Questions about neoplasia

neoplasia drawing square

Here are some really good questions about neoplasia. These are all questions from dental students in previous years’ classes – but maybe some of them will resonate with you.

Q. I don’t understand what is a non-neoplastic epithelial cell and what specifically is a neoplastic cell.

A. A non-neoplastic epithelial cell is just a regular old epithelial cell, sitting there in the skin or in a gland, doing its job and dying off when it’s supposed to.

A neoplastic epithelial cell is part of a tumor, and although it may look somewhat like a regular epithelial cell, it is able to divide and multiply on its own, regardless of external signals. We’ll talk about some other features of neoplastic cells on Wednesday – there are several! – but it’s the ability to grow on their own that really defines tumor cells. They just keep dividing, despite not being told to do so by the body. Pretty soon, there are so many that they actually make a visible or palpable mass. And if you don’t do anything, the mass will get bigger and bigger.

Q. By the definition of neoplasia (new excessive growth) I don’t understand how a non-neoplastic cell can develop into a tumor. If it is non-neoplastic how can there be no new accelerated cell growth and still develop a tumor?

A. In order to become neoplastic, regular old non-neoplastic cells have to undergo a bunch of genetic changes. You’re right: when they are not neoplastic, they don’t have this property of accelerated cell growth. They’re just regular cells that do their job and die off when it’s time.

But if a normal cell acquires certain genetic abnormalities – like the ability to go through the cell cycle without paying attention to checkpoints, or the ability to turn off the normal mechanisms that keep growth under control, or the ability to activate growth receptors when there’s not even any growth hormone attached – then that cell may end up becoming neoplastic.

Sometimes cells that acquire these abnormalities end up getting killed off by normal means (we have proteins that see when our DNA is mutated, and either fix it, or kill off the cell). But if these protective mechanisms don’t work (if a cell acquires a mutation in one of them), then the cell will live on despite all these mutated genes…and it will divide into two cells, and then into 4, and so on.

Usually there are many, many mutations that a cell has to undergo before it officially becomes neoplastic. And every tumor can have its own specific mutations – they’re not the same in every tumor.

Also: sometimes, as the cell acquires these mutations on the way to becoming a tumor cell (a neoplastic cell), it actually looks different too! This seems to be especially true for epithelial cells. As an epithelial cell starts acquiring mutations and goes down the road that leads to neoplasia, it starts showing signs of dysplasia – it grows to an unusually large size, or the chromatin gets darker, or nucleoli show up, or it starts not respecting its neighbors’ space.

These morphologic changes are pretty predictable: cells become mildly dysplastic, then moderately dysplastic, then severely dysplastic. The more dysplastic they become, the more likely it is that they will continue on down the path to carcinoma in situ (and, evenutally, invasive carcinoma).

This morphologic progression doesn’t seem to happen the same way in non-epithelial cells. Non-epithelial cells (like muscle cells, or fat cells) may undergo some visible changes as they move towards neoplasia – but those changes are not as predictable or universal as the dysplastic changes that occur in epithelial cells.

Q. And why is it restricted to only epithelial cells?

A. If by “it” you mean neoplasia: neoplasia is not restricted to epithelial cells. Any cell in the body – epithelial, muscle, bone, cartilage, blood, fat, whatever – can become neoplastic.

The restriction we talked about in class was related to the dysplasia (as mentioned above). I don’t know why the same dysplastic changes don’t seem to occur in non-epithelial cells – but they don’t.

Q. How can non-neoplastic tumors become invasive without accelerated cell growth?

A. Tumors are neoplastic, by definition (tumor is just another word for neoplasia). So all tumors have this propensity to grow autonomously; some are benign (these are not typically invasive), and some are malignant (these typically are invasive).

Q. Also, are all malignant tumors anaplastic?

A. No – malignant tumors can show any level of differentiation they want. They can be well-differentiated (in which they look almost exactly like their cell of origin), moderately-differentiated (in which they sort of look like their cell of origin), poorly-differentiated (in which they really don’t look much like their cell of origin at all), or anaplastic (in which they look absolutely nothing like their cell of origin – they’re just super pleomorphic, with big ugly nuclei, no architecture, and lots of abnormal mitoses).

That being said: malignant tumors are more likely to be anaplastic than benign tumors. Benign tumors are usually well-differentiated (they are rarely, if ever, anaplastic), whereas malignant tumors can be anywhere on the differentiation spectrum.

Granulation tissue vs. granuloma

Here’s a student question from a previous year that you might find useful.
 
Q. I have a quick clarification question for you about the difference between granuloma and granulation tissue.  I have in my notes that “a granuloma is a type of chronic inflammation where you have macrophages that surround something indigestible like a splinter.”
 
How, then, would you define granulation tissue that is present in the 3-5 days following injury? Is the difference simply that granulation tissue is not necessarily something that surrounds an indigestible particle, but rather a tissue that characterized by the presence of macrophages, collagen/fibroblasts, and blood vessels?
 
