The bone disorders

The study maladysIntroduction in that respect ar m either contrastive types of osmium disorders and these skunk call for vast implications on a patient suffering from each exceptional one of these oculus sinister disorder. There 7 master(prenominal) categories of grind away disorders listed below, each of which will be discussed in detail. genic ( transmitted) disorders, i.e. Achondroplasia, Osteogenesis imperfecta. Nutritional disorders, i.e. Rickets, Osteomalacia. Autoimmune disorders, i.e. Rheumotid Arthritis Degenerative disorders, i.e. Osteoarthritis. organise tumours, i.e. base Bone Cancer, Secondary Bone Cancer. Hormonal disorders, i.e. Osteoporosis. P rile alongts infirmity.Genetic (inherited) disorders.Achondroplasia.Achondroplasia is genetical disorder and is the of import type of unaw atomic number 18s-limbed dwarfism that takes place in benignants, occurring amongst 1 in 15,000 and 40,000 live births. It has been estimated that active 90% of cases of achondroplasty ar sporadic, and on average, there is a mature of paternal age at the effect of conception of affected individuals (Vajo et al., 2000).The literal meaning of achondroplasty is without the formation of cartilage, and sufferers hold back difficulty with overdress branch. Achondroplasia affects principally tenacious cram e.g. legs and arms. It is an autosomal Dominant Gene Defect (ADGI), and endures to the conversion of cartilage into dress up. It occurs when one of the 22 non-sex genes is mutated, and this mutated gene has now been identified to be located on chromosome 4, which is know to be the Fibroblast Growth Factor Receptor 3 (FGFR3).SymptomsAchondroplasia is typically distinguished by the formation of a long, narrow trunk and short limbs. whatsoever azoic(a) usual symptoms of achondroplasia embarrass hyperextensibilty of knocks in particular at the knees and hands, stock-still the rotation of the elbow is limited as tumesce being unable t o fully extend. Sufferers of Achondroplasia super hotly contrive a large head, short broad hands, and suffer from hypertonia (poor ponderousness tone). spinal cord compression at the cervicalmedullary junction is a nonher typical swash of achondroplasia patients (Horton et al., 2007).The location of the mutated gene associated with achondroplasia was mapped to chromosome 4p16.3 in 1994, and this was followed soon after(prenominal) by the identification of the heterozygous mutations of FGFR3 (Rousseau et al., 1994).It has been upgrade disc overed that children that have FGFR3 mutations, they p arnts in the main do non have the FGFR3 mutation, and there has withal been a immobile association between advanced paternal age, in particular over 35 years of age.DiagnosisBe understanding the symptoms of achondroplasia are precise distinguishable, the diagnosis at birth should not be a problem. thus far, it has been estimated that about 20% of individuals are not referd wit h achondroplasia at birth (Trotter et al., 2005). A commonality manner that has been employed and widely employ for the diagnosis of achondroplasia is antepartum echography. This method detects effected foetuses in the third trimester of pregnancy.The diagnosis of Achondroplasia plunder be carried out via CVS (Chronic Villus Sampling), followed by molecular gene discharges. CVS is a strain that is carried out before birth, in which cells are inspected. Molecular genetic examen is carried out in order to advert possible mutations.TreatmentThere is no clear come up toment for achondroplasia, and there are legion(predicate) tests that are ongoing in order to do find one. The use of human sireth hormone has been proposed as a possible method of diplomacyment. Tests have shown that there was an initial amplification in appendage estimate of subjects with achondroplasia, nevertheless, the semipermanent benefits of such treatment have not been made clear, and many experts d o not recommend it (Horton et al., 1992).In order to incr reliever the stature of achondroplasia patients, surgical limb lengthening is another proposed method to suspensor achondroplasia patients. The typical method compromises of different wads being broken, i.e. femur, tibiae, and humeri, after which orthopedical appliances are utilise in order to carry out decompress up stretch during the healing process. Although this method increases the standing height of the patient, this method is to a fault not recommended due to the many knottinesss arising from it. These complications let in, the need of repeated surgeries, wound infections and problems arising from the stretching of skeletal tissue such as rake vessels.Osteogenesis Imperfecta.Osteogenesis imperfecta is a operating system disorder causing imperfect de ivory formation. It effects around 1/5,000 to 1/10,000 individuals (Sillence et al., 1979). It