Chapter 25 – Tribology and biomaterials




Abstract




Mode 1: Wear from two articulating surfaces that are intended to rub together, such as the femoral head and the poly.


Mode 2: Wear from an articulating surface and a non-articulating surface, such as the femoral head and the shell.


Mode 3: Third-body wear, which is particles coming between bearings.


Mode 4: Wear between non-articulating surfaces such as the neck and the edge of the shell.





Chapter 25 Tribology and biomaterials


Iain McNamara and Majeed Shakokani



Structured oral examination question 1


Picture of THA with osteolysis shown.



EXAMINER: This is an X-ray of a THA in an elderly patient complaining of pain. What do you see (Figure 25.1)?





Figure 25.1a and 25.1b Anteroposterior (AP) and lateral radiographs of hybrid THA with areas of osteolysis around greater trochanter.




CANDIDATE: Plain radiographs of a reverse hybrid THA with a significant area of osteolysis in the greater trochanter.




EXAMINER: What do you think caused this?



CANDIDATE: Potential causes are infection, poly wear …



EXAMINER: Tell me about wear.



CANDIDATE: Wear is a progressive loss of material from the surface of a body owing to relative motion at that surface generating debris.



EXAMINER: What types and modes of wear do you know?



CANDIDATE: Well there are four modes of wear and various types of wear (I couldn’t remember how many).





  1. Mode 1: Wear from two articulating surfaces that are intended to rub together, such as the femoral head and the poly.



  2. Mode 2: Wear from an articulating surface and a non-articulating surface, such as the femoral head and the shell.



  3. Mode 3: Third-body wear, which is particles coming between bearings.



  4. Mode 4: Wear between non-articulating surfaces such as the neck and the edge of the shell.



EXAMINER: OK, how about types of wear?



CANDIDATE: There are mechanical and chemical. Mechanical includes abrasive, adhesive, fatigue, third-body and fretting. Chemical includes corrosive and corrosive fretting.



EXAMINER: Do you know how we can measure wear?



CANDIDATE: There are linear and volumetric wear which are two methods of measuring wear. Volumetric wear measures the volume of material lost in cubic millimetres per year or per million cycles. Linear wear measures the penetration of the component into the other and is measured on X-rays. For example, the bigger the femoral head the greater the volumetric wear and the smaller …



EXAMINER: Are you sure? Poly has changed over the last 50 years. So, tell me then, what’s the ideal size of a femoral head?



CANDIDATE: [I was waiting for him to ask me this question, I had some papers in mind and drawings.]


McKee and Farrar [1] used large heads and had minimal dislocation but significant wear, Charnley [2,3] initially used size 41.5-mm diameter femoral heads but had massive wear and early failure. He then used 22.25-mm femoral heads and reduced his wear, but bearing in mind that polyethylene quality wasn’t like the ones we have these days, highly cross-linked poly. There are various factors that increase wear in a THR, they include thickness < 6 mm, malalignment of components, young patients, men and activity levels.



EXAMINER: OK, let’s move on, how does osteolysis happen?



CANDIDATE: It’s a histiocytic response to wear debris.



EXAMINER: OK, what does that mean?



CANDIDATE: It’s a cascade of events that ends with osteoclast activation. It starts when the macrophages are activated by the debris. They release osteolytic factors like TNF-alpha, osteoclast-activating factor and interleukins. This activates osteoclasts and cause osteolysis. Osteolysis causes micromotion of the prosthesis which then causes further debris. Also, as the patient walks they release the debris into the effective joint space causing further inflammatory response and lysis [4].



References



1.McKee GK, Watson-Farrar J. Replacement of arthritic hips by the McKee–Farrar prosthesis. J Bone Joint Surg Br. 1966;48:245259.

2.Charnley J. Surgery of the hip-joint: present and future developments. Br Med J. 1960;1:821826.

3.Charnley J. Arthroplasty of the hip. A new operation. Lancet. 1961;1:11291132.

