Arthritis: A collection of about 100 diseases that affect the joints of the human body

Introduction 

Arthritis is a collection of about 100 diseases that affect the joins of the human body, mainly causing pain and inflammation. Indeed, the name arthritis is a combination of two Greek names from the phrasal noun joint pain. The classification of the many diseases that amount to arthritis is made based on their causes, their signs and symptoms as well as management and curative regimens (Cosman, et al, 2014). In many cases, arthritis diseases have many correlations raging from the classifying attributes indicated above. From a general perspective however, age plays a major role in a majority of arthritis cases with increase in age being directly proportional to susceptibility to any form of arthritis. Lifestyle also plays a major role in some forms of arthritis with obesity being a major exacerbating factor. However, arthritis can also be caused or exacerbated by blood related complications and other ailments making arthritis a secondary condition (Smolen et al, 2016). Among the most common forms of arthritis are osteoporosis, osteomalacia, rheumatoid arthritis, gout, and osteoarthritis whose particularization from a comparative perspective forms the essence of this research paper. 

Overview of the Diseases 

Osteoporosis 

Osteoporosis affects the bones rather than the joints and a secondary factor has to come into play for the advent of osteoporosis to be discovered. In definition, osteoporosis is a disease that occurs when for some reason, the bones become extremely weak and susceptible to fracturing upon minute pressure. Common breakages associated with the disease include broken limbs and broken spinal column. The results of the disease cause chronic pain as well as the inability to carry out normal life functions (Cosman, et al, 2014). 

Osteomalacia 

Osteomalacia is a deficiency disease that results in the weaknesses of the bones due to the lack of bone forming and maintenance minerals such as vitamin D. The disease can affect individuals at any point of growth with the version affecting small children being referred to as rickets. The condition is in most cases mild and treatable through the introduction of the mineral that had been deficient in the body. Apart from vitamin D, osteomalacia can be caused by deficiencies in phosphate and calcium. Bone brittleness hence ease of fracturing can be a result of the disease but even without breakage, the advent of the disease can cause pain and distortion of both bones and muscles (Zhang et al, 2016). 

Rheumatoid Arthritis 

Rheumatoid arthritis is specific to joints and entails the warming and swelling of joint which results in chronic pain. This is caused by an autoimmune disorder, which causes the natural immunity system within the body to react adversely towards a certain part of the same body. The immune disorder has been associated with type major histocompatibility complex (MHC) antigen HLA-DRB1. The most common joints to be attacked by this disease are the wrist or other joints of the hand albeit other body parts can also be affected that do not have joints. These secondary non-joint related effects may include a lower red cell count, the inflammation of the chest cavity around the lungs or the heart. Therefore, whereas rheumatoid arthritis is mainly a disease of the joints, it can affect the whole body and be even life threatening (Smolen et al, 2016). 

Gout 

Gout is a blood related joint inflammation disorder that has a tendency of attacking the big thumb of the foot or the hipbone. It is mainly attributed to the increase of uric acid in the blood which in turn causes joint inflammation and debilitating pain within 12 hours of its advent. However, the disease may also affect the vital organs in the body and result in tophi, kidney stones and urate nephropathy. The disease has been closely associated with lifestyle issues with most a higher propensity for the disease being found among those who eat meat and drink beer excessively or are obese. The pain in the joint is caused by the deposition of uric acid crystals at the joint (Rees et al, 2013). 

Osteoarthritis 

Osteoarthritis is a disease of the joints that causes their swelling, distortion, and inability to move in ways that are natural to the joint, limb or digit. This results from the breakdown of the joint cartilage and the bone underlying the said cartilage. Ordinarily, the onset of pain and other adverse symptoms only happened after some extreme activity to the joint such as overuse or exercises. With time however, the joint will become visibly distorted and the pain constant. Among the bones and body parts commonly affected include the fingers of the hand more so the thumb, the lower part of the neck, the knees and also the hip joints. The advent of the disease will be mild with debilitating symptoms taking years to commence. The effects of the disease are mainly limited to the joints (Berenbaum, 2013). 