occurs as a result of a poor feeling of collagen or a lack of co llagen production, and bathroom lead to slim jams that are easily broken and have a low organise mass. Another distinguishable characteristic of osteogenesis imperfecta patients is an s-shaped spine that croupe ultimately break.Osteogenesis imperfecta occurs as a result of mutations in the genes that encode the chains of type I collagen. Type I collagen is the main protein found in chock up. Genetically inherited cases of osteogenesis imperfecta normally show very subdued symptoms. However, spontaneous cases are a lot more severe.SymptomsThe symptoms of osteogenesis Imperfecta range in severity, from intrauterine fractures and perinatal lethality, to very mild fractures.DiagnosisThe diagnosis of osteogenesis imperfecta in individuals with a family story of the unsoundness is or else simple, but more difficult in those that do not have a family history.Generally osteogenesis imperfecta is diagnosed clinically, and based on the physical symptoms associated with the disease Osteogenesis imperfecta offer be diagnosed via a collagen biopsy test, which is a saucily method. This test is known to identify 90% of osteogenesis imperfecta cases.Ultrasound is another method that privy be use for diagnosis, and merchantman detect more severe types of Osteogenesis imperfecta, even at the foetus phase and overly 16 weeks into pregnancy.Test such as those that include culturing cells, and observing the collagen produced understructure also be carried out, as well as using blood samples to examine mutations of the collagen manufacturing genes. Although these types of tests tramp be effective in the diagnosis of osteogenesis imperfecta to some extent, they are generally no more than 85% accurate.TreatmentCurrently there is no known cure for osteogenesis imperfecta. However particular emphasis has been placed on prevention on imperfection and maintaining sun-loving pearls particularly in boyisher children.Supplements of calcium and atomic number 15 dish up increase organise density. Also Biophosphates are employ, and these are drugs that serve well decrease the rate of fig out resorption. Biophosphates have been clearly shown to prevent machinate fractures from occurring and also increasing the lift up strength and density. Growth hormones has been previously proposed as a possible treatment for osteogenesis imperfecta (Kruse and Kuhlencordt, 1975). However this has been later dismissed, and although the use of growth hormone in combination with Biophosphates may be a useful treatment, this has not merely been tested.Metal bone plates are also utilise for patients with more severe fractures, and helps to prove and reduce fractures of the affected bones, mainly long bones e.g. arms and legs. Nutritional disorders.Rickets and Osteomalacia.Rickets is a nutritionary bone disorder which is found in children. It is known to affect about 1 in 1000 children in the UK wholly. A very corresponding disorder takes place amongst a dults and this is known as osteomalacia.Both these disorders occur as a result of abnormal mineralisation (calcification) of bone and cartilage. The tree trunk transfers calcium and vitamins from the bone into the blood due to vitamin need i.e. deficiency in Vitamin D and calcium. This demineralization by and by leads to bone deformity, and thus the bones become soft and very vulnerable to fractures.There are many reasons that cause vitamin deficiency that subsequently leads to rickets and osteomalacia. Some of which include nutritional deficiency (poor nutrition), poor life-style (lack of work out), insufficient sunlight image (remaining indoors for long full stops of duration) and abnormal metabolism (liver and kidney disease, chronic renal failure etc) (de Menezes Filho et al., 2006). Another main cause of rickets in children is due to the baby receiving a lack of vitamin D in the womb from the mother who may also be deficient in vitamin D.SymptomsSymptoms of rickets and osteomalacia include Growth retardation. Deformities in the upper and lower limbs. depleted weight gain in children. High vulnerability to bone fractures. Bone imposition. Muscle weakness. Pelvic flattening. Bowing legs. Defects in structure of teeth.DiagnosisA physical testing will beginning(a)ly help to identify bone deformities and multiple fractures. A medical history check can also help to identify a possible genetic link.The levels of parathyroid hormone and alkaline phosphate will increase in the blood as a result of deficiency in vitamin D and calcium. These hormones are prudent for the transfer of minerals and vitamins from the blood to the bone. This rise in the bloodstream is a study sign of rickets and osteomalacia, and blood tests carried out to see this elevated rise of these hormones is a salutary method for