4.Ingham E, Fisher J. The role of macrophages in osteolysis of total joint replacement. Biomaterials. 2005;26(11):12711286.


Structured oral examination question 2




EXAMINER: Tell me about synovial fluid.



CANDIDATE: Synovial fluid is produced by the synovial membrane in the joint. It is a dialysate of blood plasma without the clotting factors, haemoglobin or RBC. It contains hyaluronic acid, lubricin, proteinase, collagenases and prostaglandins. The main function is to lubricate articular cartilage and nourish it through diffusion. It exhibits non-Newtonian flow characteristics.



EXAMINER: Tell me about lubrication.



CANDIDATE: Lubrication is when a film of lower shear strength is present between two bearing surfaces, reducing friction. There are two main hypotheses surrounding joint lubrication in synovial joints.



EXAMINER: What is friction?



CANDIDATE: The resistance of two surfaces to slide against each other.



EXAMINER: Tell me about the two hypotheses surrounding joint lubrication in synovial joints.



CANDIDATE: The first is fluid-film lubrication, in this hypothesis the joint surfaces are separated by a fluid film which fully supports the applied load, preventing contact between the surfaces. The minimum thickness of the fluid film must exceed the surface roughness of the bearing surfaces in order to prevent asperity contact.


The second is boundary lubrication. In this situation, the bearing surfaces are in contact but separated by a boundary lubricant of molecular thickness, which prevents excessive bearing friction and wear. In boundary lubrication the load is carried by the surface asperities rather than by the lubricant.


It is thought that fluid-film lubrication dominates in synovial joints. However, realistically, both fluid-film and boundary lubrication occur in synovial joints, depending on the specific joint in question and the particular type of loading applied.



EXAMINER: Do you know the lambda ratio?



CANDIDATE: This is the ratio of fluid film thickness to surface roughness, in fluid film it’s 3 and in boundary it’s less than 1.



EXAMINER: Can you tell me about the different types of fluid-film lubrication?



CANDIDATE: There are various types of lubrication, they include hydrodynamic lubrication (HD), elastohydrodynamic (EHD), micro-elastohydrodynamic (MEHD), squeeze film, weeping and boosted lubrication.


In hydrodynamic lubrication there is no contact between the joint surfaces. The surfaces are separated by a thin fluid film which supports the applied load. In simplistic terms, the movement of the joint surfaces in parallel with one another creates a thin, wedge-shaped fluid film between the surfaces which prevents them from contacting one another.


A model that is more likely in synovial joints is elastohydrodynamic (EHD) lubrication. In this model, the cartilage is not considered to be rigid, as it is in the previous model; rather it is elastic and deformable. In EHD lubrication, elastic deformation of the bearing surface enlarges the area of the surface and traps pressurized fluid. This in turn increases the capacity of the fluid film to carry load and decrease stress within the cartilage.


A modification of the elastohydrodynamic model of lubrication is micro-elastohydrodynamic lubrication (MEHD). The micro-elastohydrodynamic lubrication model assumes that the asperities of articular cartilage are deformed under high loads. This smoothes out the bearing surface and allows a fluid film to be created which is sufficient for fluid-film lubrication.



EXAMINER: Tell me about weeping lubrication.



CANDIDATE: Weeping lubrication happens when cartilage is compressed – tears of lubricant fluid are generated from it. Contrary to boosted lubrication where the water is compressed into the cartilage leaving behind a concentrated fluid pooled with hyaluronic acid in the joint.



EXAMINER: What are asperities?



CANDIDATE: These are the projections from the articular surface; the taller they are, the rougher the surface, also increasing friction.



EXAMINER: OK, what types of lubrication happen in prosthetic joints?



CANDIDATE: Well, it is believed that boundary lubrication predominates but mixed conditions do occur. Lubrication occurs through a pseudosynovial fluid that is created over the surfaces.