Comparative Analysis 

Pathophysiology 

In biology, pathophysiology which is also referred to as physiopathology relates to where pathology meets with physiology in the analysis of the advent and progress of a condition. Pathology relates to the general effects and progress of a disease while physiological relates to the physical condition of the body. Physiopathology, therefore, comes into play when the progress of a disease begins to affect the physical state of the body. Arthritis mainly affects the bones and by extension the muscles hence a majority of the physiology is premised in the endocrine musculoskeletal systems. However, some diseases such as osteomalacia will also affect the muscles and will have a neurological effect. Extreme cases of Rheumatoid arthritis may also affect the heart leading to a cardiovascular pathophysiology (Smolen et al, 2016). 

Most diseases that fall under arthritis engender a conjunction between pathology and physiology thus making physiopathology paramount in defining and understanding these diseases. With regard to osteoporosis, the advent of the disease is not caused by the existence of any pathogen based ailment in the body. It occurs naturally through the normal wear and tear activities of life. Two main factors will, therefore, come into play; the first is how strong the bones were ab initio, based either on genetics or nutrition (Cosman, et al, 2014). The second factor is how the body has been used over time. The combination of weaker bones and high use or abuse will lead to a high susceptibility for the advent of osteoporosis. From a pathophysiological perspective, it is important to note that no matter how much osteoporosis develops pathologically, it will never manifest physiologically unless an outside force causes a fracture. This is the pathophysiological peculiarity of osteoporosis as compared to all other arthritis. A careful or lucky patient can live with the condition for years as it develops pathologically without any physiological effects (Cosman, et al, 2014). 

The pathophysiological exact opposite of osteoporosis is gout. In the exact opposite of how the pathological advent of osteoporosis does not manifest physiologically, the advent of gout has physical manifestations within hours of its advent (Rees et al, 2013). However, these physiological manifestations are not visible ab initio but involve extreme and debilitating pain. With passage of time, as gout continues to progress pathologically, the affected part will swell and also redden. Therefore, with regard to gout, the pathological and physiological progression are contemporaneous and correlated. The more the uric acid levels increase in the body, the more the acid crystals are deposited in the affected joint or body part thus the more the physiological manifestations of pain, reddening and swelling increase (Rees et al, 2013). This is as opposed to osteoporosis whose physiological manifestations have little to do with the pathological progression of the disease per se but rather on the external pressure applied to the bones thus causing fractures. 

The above analysis also establishes that osteomalacia correlates with gout and differs with osteoporosis from a pathophysiological perspective. Pathologically, osteomalacia, being a deficiency disease continues to exacerbate with the increase in deficiency on the nutrient that is causing the disease (Zhang et al, 2016). The disease may also retrogress with the treatment more so one that includes introduction of the right amount of the deficient nutrient. However, the nutrient is important that the start of osteomalacia pathologically will be closely followed by the physiological manifestations of pain and distortion of both bones and muscles. The exacerbation of the disease pathologically also results in the increase in physiological manifestations and vice versa (Zhang et al., 2016). 

Rheumatoid arthritis is also very similar in pathophysiological progression with gout hence places it in league with osteomalacia and contrary to osteoporosis. From a parenthetic perspective, rheumatoid arthritis develops when the body defence begins to react adversely to a body part. Just as with gout, the physiological manifestation of the advent of rheumatoid arthritis will be very rapid but not initially visible (Smolen et al., 2016). The rheumatoid arthritis patient will experience a lot of pain and discomfort but visible manifestations will only come in with the pathological development of the disease. The same will also apply to the retrogression of the symptoms upon treatment. 