diagnosis.X-rays can also show the demineralisation of the bone and reveal any abnormal bone structures.Treatment surrogate vitamin D, calcium, and oth er necessary minerals in patients with rickets and osteomalacia is very important, and is the main method of treatment.Babies that cleard a lack of vitamin D whilst in the womb of their mother, or a shortage from their mothers milk should be given vitamin drops, e.g. Abidec, to help increase their levels of vitamin D.Food rich in Vitamin D and calcium are passing advised, and offer a replacement for their deficiency. These types of food include oily angle (tuna, salmon herrings, mackerels), dairy products (milk, yoghurt), liver, Vitamin supplements can also be prescribed from a doctor.An injection of vitamin D (calciferol) is also purchasable and can last up to a year before another injection is needed. Adequate exposure to sunlight is also highly recommended.Autoimmune disorders.Rheumatoid arthritis (RA).It has been estimated that at to the lowest degree 1 in 100 the great unwashed suffer from RA, and that in the UK alone there are about 400,000- 500,000 sufferers. It is a chr onic inflammatory disease mainly affecting synovial membrane, cartilage and bone. This then can lead to marijuana cigarette destruction, which is typically distinguished by gradual bone erosion, and is the main cause of disability in RA.RA causes the immune system to parachuting producing antibodies, which attack the lining of joints (synovium), and tissues ( tendons), and so thus resulting in irritation and swelling. In response to this, the body releases a special synovium thickening chemic which causes the joint to wear away and loose its shape, and eventually the joint is altogether destroyed. RA is also systemic and can riddle to other tissues and other parts of the body causing more problems mainly in the hands, feet and spine. In very severe cases the disease can spread to organs and this can be very critical. RA does not occur at a particular age group, and the disorder can develop at any age in sufferers lifetime. However, more comm save RA occurs in patients that ar e between the ages of 30 to 60 years old. The causes of RA are thus far relatively unknown, however that have been several theories involving possible genes that can cause RA (Barton and Worthington, 2009). RA may also occur as a result of pollution (bacteria, fungi, viruses).SymptomsSymptoms of RA include Swelling of joints. Stiffness, particularly early in the morning. Inflammation. Formation of rheumatoid nodules, which appear on hands, feet and elbows. Flu desire symptoms such as fever. Weight issue.DiagnosisThe diagnosis of RA is sooner difficult, due to the fact that the main symptoms of RA inflammation and joint stiffness/swelling, and these symptoms can be commonly associated with other diseases/disorders. A full family history is looked at first in order to establish any familial traits of RA in the patient.Imaging techniques such as X-rays, CT scans and ultrasound can used to look at rheumatic erosion (the slice of bones/joints). However, it can be difficult to diagno se RA in the early stages of the disorder, as there may not be any physical changes during these stages.The cytokines TNF (tumour necrosis factor) and IL-1 (Interlukin-1) are amenable for just inflammation which occurs in stack that suffer from RA. Both of these cytokines are present in the joint of passel with RA, and checking for the strawman of these cytokines at joints is a method used to diagnose RA.ESR (erythrocyte sedimentation rate) is also another blood test that can be used to diagnose RA. It is a measure of the rate in which red blood precipitate in a period of 1 hour, and is a non specific measure of inflammation.The CRP test (C-reactive protein test) is the second nearly(prenominal) popular diagnosis test for RA. In response to inflammation of tendon/ligaments, the liver produces C-reactive proteins, and this test is used to detect the movement of these proteins in the blood. The antibody RF (Rheumatoid factor) is present in the blood of sufferers of RA. Therefo re blood tests to identify the presence of this antibody in the blood, 8 out of 10 times will diagnose a person that is suffering from RA.TreatmentCurrently there is no clear treatment for RA, however there a few drugs available that either help tranquillise some of the symptoms, or to help veer the disorder. Pain killers such as paracetamol and ibuprofen can help relieve some of the symptoms of RA.NSAIDs (non-steroidal anti-inflammatory drugs) are also a set of paroxysm killers e.g. diclofenac, ibuprofen and naproxen, and help to control joint pain and stiffness. Although these drugs help with the symptoms of RA they do not directly impede the development of RA. Furthermore, there are many common side effects associated