Different surfaces have different affinity to the lubricant, this is called wettability and can be measured by the angle of contact at the edge of the drop of the lubricant applied to that surface. For example, ceramics are more hydrophilic than metals, thus they have improved lubrication and lower friction (Figure 25.2).





Figure 25.2 Lubrication [I drew this picture at the same time].




EXAMINER: OK, so what else decreases friction in the joint?




CANDIDATE: The cartilage.



EXAMINER: So, tell me about cartilage.



CANDIDATE: Cartilage is a highly differentiated connective tissue made of cells, extracellular matrix (ECM) and water. The cells are chondrocytes and ECM includes fibres, collagen (mainly Type II), elastin, proteoglycans, cartilage oligomeric proteins (COMP) and cartilage matrix protein (CMP).


COMMENT: If you have answered all questions and they have time they might ask you a question to fill the 5-minute time. Cartilage is a very common question and you need to know it by heart. I used the above definition (cells, matrix and water) to answer questions on bone, cartilage, meniscus, ligaments and tendon and just changed the cell component and the ECM (i.e. it is made of water, cells and matrix).


This definition helped me to relax and start building up for that station.



Structured oral examination question 3



Bone




EXAMINER: What makes up bone?



CANDIDATE: Bone is a highly differentiated connective tissue made up of cells (10%) and extracellular matrix 90% (ECM). The cells are: osteoblasts, osteoclasts, osteocytes, bone lining cells. The ECM contains inorganic and organic matrix, the inorganic matrix includes calcium hydroxyapatite and osteocalcium phosphate. The organic matrix includes collagen Type I, proteoglycans, non-collagen matrix proteins (osteocalcin, osteonectin, osteopontin), growth factors and cytokines.


Bone is the primary reservoir of calcium, and also contains the haematopoietic marrow and plays a mechanical role in supporting the body’s tissues. It can be divided into woven bone which is immature bone with randomly organized collagen fibres and no lamellae making it weak but flexible. It’s found in growing bone and pathological bone.


Lamellar bone is mature bone with organized layers and its structure is arranged according to the stress on the bone. It is found at the periosteal surfaces.


Cortical (compact) bone forms the cortex of long bones. Also in flat bones it comprises 80% of the adult bone.



EXAMINER: Can you draw cortical bone for me (Figure 25.3a)?





Figure 25.3a Drawing of cortical bone.




EXAMINER: Which cell forms the majority of the bone cells?




CANDIDATE: The osteocyte forms approximately 90% of bone cells, it forms from osteoblasts. It controls the calcium and phosphorus metabolism responding to chemical, mechanical and electrical stimuli.



EXAMINER: Tell me about the osteoclasts.



CANDIDATE: Osteoclasts are large multinucleated giant cells; they differentiate from haematopoietic precursors. They resorb bone within pits or depressions known as Howship’s lacunae. When laying on bone they have a contact area called ruffled borders which increase their surface area. Bisphosphonates work on the ruffled borders.



COMMENT: I was drawing something like this as I talked (Figure 25.3b).





Figure 25.3b Osteoclast.




EXAMINER: How does the blood reach it?




CANDIDATE: Bone receives 5–10% of cardiac output. There are various systems that supply it: nutrient artery system (high-pressure), metaphyseal–epiphyseal system and periosteal system (low-pressure). The nutrient artery enters mid diaphysis and divides into ascending and descending branches supplying the inner two-thirds of the cortex. All three systems are interconnected, and the direction of flow is centrifugal (inside to out).



EXAMINER: How is bone metabolized?



CANDIDATE: A complex interplay and interaction of various hormones, growth factors and cytokines regulate plasma calcium and phosphate levels. They include vitamin D, PTH and calcitonin.



EXAMINER: How does vitamin D regulate calcium?



CANDIDATE: Vitamin D is either taken through diet or activated in the skin by ultraviolet light. Vitamin D enhances the absorption of calcium and phosphorus from the small intestine and enhances osteoclast resorption from bone. In the kidneys it causes increased calcium retention and phosphate excretion (Figure 25.3c).