Osteoarthritis on the other hand, can be considered as the osteoporosis of the joints. It involves the normal wear and tear factor but for the joint based on nature and nurture. As with osteoporosis, the advent of physiological manifestations will take some time before being felt as the disease progresses pathologically. However, osteoarthritis differs exponentially from osteoporosis in that when the disease progresses pathologically to some extent, physiological manifestations will appear without any external force input. The affected joint may initially only ache when moved but with time, it will ache even at a point of rest. Further, the joints will also swell and get distorted. Finally, osteoarthritis and osteoporosis are similar as once the disease progresses physiologically, pathological mitigation will not result in physiological improvement unlike gouts, rheumatoid arthritis, and osteomalacia (Smolen et al, 2016). 

Etiology 

Etiology in biological sciences entails the study of causes of a disease as well as the reason for the advent of the said disease. With regard to arthritis, the causes of the disease differ greatly. Two of the referenced diseases are caused by natural causes; osteoarthritis and osteoporosis which are similar in causation with the main differences being in how the diseases progress and which parts of the body they affect. Osteoarthritis and osteoporosis both develop from the normal functions of life and, therefore, like many forms of cancer, their development is based on a combination of genetics and lifestyle, a combination commonly referred to as nature and nurture (Cosman, et al, 2014). The nature part is mainly genetics and involves how strong the bones initially are for osteoporosis and how well formed the joints initially were for osteoarthritis. 

The better the bones or joints initially, the lower the likelihood of the advent of osteoarthritis and osteoporosis. Better genes may also ensure a later advent of the said diseases. The nurture part involves the kind of nutrition that was taken by an individual which had either a positive or negative impact on the bone or joint respectively. Finally, the nurture part also involves how the joints and bones have been used over time. The harder the joints or bones have been used over the time the higher the propensity of development of osteoarthritis or osteoporosis respectively. It can, therefore, be said that the etiology of osteoarthritis and osteoporosis is limited to the bones and/or the physical body (Cosman, et al., 2014). 

The other three forms of arthritis; rheumatoid arthritis, gout, and osteomalacia have their etiology based on non-bone related issues with only their manifestations affecting the bones themselves. Gouts and osteomalacia have their cause mainly premised on nutrition and lifestyle, which has little to do with bone structure or movement. The advent of gouts is mainly caused by the consumptions of foods that lead to the deposition of too much uric acid in the blood. As the blood flows within the body, crystals of the uric acid become deposited in a joint thus causing the advent of the arthritis named gout (Rees et al., 2013). 

Similarly, the cause for osteomalacia is the lack of minerals in the diet, hence in the blood. These minerals include Vitamin D, calcium, and phosphate (Zhang et al., 2016). The deficiencies make it impossible for the body to either form bones properly or maintain them properly, leading to the disease. Finally, rheumatoid arthritis is caused by a long term autoimmune disorder that happens when the natural immunity of the body for some reason affects a part of the same body. This means that the advent and proliferation of rheumatoid arthritis has nothing to do with the bones or joints that will eventually be affected by the disease (Smolen et al., 2016). Therefore, whereas all the 5 diseases affect the bones, only osteoporosis and osteoarthritis originate from the bones or joints with the rest originating elsewhere then affecting bones and/or joints. 

Manifestations 

In biology, the manifestations of a disease are its signs and symptoms through which the existence of the disease in an organism can be identified and/or diagnosed. The five diseases forming the basis for this research paper are members of the group arthritis and therefore have some primary manifestations that relate to one another. However, the diseases also have some major peculiarities that separate them from other diseases within the same group. Osteoporosis for example, has symptoms that remain hidden until an event happens to reveal it. This event is related to the application of sudden or forceful pressure on the bone thus forcing it to break. 

Whereas all bones can break upon application of enough pressure, with osteoporosis very little pressure will result to a major fracture. For example, the lifting of an object can result in a fracture in the backbone of a small tap with a hard object result in the fracture of a limb. Therefore, osteoporosis does not manifest by itself but will require a secondary force (Cosman, et al., 2014). Osteomalacia on the other hand, has definite manifestations that will take place without external force as the disease progresses. These include pain in the bones and joints especially along he spinal column and the legs. As the disease progresses, muscles will weaken making walking difficult and changing gait. The pelvic may then flatten and the bones bend. The bones and joints will also become weak leading to ease of fracturing (Zhang et al., 2016). 

