Dr Pip Garner
Dr Pip Garner is a bone biologist and post doctoral research fellow at the University of Leeds who works on the variability in the human spine. As well as research and lecturing, in 2012 she was recognised by The Society of Biology for her science public communication work which has included demonstrations at the Cheltenham Science Festival and the organisation of a forensics summer school.
So at school you’re always told the body is made of cells. It’s a little white lie.
On becoming interested in science
I’ve always been curious. I was always that kid that went on the field trips to…we used to have a field study centre near our school that we used to go on three or four times a year. I was always the kid that got asked to stop asking questions! Or stop answering questions, or I was always fascinated how everything worked, specifically how the human body worked. You know, what would gross most people out I’ve always been fascinated with. And it’s the same with most of my family actually, I think.
But when I was ten my dad got cancer. And I think that was…it was quite a hard time but it also made me want to know; I spent a lot of time in the hospital with him and made me want to know more about what actually happens when the body goes wrong as well. So from then I wanted to be a science researcher. I never wanted to be a doctor, I always wanted to be the person who found stuff out behind the scenes. And I thought I wanted to go into cancer research but as I developed I actually fell in love with bone research, but that’s what got me started.
On becoming a bone biologist
So, my background, I came from being a medical scientist specialising in anatomy. I’ve always loved to know about the human body and how it works, um, and from there I ended up getting interested in bone. So my PhD was in disconnections within bone and how that alters when we age ‘cause bone is a very specialised tissue, it’s very, very dynamic. A lot of people just think bone is a dead material. We actually know it’s living and it changes every day. Your bone is not the same from one day to the next. And so we wanted to look at, when you get old, why sometimes this…it can’t heal properly or it breaks. So something like osteoporosis or also looking at something like osteoarthritis.
On current research
I’m looking at actually characterising the human spine. So I’m taking the techniques that I learnt in my PhD, which was to look at how cells communicate – or in the case of something like osteoporosis how they’re no longer communicating – and look at strength things, so bone’s like a honeycomb, it’s like a Crunchie bar. And the struts break, so I’m trying to map where those struts break and figure out why people have osteoporotic fractures in the spine. And then we’re trying to relate that to something. Maybe it’s the shape of the spine, maybe it’s the intervertebral discs, if they’ve lost height or something like that. So it’s a bit of a pluto study trying to look at all different things and how they might interact.
So I’m going to be working with a much bigger group of actual medical engineers that work at the University of Leeds, and in particular some computer modellers. They do some very fancy techniques with something called finite element modelling and that’s hopefully going to be used when we plug in…what we’d like from medicine, and regenerative medicine and surgery techniques, is to make patient specific treatments but unfortunately that’s not always possible. But what we are trying to do is if we can gain enough information about an individual person, put that into some sort of computer model, and then that will predict what the best treatments for that person would be. Whether it’s a certain kind of surgery, whether it’s using a certain kind of, say, bone_cement, these sort of ideas. So it should be used by, hopefully, surgeons to predict, like I say, what the best treatment is. We call it patient stratification.
On artificial replacement research
So at Leeds we kind of look at it from two ways. So we have a lot of simulators that can test things like artificial joints. So, looking at hips was the first one we looked at. We’re quite extensively looking at knees, um, total disc replacements, they go into the spine to replace the intevertebral discs and we’ve also just started on something like the ankle. And our sort of job, we think, at Leeds, is to try and get the best materials, um, make sure they’re put in the best way to make them last longer for the patient. And if they are failing, if they’re not working as well as they should, why? What are those specifics?
But then the other way we’re also looking at it is, if the technology’s all well and good putting in artificial joints, and they’re much better than they’ve ever been, but we’d actually like the body to heal itself. That’s sort of the holy grail of what we’re going towards. So looking at regenerative medicine. So one of the things we’re looking at is, so, if you need to replace a piece of tissue at the moment, putting it just from one person to another or from an animal donor into a person, it’s going to be rejected. The immune system’s going to take over and you either have to have a patient on immunosuppressive drugs for the rest of their life, as they would if they had an organ transplant, or you can have a piece of tissue that isn’t going to work for very long. So we actually have a technique to take out the cells, because it’s the cells that set off this reaction.
So then if you take the cells out, we’re left with what you call a biological scaffold. We can put that into the body and the body puts its own cells back in. So that’s quite a cool way to get the body to fix itself.
They’re actually natural scaffolds. There are some people looking at synthetic scaffolds, but we use natural scaffolds. So it’s tissue. So if we want to replace a piece of tendon we actually take a piece of tendon and then take the cells out. And what we’re left with is something we call extracellular matrix.
So at school you’re always told the body is made of cells. It’s a little white lie. We tend to be made of lots of extracellular matrix with a few cells in it. So we take the cells out and what we’re left with we test microscopically to check we’ve definitely got all the cells out and then we mechanically test as well to check that it still works how it should, and amazingly, it does.
On future discoveries and research
I hope we discover more of the fundamentals of why things go wrong. So we’re trying to fix all these diseases but actually we don’t know how they start, a lot of them. So, I know that’s not very specific but I’d quite like a generic, across the board, better understanding of how things work because we’re never going to be able to fix them properly unless we know that. So for me, I suppose, why some people fracture with osteoporosis and some people don’t. I think that’s quite an achievable goal. But overall, why things happen!