Figure 25.3c Vitamin D metabolism.



Structured oral examination question 4



Bone grafts



EXAMINER: So, you have a patient with a tibial plateau fracture on your operating table and you find a big bony defect that needs filling. How do you approach that?



CANDIDATE: Bearing in mind this is a basic science station I went straight for the kill and mentioned bone graft.



EXAMINER: What types of bone grafts do you know?



CANDIDATE: There are autografts, allografts and zenografts. Also, there is demineralized bone matrix (DBM), synthetic, bone morphogenetic protein (BMP) and stem cells.



Autograft utilizes bone obtained from the same patient receiving it. It can be harvested locally or from a distant site like the iliac crest. It has all the good properties of a graft, it is osteoconductive, osteoinductive and osteogenic. It can be cancellous, cortical or vascularized. Cortical provides structural support whereas cancellous is used for its osteogenic properties.



Allografts are obtained from a different patient than the one receiving it. They are taken from cadavers or living donors such as femoral heads. They are available in different methods depending on their processing and preservation, deep frozen–70°C, freeze dried –169°C and fresh. They are not as good as autograft as they have osteoconductive properties only and some osteoinductive properties.



EXAMINER: What would you use for your case?



CANDIDATE: Well it depends on the individual case, but I would prefer to use autograft as it has no immunogenicity, no risks of disease transmission and is cheap, but it has donor site morbidity whereas allografts have no donor site morbidity, but are slow to incorporate …



EXAMINER: Ahhh, what’s graft incorporation?



CANDIDATE: It is the process by which invasion of the graft by the host cells and the graft is then replaced either partially or completely by host bone or rejected. This happens in stages:





  1. 1. Inflammation, stimulated by the necrotic debris.



  2. 2. Osteoblast differentiation from precursor cells.



  3. 3. Osteoinduction where osteoclasts and blasts are stimulated.



  4. 4. Osteoconduction: new bone starts to form.



  5. 5. Remodelling, which continues for years.



EXAMINER: So, we know how an autograft is taken, do you know the process of allograft donation and bone banking?



CANDIDATE: Yes, living donors are consented and in case of cadavers as long as there is lack of objection from next of kin then it can be harvested.


The donors get screened for comorbidities and bloods are taken. They are screened for history of intravenous drug abuse, malignancy TB, steroids. Bloods for hepatitis B & C, HIV, syphilis and Rhesus status.


The graft goes through processing of cleaning then preservation. The graft gets debrided from unwanted tissue, treated with ethanol/antibiotic soaks/irradiation and then preserved either fresh, fresh frozen or freeze-dried.



EXAMINER: OK, quickly tell me about the synthetics and what you are going to use for this tibia?



CANDIDATE: (I realized I have told him all about bone graft but not told him what I will use).


Synthetics are commercially available products. The main constituents are either calcium sulphate, calcium carbonate, calcium triphosphate or hydroxyapatite. I will use calcium phosphate derivative because Russell et al. (JBJS Am 2008) performed an RCT of autograft vs. calcium phosphate cement in tibial plateau fractures and showed significantly reduced rates of subsidence, also Buckley published similar results in 2009 in calcaneal fractures.



References



1.Russell TA, Leighton RK. Comparison of autogenous bone graft and endothermic calcium phosphate cement for defect augmentation in tibial plateau fractures. A multicentre, prospective, randomized study. J Bone Joint Surg Am. 2008;90(10):20572061.

2.Johal HS, Buckley RE, Le IL, Leighton RK. A prospective randomized controlled trial of a bioresorbable calcium phosphate paste (alpha-BSM) in treatment of displaced intra-articular calcaneal fractures. J Trauma. 2009;67(4):875882.

Sep 7, 2020 | Posted by in ORTHOPEDIC | Comments Off on Chapter 25 – Tribology and biomaterials

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