Rheumatoid arthritis affects both joints and other body parts including the skin and vital organs such as the kidney, lungs, and the liver. The initial manifestation involves only one joint that will swell, become tender, warm, and stiff. With time however, the symptoms will manifest in more joints in the body. An extreme manifestation is the development of synovitis, which will result in the loss of movement in the part of the body served by the affected joint. A rheumatoid nodule can also develop on the skin near the affected joint, mainly towards the end of a limb. These are the ordinary signs of rheumatoid arthritis with the effects on vital organs being considered as related complication (Smolen et al., 2016). 

The normal manifestation of gouts includes the most common, which is the reddening, heating up, and extreme pain on the big toe. However, the joint pain can also affect the heels, the knees, the wrist and the finders. The amount of pain experienced is usually inversely proportional to the temperature the patient is in. On rare occasions, the patient may also feel fatigued or develop a high fever (Rees et al., 2013). The symptoms of osteoarthritis closely relate with those of rheumatoid arthritis and include the swelling, distortion and pain in the hands, feet, spin, hips, and knees. The main difference between osteoarthritis and rheumatoid arthritis is that with osteoarthritis, the pain reduces with rest or lack of use of the joints (Berenbaum, 2013). 

Possible Complications 

Osteoporosis does not have possible pathological complications by the physiological manifestations through multiple fractures can increase to the point of completely eliminating the possibility of movement. Fracture in the spine or the skull can also cause neurological complications (Cosman et al., 2014). Few complications are related with osteomalacia save for the possible advent of hypophosphatemia for phosphate based osteomalacia (Zhang et al., 2016). Rheumatoid arthritis however, has the highest propensity and wide for complications. These include fibrosis of the lungs, renal amyloidosis, myocardial infarction and stroke. From a neurological perspective there is a risk of Peripheral neuropathy and mononeuritis multiplex (Smolen et al., 2016). Gouts on the other hand, have known complications in the case too much uric acid crystal deposits take place leading to the formation of tophi. Excessive tophi can however lead to bone erosion. Precipitation of uric acid in the kidneys can also result in the formation of Kidney stones. The probable complication for osteoarthritis is joint effusion (Berenbaum, 2013). 

Current Diagnostic and Treatment Modalities 

The diagnosis and treatment of osteoporosis mostly begins when the diseases have manifested through a fracture. Several diagnostic regimens have been developed including conventional radiography which is combined with CT scans or an MRI. However, the most recognized diagnostic system currently is the Dual-energy X-ray absorptiometry (DXA) (Cosman et al., 2014). To exceed the level of weakness or damage to the bone, chemical biomarkers are used. Osteoporosis is mainly controlled through change of lifestyle and increased care to avoid fractures. From a pharmacological perspective however, Bisphosphonates are used to reduce propensity for fractures. Postmenopausal osteoporosis has also been shown to be effectively treated through Teriparatide. Raloxifene is also used only to prevent the debilitating spinal fractures (Cosman, et al., 2014). 

Being a deficiency based condition, osteomalacia is mainly diagnosed through testing of levels of minerals such as Vitamin D in the body. The technetium bone scan is also used to diagnose osteomalacia. Common treatment mainly involves the administration of vitamin D but will vary on whether the disease is caused by lack of minerals or malabsorption. Weekly administration of vitamin D for 6 weeks cures osteomalacia caused by basic deficiency but in the case of malabsorption, daily injections or oral dosing for the same duration will be necessary (Zhang et al., 2016). Rheumatoid arthritis is diagnosed using both x-rays and blood tests. MRI and ultrasound can also be used. Blood tests involve the rheumatoid factor (RF) and the measurement of Anti-citrullinated protein antibodies (ACPAs). Rheumatoid arthritis has no known cure but its adverse symptoms can be controlled pharmacologically using disease-modifying antirheumatic drugs (DMARDs) and benzodiazepines such as diazepam for pain relief (Smolen et al., 2016). 

