaturation, X linked recessive Type IIC – snow capped teeth, AD Genetic studies show that multiple mutations in the AMELX gene in the type IIA AI whereas IIA & C the gene defect is unknown. Clinical features – Affected teeth are normal in shape but exhibit a mottled, opaque white brown yellow discoloration.The enamel is softer than normal and tends to chip from the underlying dentin. Radiographically the affected enamel exhibits a radiodensity that is similar to that of dentin. – Type IIA the surface enamel is mottles and agar brown. Enamel is soft enough to be punctures by an explorer – Type IIB shows lionization that is male exhibit differebti pattern in deciduous and permanent teeth. The deciduous teeth are opaque white with a translucent mottling; the permanent teeth are opaque and may darken with age.Female patients exhibit a similar pattern in both dentitions. The teeth demonstrate vertical bands of white opaque ena mel and normal translucent enamel. Radiographically the bands are not perceptible. – Type IIC exhibits a zone of white opaque enamel on the incisal or occlusal third of the crown. AI type IV – hypomaturation hypoplastic with taurodontism This type of Ai exhibit enamel hypoplasia in combination with hypomaturation. Classified into Type IV A hypomaturation hypoplastic Type IVB hypoplastic hypomaturation Genetic defects in both groups is unknownType IV A the predominant defect is one of enamel hypomaturation in ehich the enamel appears mottled yellowish white to yellow brown. Pits are seen frequently on the buccal surface of the teeth. Radiographically the enamel is similar to dentin in density and large pulp chambers may be seen in addition to varying degree of taurodontism Type IVB the predominant defect is one of enamel hypoplasia in which the enamel is thin; the enamel that is present demonstrates hypomaturation. Radiographically there is decrease in the thickness of the enamel.Both these types are seen in the systemic disorders, trich dento osseous syndrome. Other features seen are kinky hair, osteosclerosis and brittle nails. b. enamel pearl Refers to the presence of enamel in unusual locations mainly the tooth root. These are hemispheric structures that may consist entirely of enamel or contain underlying dentin and pulp tissue. These are thought to arise from a localized bulging of the odontoblastic layer. This bulge may provide prolonged contact between Hertwig’s root sheath and the developing dentin, triggering induction of enamel formation. t is found most frequently on the roots of maxillary molars. The enamel pearls precludes normal PDL attachment with CT. Dentin defects c. dentin dysplasia It is a rare disturbance of dentin formation characterized by normal enamel but atypical dentin formation with abnormal pulpal pathology. It is an abnormality that maps to the same site on ch 4 as does DI type II & III. It too may be an alleli c variant. Classified into Type I radicular dentin dysplasia Type II coronal dentin dysplasia Both these patterns appear to be hereditary diseases, transmitted as an autosomal dominant characteristic.Clinical features – Type I both dentitions are affected although the teeth are clinically normal. The teeth are extremely mobile and exfoliated prematurely – Type II both dentitions are affected. Deciduous teeth have the same color as that in DI but the permanent dentition is normal. – Type I both dentitions roots are short blunt and conical. In deciduous pulp chambers and root canals are completely obliterated. Permanent teeth crescent shaped pulpal remanant remains. Periapical radiolucencies involving intact teeth are present. Type II deciduous dentition presents with completely obliterated pulp chambers. Permanent teeth exhibit an abnormal large pulp chamber in the coronal portion. Histologic features – Type I a portion of coronal dentin is normal. Most of the pulp is obliterated by calcified tubular dentin, osteodentin and fused denticles. New dentin forms around these obstacles giving the characteristic appearance described as Lava flowing around the boulders. – Type II deciduous teeth exhibit amorphous and atubular dentin in the radicular portion while coronal dentin is normal.Permanent teeth same but the pulp has multiple pulp stones. d. regional odontodysplasia It is a localized non hereditary development abnormality of teeth with extensive adverse effects on the formation of enamel, dentin and pulp. Proposed causes – abnormal migration of neural crest cells – latent virus – local circulatory deficiency – local trauma or infection – hyperpyrexia – malnutrition – radiation therapy – somatic mutation pathosis associated with RO – ectodermal dysplasia – epidermal nevi – hypophosphatasia – hydrocephalus neurofibromatosis – Rh incompatib ility – Vascular nevi Clinical features – maxillary teeth esp anterior are most commonly affected – female predilection with a ratio of 1. 