with NSAIDs including diarrhoea, nausea, change magnitude risk of myocardial infarction etc.Disease modifying anti-arthritic/antirhumatic drugs (DMARDS) are drugs that function by stoppage the affect of certain chemicals i.e. TNF spare-time activity the damage of bone, joints, tendons and ligaments. These drugs not only ease the pain and stiffness related to RA, but also slow the progression of the condition.Maintaining a healthy lifestyle for an individual suffering from RA is also vital as it reduces the chances of win complications arising from the disease. There are also many therapies e.g. acupuncture, hydrotherapy, and also arthroplasty which can significantly help with the pain and joint stiffness linked to the disorder.Degenerative disorders.Osteoarthritis (OA).Osteoarthritis is an age-related disease that last has an effect on each individual, who live onto they senior years (Wong and Carter, 2003).The pain associated with osteoarthritis typically emerges from the degeneration of the cartilage between the joints, as a result of primary osteoarthritis, or from trauma bringing about the mischief of cartilage (Temenoff and Mikos, 2000). Given that cartilage demonstrates a poor ability to self-repair, these injuries are sustained for years and can ultimately bring about further degeneration (secondary osteoarthritis) (ODriscoll, 1998). The degeneration of cartilage causes bone ends to become exposed, and the deposition of new osseous tissue on the bone ends. This also reduces the space in the joint cavity and limits movement (Gerard J. Tortora, 2007). The underlying bone also forms osteophytes (spikes) which grow outwards due to the bone compensating for the loss of cartilage, and this hinders joint movement and causes pain. It has been estimated that roughly 36 million Americans are diagnosed with this form of arthritis (Temenoff and Mikos, 2000). Osteoarthritis is also the main reason as to why many individuals undergo hip and knee replacement surgery (Wilson et al., 2005), and is also the main cause of mobility impairment in elder individuals (Buckwalter, 1997).SymptomsAcute pain causing stiffness and lack of joint movement is the main symptom of OA. The capsule surrounding joints become big due to infl ammation and this reduces mobility, and thus muscles at the joint become weaker. otherwise symptoms include spasm and contractions in the tendons accumulation of fluid at joints, muscle weakness, and hardy bone enlargements in small joints i.e. fingers and toes.DiagnosisThere is no single test used to diagnose OA. A physical examination can show a lack of mobility, joint weakness and swelling. X-rays can show the loss of joint space and in extreme cases the presence of osteophytes. TreatmentThere is advanced research going into ways to manoeuver cartilage to help patients suffering from OA, although a major breakthrough has yet been developed. Instead a healthy lifestyle i.e. loss of weight and exercise is highly advisedSufferers are advised to exercise the affected subject field as this will enable better support for affected joints and strengthen the muscles surrounding the joint. This also helps in increasing the mobility of the joints, balance and posture. Drugs such as NSAID s (non-steroidal anti-inflammatory drugs) i.e. ibuprofen can help in relieving pain and cut inflammation. However the long term use of these types of drugs can cause many adverse reactions.Bone tumours.A Bone tumour is the neoplastic growth of tissue in bone i.e. cells in tissue continually dividing resulting in the formation of the tumour, and can be benign or malignant. This tumour can further spread throughout the body via the lymph system. The lymph system contains lymphocytes and phagocytes, and a further function of the lymph system is to remove worn out red blood cells.There are two main categories of bone tumours, primary bone tumours and secondary bone tumours. autochthonic bone tumours can be place or can spread (malignant), and these bone tumours derive from within the tissue. Primary tumours can be further divided into benign tumours and cancer. Secondary bone tumours derive from other tumours from a different part of the body and spread to the tissue via the blood.Th e mutation of the P53 gene which suppresses bone tumour is thought to responsible for the formation of bone tumours however the exact cause is still not fully known.There are many different types of bone tumours, of which the most common are listed below, including symptoms, diagnosis and treatments. Osteosarcoma- This is the most common type of bone tumour, and as well as Ewings syndrome (see below), is the most aggressive type of bone tumour. It affects people at an early age (5-25years), and is rare in people of above the age of 30. Osteosarcoma is a malignant tumour and eventually will spread