The diagnosis of gouts is undertaken through identification of monosodium urate crystals in synovial fluid or a tophus. The initial treatment of gout is through administration of Nonsteroidal anti-inflammatory drugs (NSAIDs) (Rees et al., 2013). Those who are intolerable to NSAIDs can be treated with Colchicine. Joint injection with the steroid Glucocorticoids has also been found to be effective. Recently, Pegloticase was also approved for the treatment of gouts. Osteoarthritis is a progressive disease and its diagnosis is done through monitoring the continued changes in the shape and nature of the affected joints. X-rays can play a role in the continued monitoring process to show how the joints have been changing over time to differentiate between osteoarthritis and normal ageing. Known treatments for osteoarthritis include pharmacological intervention, surgery as well as alternative medical approaches (Berenbaum, 2013). Pharmacological treatments include the use of NSAIDs such as Naproxen and COX-2 selective inhibitors such as celecoxib are used. Joint replacement surgery has been proven to be effective in the treatment of osteoarthritis including the replacement of knee joints and hip joints. Alternative medicine includes the use of Glucosamine and chondroitin as well as Avocado/soybean unsaponifiables (ASU) (Berenbaum, 2013). 

Conclusion 

It is clear from the instant research that all the aforementioned diseases; osteoporosis, osteomalacia, rheumatoid arthritis, gout and osteoarthritis all qualify to be under the group arthritis as they all eventually affect human structure and movement components. These mainly include joints and bones with a number of them also affecting muscles. Two of the diseases; osteoporosis and osteoarthritis can however, be considered as a normal part of the aging process. These are the culmination of the wear and tear of the human structure during the course of life. The extent of wear and tear is affected by the nature and nurture of specific individuals. Osteomalacia and gout are both nutritional ailments the first caused by lack of minerals and the latter too much uric acid. However, Rheumatoid arthritis is independent as it is caused by an immunity disorder that causes the natural immunity system to attack a part of the body. Most of these diseases save for osteomalacia are mainly common among the older population. Gout and osteomalacia can be treated with a possibility for full recovery. There is however no known cure for rheumatoid arthritis and its treatment requires observation and control. With regard to the wear and tears diseases aforesaid, treatment only involves protecting the affected parts or replacing them through surgery. 

References 

Berenbaum, F. (2013). Osteoarthritis as an inflammatory disease (osteoarthritis is not osteoarthrosis!).  Osteoarthritis and Cartilage ,  21 (1), 16-21 

Cosman, F., De Beur, S. J., LeBoff, M. S., Lewiecki, E. M., Tanner, B., Randall, S., & Lindsay, R. (2014). Clinician’s guide to prevention and treatment of osteoporosis.  Osteoporosis international ,  25 (10), 2359-2381 

Rees, F., Jenkins, W., & Doherty, M. (2013). Patients with gout adhere to curative treatment if informed appropriately: proof-of-concept observational study.  Annals of the rheumatic diseases ,  72 (6), 826-830 

Smolen, J. S., Breedveld, F. C., Burmester, G. R., Bykerk, V., Dougados, M., Emery, P., ... & Scholte-Voshaar, M. (2016). Treating rheumatoid arthritis to target: 2014 update of the recommendations of an international task force.  Annals of the rheumatic diseases ,  75 (1), 3-15 

Zhang, Q., Doucet, M., Tomlinson, R. E., Han, X., Quarles, L. D., Collins, M. T., & Clemens, T. L. (2016). The hypoxia-inducible factor-1α activates ectopic production of fibroblast growth factor 23 in tumor-induced osteomalacia.  Bone Research ,  4 , 16011