The reflections on the central role of inflammation in both human health and human disease in this blog post considers the chapters ‘Acute Inflammation’, ‘Classification of Inflammation’, ‘Chronic Inflammation’, ‘Healing and Repair’, and ‘Infection and some Infectious Diseases’ in the prescribed textbook General Pathology by J.J. Rippey. This post explores the physiology of inflammation in different pathological situations, namely injury due to various aetiologies and infection, and its role in healing leading to human health as well as its role in human disease and how it contributes to the overall pathology.
In reading the relatively simple and concise definition of inflammation as “the reaction of vascularised living tissue to local injury” (Rippey, 1994: 125) I felt that it doesn’t quite convey the vast impact that inflammation has on the human body! It is a process that we can experience almost constantly in different forms due to the many injuries that a body can experience over a lifetime, ranging from very minor to very severe. For every injury that our bodies experience inflammation follows, it is the initial response of the body – the almost daily minor mechanical injuries of little bumps leading to small bruises and minor cuts in the skin from accidents in the kitchen or garden, as well as exposure to the many infective microbes on a daily basis that our body deals with without our conscious knowledge, will mean that some part of our body is in one stage of inflammation or another almost constantly. Acute inflammation is a linear progression of events in response to a stimulus and is pertinent to the examples just mentioned. (Leisegang, 2012) It is also pertinent to my own seasonal run-in with inflammation – in the winter, due to the cold weather and not having the greatest peripheral circulation, I experience the discomfort of mild chilblains in some of my toes. These chilblains display the cardinal signs of inflammation of rubor (redness), calor (heat), tumor (swelling) and dolor (pain), as well as functiolaesa (loss of function) as it is sore to walk on them! (Martini & Nath, 2009) The stimulus for this inflammation is an idiopathic abnormal vascular response to cold causing slight tissue injury. (Raza, 2006) The chemical composition of the interstitial fluid is altered because of the cold changes and damaged cells release prostaglandins, proteins and potassium ions. (Martini & Nath, 2009) This in turn triggers the inflammation process, which is ‘designed to neutralise the injurious agent in some way’ (Rippey, 1994) and to remove the consequences of the injury, such as any necrotic cells (AFP785, 2009) and to facilitate healing. I’m not going to go into the process of the inflammatory response itself as it is covered very well in the video below. (Khanacademy, 2010)
So far I have been looking into acute inflammation with my mild winter chilblains as an example. I want to take this example further by looking into classification of inflammation. This is done taking into consideration the duration of the inflammation, the nature of the inflammatory exudate, and the site of the inflammation. (Rippey, 1994) In reflecting on what I have been taught I would classify the inflammation I experience each winter as acute in duration, with very mild serous exudation, and with the anatomical site of perniosis. “Inflammation, although a response to a stimulus, may contribute to the overall pathology” (Leisegang, 2012: 16). Acute inflammation may go on to develop into chronic inflammation for many different reasons – chronic inflammation is a circular progression of the inflammatory response which is prolonged and where ‘destruction and inflammation are proceeding at the same time as attempts at healing’. (Rippey, 1994) The differences between acute and chronic inflammation at tissue level can be seen in the diagram below. An example of chronic inflammation is osteomyelitis, where the inflammatory response to the infected bone causes swelling which leads to ischaemia and necrosis because of the unyielding nature of the bone. The dead bone prevents draining of pus, delays healing and leads to a chronic inflammatory situation needing medical treatment. This is demonstrated in the lower diagram.
In the past month our household has been hit by the recent seasonal virus, a rather nasty cold that started with a sore throat. This has been the result of an infection with a parasitic micro-organism termed a pathogen which probably gained access to my family members’ bodies via direct spread through inhalation and then overcame the body’s defence mechanisms. The portal of entry was probably the epithelium of the throat due to the first symptom of the cold. The pathogen was then able to multiply and cause tissue damage leading to local inflammation and later accompanied by the systemic effects of inflammation being malaise, increased body temperature and decreased appetite. (Rippey, 1994) Luckily, the immune system of my family members worked well and without the need to take medication the ultimate result of this experience was recovery! The diagram above shows how the body’s immune system in conjunction with the inflammatory process worked to fight off the infection. In reflecting on this chapter in the textbook I remembered when I had tick-bite fever a few years ago. I was walking a wilderness trail in Hluhluwe-iMfolozi National Park when, unknowingly, I was bitten by a tick and infected with Rickettsia conorii. The first I knew of this was a week later when I had an unusual and persistent headache, stiff neck, and a swollen, blackish, crusted eschar on my upper thigh. Luckily the tick-bite fever was diagnosed and treated before the maculopapular rash appeared! (Rippey, 1994)
After the inflammatory response comes healing and repair. The video above clearly shows the process of wound healing and repair. I have personally been able to witness this over the past month on a macroscopic level as my partner healed from a hernia operation. His surgical wounds healed by first intention, a process that will take about six weeks to complete. Being a month into this process I think he is at the point where the collagen fibres have been laid down, probably the type-I fibres at this point, and the scar is contracting slowly to increase tensile strength. The diagram below shows the process of healing by first intention. (Rippey, 1994: 160) I have spent many happy hours explaining this all to him 🙂 I’m not entirely sure how much he has enjoyed the experience though!
In conclusion, by reflecting on the physiology of inflammation in different pathological situations – namely injury due to cold, infection and mechanical injury due to surgical wounds, also in the pathophysiology that occurs during chronic inflammation – I feel I have come to understand the central role that inflammation plays in human health and human disease.
AFP785, 2009. Pathlogy: Acute Inflammation. Available at: <http://www.youtube.com/watch?v=3oUxDsZp71Y> [Accessed on 7 April 2013].
Elcheguevarra, 2012. Wound Healing – Integumentary System 3D. Available at: <http://www.youtube.com/watch?v=iXfM13u3mp8> [Accessed on 7 April 2013].
Khanacademy, 2010. Inflammatory Response. Available at: <http://www.youtube.com/watch?v=FXSuEIMrPQk> [Accessed on 7 April 2013].
Leisegang, K., 2012. Module Descriptor: general pathology NAT311. University of the Western Cape, unpublished.
Martini, F.H. and Nath, J.L., 2009. Fundamentals of Anatomy and Physiology. 8th ed. San Francisco: Pearson Benjamin Cummings.
Raza, N., 2006. Chilblains at Abbottabad, a moderately cold weather station. Journal of Ayub Medical College, 18(3), pg25-28. [online] Available at: <www.ayubmed.edu.pk/JAMC/PAST/18-3/06Naeemraza.pdf> [Accessed on 7 April 2013].
Rippey, J.J., 1994. General Pathology. Johannesburg: Witwatersrand University Press.