4:1 – the affected teeth fail to erupt and their shape is markedly altered – the erupted teeth show small irregular crown that is yellow to brown with rough surface – on x ray they have a very thin enamel and dentin surrounding an enlarged radiolucent pulp – There is lack of contrast between enamel and dentin.Histologic features – marked reduction in the amount of dentin and widening of predentin layer – presence of large areas of interglobular dentin and an irregular pattern if dentin – the reduced enamel epithelium around nonerupted teeth show many irregular calcified bodies known as enameloid conglomerates (also seen in AI) e. hypercementosis It is a nonneoplastic deposition of excessive cementum that is continous with normal radicular cementum Clinical and radiographic feat ures in x ray affected teeth demonstrate a thickening or blunting od the root – the enlarged root is surrounded by the radiolucent PDL space and intact dental lamina – may be isolated or involve many teeth – premolars are involved more frequently – predominantly in adults and the frequency increases with age – factors associated with hypercemntosis i. local 1. abnormal occlusal trauma 2. adjacent inflammation 3. unopposed teeth ii. systemic 1. acromegaly 2. arthritis 3. alcinosis 4. paget’s disease 5. rheumatic fever Histologic features – periphery of root exhibits deposition of an excessive amount of cementum – this may be hypocellular or ostecementum – the material is arranged in concentric layers Anomalies of mineralization a. amelogenesis imperfecta type III hypocalcifeid in this type the enamel matrix is laid down appropriately but no significant mineralization occurs. Classified into Type III A – autosomal d ominant Type IIIB – autosomal recessiveIn both gene defect is unknown. Most common type of AI. Teeth are norma on eruption but the enamel is very soft and easily lost. Enamel is yellow brown on eruption and turns to brown black due to staining. Autosomal recessive are more severe than the dominant type. Radiographically the density is similar for both enamel and dentin. CONCLUSION An understanding of the many disturbances of development of teeth is predicated upon s thorough understanding of the embryology of these structures.Genetic factors are undoubtedly of importance in the development of these defects. REFERENCE: ? Oral pathology by Shafer ? Oral pathology by Somes and Southam ? Oral & maxillofacial pathology by Naville ? Developmental defects of teeth by www. UNC DENTISTRY. com ? Oral histology by Orban’s ? Oral histology by Tencates ? Normal and abnormal dental development- by Isabelle Miletich & Paul T. Sharpe Human Molecular Genetics, 2003. ? Mouse models of t ooth abnormalities Eur J Oral Sci 2008; 116: 1–10

How Does Fatigue Affect Labour Productivity

1) How does fatigue affect Labour Productivity? Fatigue affects labour productivity by impairing the ability of a worker to carry out his/her required duties as expected and in a safe manner. With increase in fatigue comes a reduction in muscular strength, attention to details and loss of concentration. A worker or employee who is gradually losing strength, losing concentration and not giving attention to details is usually more prone to mistakes and would not be able to work at his/her optimum level.Fatigue has also been known to affect employee health. A common example is Chronic fatigue syndrome (CFS), which is a debilitating chronic illness affecting various people worldwide (Lin et. Al. , 2011). Those affected endure chronic, incapacitating physical and mental fatigue that is not relieved by rest. This illness is exacerbated by physical or mental exertion and is accompanied by impaired memory and concentration, unrefreshing sleep, muscle and joint pain, and other defining sympto ms (www. ncbi. nlm. nih. gov).It doesn’t require rocket science to assert that an employee/worker whose health is adversely affected would never perform any given task to satisfaction. 