throughout the body. It is also known to start in the cavities within the bone, and is it affects long bones mainly the knee.Osteosarcoma is diagnosed via examination and imaging techniques such as magnetic resonance imaging or CT scan.Osteosarcoma if commonly treated by surgery and chemotherapy before and after the surgery. Ewings Sarcoma- Just same(p) Osteosarcoma, Ewings sarcoma affec ts people at a young age (5-15 years), and also the selection rate up to 3 years is a 60% chance. Ewings sarcoma in mainly found in the lower extremity, than the upper extremity (Eggli et al., 1993)Some of the symptoms of Ewings disorder include pain and swelling, warmth of the local area, and the appearance of onion plant undress.Ewings disorder can be diagnosed via MRI and CT scans.Treatments of Ewings disorder include surgery, radiation and multi-drug chemotherapy (Eggli et al., 1993). Chondrosarcoma- This bone tumour affects the chondrocytes of cartilage tissue and subsequently, the tissue eventually becomes cancerous. Chondrosarcoma can occur at any age, and this tumour grows slowly and normally without any pain. Lymphoma- Lymphoma is cancer of lymphatic cells, and usually begins in the lymph node, but can also form in the bones. Multiple Myeloma- This bone tumour occurs as a result of bone marrow cells befitting cancerous and can cause osteolytic bone damage. It usually occ urs in people above the age of fifty five, and men are twice more likely to get it than women.The main symptom of multiple myeloma is pain, as well as normochromic anemia, spinal cord compression and renal insufficiency.Multiple myeloma can be diagnosed via MRI and CT scans.Chemotherapy, bone marrow transplant as well as Bisphosphonate drugs are some of the main treatments for multiple myeloma. Osteroid Osteoma- This tumour occurs as a result of the matrix of bone becoming cancerous. It normally occurs twice as often in males than females. It more commonly takes place in the proximal femur, then mainly in the tibia, followed by posterior elements of the spine and the humerus (Bloem and Kroon, 1993). gross symptoms include dull pain which gets worse during the night, an increase in skin temperature, increased sweating and abnormal growth.Radiological scans and CT scans are common methods for diagnosis.Non-steroidal anti-inflammatory drugs are given as part of the treatment for ostero id osteoma as well surgical removal. Osteoblastoma- Osteoblastoma is a benign tumour in bone tissue and occurs when osteoblast cells become cancerous. It is mainly common in children and young adults. Pain and bone mass reduction are the main symptoms of osteoblastoma. regularity of diagnosis for osteoblastoma includes x-rays, microscopic examination of osteoblast cells and a biopsy.Surgical removal of the tumour is a common treat for this bone tumour as well as cryosurgery, radiation and chemotherapy.Hormonal disorders.Osteoporosis.Osteoporosis results in bones becoming porous and these pores become bigger (2 times bigger) in cancellous cortical bone. It occurs as a result of a reduction in bone mineral density (bone mineralisation). It is a direct disease of the bone as compared to some of the other bone disorders mentioned above. During osteoporosis the rate of bone renewal is gradual than bone breakdown and it commonly affects the hip, wrists and spine. It is estimated that ov er 3 million people in the UK alone suffer from osteoporosis.There are two main types of osteoporosis (Type I and Type II).Type I osteoporosis occurs mainly in females following menopause. Following menopause there is a deficiency in oestrogen and testosterone and this disorder is known as postmenopausal osteoporosis.Type II is mainly caused by a poor lifestyle i.e. excess smoking and drinking. This leads to a deficiency of calcium and vitamin D as a result of disorders of the intestine. The deficiency may also arise from kidney disorders caused by a poor diet (too much fast foods and fizzy drinks) and excess alcohol consumption. Also people continuously taking drugs mainly corticosteroid drugs will have a loss of bone density.SymptomsOsteoporosis does not have any specific symptoms however its main outcome is an increased risk of bone fractures and breaks, and also an increased risk of falling due to fractures of the wrist, spine and hip.DiagnosisBone mineral density (BMD) test to measure bone mineral density was the first test used to diagnose osteoporosis. There are many different types of BMD tests, the most common being quantitative ultrasound. This is a very good method for diagnosis and is also a much safer approach than x-rays and radiography, which can also be used to diagnose osteoporosis.Blood tests to identify deficiencies in calcium and vitamin D are a further method for diagnosis.Treatmentshormone replacement therapy (Hormone Replacement Therapy) was initially used to treat postmenopausal osteoporosis, however its used was later stopped due to its many side effects e.g. heart cancer, blood clotting, stroke etc.Bisphosphonates can be used to treat osteoporosis and it functions by slowing down the breakdown of bone, in order for the body to cope with bone renewal. Bisphosphonate intolerancy was then later discovered in 20 % of people.Calcitonin drugs are another type of drug used to treat osteoporosis. Calcitonin is produced naturally in the thyro id gland, and calcitonin drugs work by directly inhibiting osteoclast activity. Calcitonin is also found naturally in salmon. atomic number 38 Renelate is another drug that can be used and helps to promote bone renewal.Calcium and vitamin D supplements also help to slow down osteoporosis. set is also highly advised for osteoporosis sufferers and has been shown to maintain or increase bone mineral density especially in postmenopausal women.Pagets disease.Pagets disease is a bone disorder associated with a disorder in bone remodelling, and affects 10% of elderly people (Barker et al., 1980). Furthermore it is more prominent in males than females. In Pagets disease there is an increase in bone remodelling which is also disorganised, and this caused by a primary abnormality of osteoclast cells (Hosking et al., 1996). The bone turnover is increased by 40%, and in addition, bone is grown in areas where bone is not needed and removed from areas where bone is required.Pagets disease is now referred to as osteoclast pagetic disease. In the disorder, the osteoclasts which are bone cells responsible for the removal of bone are targeted. over a period of time osteoblast activity subsequently increases in response to osteoclast activity, and helps in forming new bone. However, the new bone that is formed is a lot larger and thicker because of the very fast remodelling process, but critically the inner parts of the bone are porous, and a lot more fragile and tender. This therefore makes the bone more venerable to fractures and breaks. Below is an illustration of a particular deformity associated with Pagets disease sufferers (see Figure 2.)Symptoms/complications union pain and bone paint are common symptoms associated with Pagets disease. As the disease progresses the swelling and involution of the bone leads to the expanding bone becoming weaker. Also the initial symptoms of Pagets disease are not clear but do become clearer over time as the disorder develops.Fractures of long bones e.g. tibia, femur, pelvis, spine, skull are common symptoms of Pagets disease as well as skeletal deformity.Arthritis is a common complication which arises from Pagets disease and occurs mainly in the proximal ends of long bones.A further complication of Pagets disease is Gout. Gout arises from the excessive production of uric acid and salts leading to gouting arthritis, which is a disease of uric acid metabolism. The build up of uric acid and salts in the bloodstream leads to accumulation at the bone joints/cartilage which then causes kidney stones. Bone tumours, and in particular cancellous bone tumour can arise as a result of gout.The dysregulation of bone can also cause an increase in blood circulation and can consequently bring about heart failure.Compression of nerves is also seen in sufferers of Pagets disease and is caused by bone expansion and this brings about complications in movement. Also nerve compression in the skull brings about a loss of hearing and v ision.DiagnosisX-rays is a very clear method to help detect bone expansion, bone loss and bone deformity.Alkaline phosphate which is a by-product of any type of bone disease/disorder is present in the bloodstream, and so blood test can help to identify the presence of these.TreatmentBisphosphonates and calcitonin are common drugs used to treat Pagets disease. These drugs bind to osteoclast cells and increase their activity, thus reducing their breakdown, and reabsorption of bone into the bloodstream.Pain killers can also be taken to help ease bone pain and neuralgic pain.It is also advised that Pagets disease sufferers should receive adequate sunshine, adequate amounts of vitamin D, and maintain a healthy lifestyle i.e. healthy diet and regular exercise.ReferencesBarker, D.J., Chamberlain, A.T., Guyer, P.B., and Gardner, M.J. (1980). Pagets disease of bone the Lancashire focus. Br Med J 280, 1105-1107.Barton, A., and Worthington, J. (2009). Genetic susceptibility to rheumatoid arthr itis an emerging picture. Arthritis Rheum 61, 1441-1446.Bloem, J.L., and Kroon, H.M. (1993). Osseous lesions. Radiol Clin North Am 31, 261-278.Buckwalter, J.A.a.H.J.M. (1997). Articular Cartilage. Part II Degeneration and Osteoarthrosis, Repair, Regeneration, and Transplantation. 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