2) Major factors that contribute to increase in fatigue in workers. * Working conditions * Noise: Wokocha and Sopruchi (2010) in their study explained that noise effects are both health and behavioural in nature. He further said that unwanted sound can damage Physiological and psychological health. And any worker whose health is affected cannot perform any given task properly.Noise pollution can cause annoyance and aggression, hypertension, high stress levels, tinnitus, hearing loss, sleep disturbances, fatigue, make conversation difficult as well as leads to productivity losses due to poor concentration. * Heat stress: heat stress occurs when the body takes in and/or produces more heat than it gives off, thus raising the core body temperature beyond normal. It could happen due to the combinati on of high air temperature, high humidity, high radiation heat input, high energy expenditure (due to physical workload) and high metabolism (Groover, 2007).Heat usually hampers the ability of an employee to work efficiently. * Cold * Humidity * General state of health of employees * Nature of work * Posture during work * Muscular exertion * Tediousness * Stress * Repetitiveness with a short cycle. * Jobs that require high concentrations * Eye strain ( Kanawaty, 1992) 3) How the use of machines negatively affect workers The use of machines especially in manufacturing industries is usually accompanied with noise, vibration, monotony, and high concentration on the part of the workers who use them.The accumulated effects of vibrations usually affect the hands and the arms; monotony creates boredom and a job that requires a high level of concentration usually requires a lot of energy. All these contribute to a gradual reduction in muscular strength and an increase in fatigue; as fatigue increases, attention and concentration decreases, making the worker more prone to injuries and a subsequent loss in productivity. 4) The reasons for giving workers more relaxation allowances for using some machines while others require less.More relaxation allowance| Less relaxation allowance| 1) Partial or complete absence of noise reduction components on machines| Presence of noise reduction components on machines. | 2) A high level of machine vibration| A considerable level of machine vibration| 3) Attention not given to reduction of vibration and noise. | Ergonomically built machines with attention given to noise and vibration reductions. | | | References. Jin-Mann S Lin, Stephen C Resch, Dana J Brimmer, Andrew Johnson, Stephen Kennedy, Nancy Burstein and Carol J Simon(2011).The economic impact of chronic fatigue syndrome in Georgia: direct and indirect costs. Journal of Cost Effectiveness and Resource Allocation. Volume 9. Retrieved from http://www. resource-allocation. com/co ntent/9/1/1 on 15/11/2012 Wokocha G. A. and Sopruchi Ihenko (2010). Industrial Noise Level and its Impact on Oil Company Workers in Rivers State, Nigeria. Middle Eastern Finance and Economics ISSN: 1450-2889 Issue 8. Retrieved from http://www. eurojournals. com/MEFE. htm on 15/11/2012. Groover, M. P. (2007). Work Systems and The Methods; Measurement and Management of Work. pp 661

Healthcare Past Essay - 927 Words

Healthcare: Past, Present and Future Nervahna Crew MUSTAFA ABDELWAHID Policy, Politics and Ethics In January 22, 2012 Pick two similar federal policies that were discussed over a span of two different administrations. For example, President Clinton’s and Obama’s health care policies or President’s George H.W. Bush’s and George W. Bush’s foreign policy. Discuss the historical perspective of the time when each policy was discussed or implemented. What was the context or the problem of the day and the urgency for the policy? Analyze the social, economic, and political environments for the times the policies were discussed or implemented. Criticize each policy for its effectiveness of the time. Use four to five credible and reputable†¦show more content†¦President Bush had this idea of imposing a tax break for those that were buying health care coverage would be able to itemize this as a deduction for taxes. The bottom line is that you could find yourself receiving a credit or paying an additional sum for the insurance coverage you have. It always comes down to money with Bush when more often than not, those that can afford to take a high deductible plan and pay the out of pocket expenses would get that money back if this would have passed. This wouldn’t have benefits all families with the economy being what it was during his administration. Obama’s hands-off style may be his way of avoiding what befell the Clintons during the 1990s. Most of us recall the secrecy that Hillary Clinton insisted on, behavior that upset her allies on Capitol Hill and fueled her critics with enough fodder to kill reform quickly. On the other hand, Shields also noted that Obama may have â€Å"overlearned† that lesson and is giving too much away by outsourcing reform. Health Reform and Obama’s Leadership the healthcare blog By Rahul Parikh. 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