A. Yes! You’re on the right track. I think it might be helpful to think about the differences between granulation tissue and granulomas in two categories: function and composition.
 
Function
The function of granulation tissue is to provide the building blocks necessary for the healing of the injured tissue. The function of a granuloma, on the other hand, is to surround and (hopefully) digest foreign substances (splinters, difficult-to-kill bugs like mycobacterium tuberculosis).
 
There really isn’t any crossover, either – you don’t see granulation tissue at the site of a foreign body, and you don’t see granulomas forming in wound healing. So the functions of granulation tissue and granulomas are quite different.
 
Composition
Their composition is different too. Granulation tissue is composed of blood vessels, fibroblasts, and loose extracellular matrix. Granulomas are composed of macrophages and (often) a collar of surrounding lymphocytes. Macrophages do participate in wound healing, but they’re not part of granulation tissue. So the composition of granulation tissue and granulomas are very different too.

Why so sad, Prometheus?

Yeah, an eagle is pecking a little at his liver – but seriously, his face shows a disproportionate degree of anguish.

Prometheus is in a bind (literally: the painting is “Prometheus bound” by Rubens) because Zeus is pissed that he stole the secret of fire. As punishment, Zeus sends an eagle to eat Prometheus’ liver. But the liver has an incredible capacity for regeneration – so overnight, Prometheus’ liver grows back. So Zeus sends the eagle again, and the liver regenerates again…you get the idea.

While it’s probably pretty uncomfortable to have an eagle pecking at your liver, the reason Prometheus is so incredibly upset is probably because to the ancient Greeks, the liver was considered to be the seat of one’s soul and intelligence. Had the eagle been pecking at Prometheus’ spleen, say, or his kidneys, maybe it wouldn’t be such an insult. Of course, these organs can’t regenerate as prodigiously as the liver can – so although Prometheus would be less offended, he’d also be dead.

 

Hey, how are you doing?

We ask each other this question so often – and yet we really don’t expect anything other than “Great!” or “Busy!”

I know we can’t (and shouldn’t) share everything with everyone. That makes sense.

But in dental and medical school, there’s something else going on. Everyone is really smart and talented and gorgeous, and you can’t help but compare yourself – and your skills – with others. So to save face, there’s an implicit rule that you don’t show your real, vulnerable self. You laugh and bitch about tests being hard, but you don’t really talk about how scared and exhausted you really are.

So if you’re not doing well, and you look around and see everyone else laughing and and smiling, you might very well think that you’re the only one who is miserable.

I’ve been thinking about this a lot, because I have had lots of conversations with students over the years, and one of the most common things I hear is some variation of “I just don’t think I belong here.” And I always say, “You most definitely DO belong here; you were chosen from many for a reason; and you are most definitely not alone.” Which may be reassuring to that particular student – but that’s as far as it goes; it doesn’t help the rest of the students who feel that way.

I think we need to talk more about these hidden things. I don’t want to take up a lot of your time, but I think it’s important that you know you are not alone, and that there are things you can do that will get you through tough times.

So from time to time, I’ll be sending out short surveys with questions about mental health/wellness. I’ll use Google forms, so that no emails or names are associated with the responses. That way, we can actually be real and say what we really feel.

Here is the first little survey. It only takes about 5 minutes to do. This whole thing is totally optional, of course – and as I mentioned, totally anonymous. I’ll briefly show you the results in class, and then I’ll post a bunch of resources, videos, and journal articles in case you want to know more.

If you want to participate, please respond by Sunday night (5/29), so I can have a few days to gather the data and make some sense out of it. I’ll send out a quick reminder email Sunday evening.

I’m really curious to see what we find, and really hopeful that you’ll get something useful out of it.

Inflammation lecture summary

Inflammation is a really important topic for you to understand. You’ll be expected to recognize and understand the importance of inflammatory cells in oral pathology lesions. And you’ll also be causing some serious inflammation if you keep poking people with those long sharp silver things.

To help you as you’re studying, I put together a lecture summary (like I did for the Cell Injury lecture) that covers the most important points from the inflammation lecture. Our exam questions will come directly from this summary – so if you understand the concepts in the summary, you should do well on this part of the exam.

If you want a little more in-depth stuff to read, here are a couple posts from my Pathology Student website. Note: these posts are totally optional! They go into a little more detail than you’ll need to know for our exams – however, sometimes it’s helpful to have a different explanation of our content. So use them (or don’t) however you see fit.

  • Neutrophil vs. monocyte. Quick review of what each of these cells looks like and does.
  • How to differentiate acute from chronic inflammation in histologic sections. Hint: it has to do with “busy-ness” and Micky Mouse ears. This is something you’ll need to do in oral pathology – so might as well learn now!
  • Ode to the Granuloma. When my kids were little, whenever they’d hear “granuloma,” they’d bust out a version of “My Sharona,” substituting “gran-u-lo-ma” for “My Sharona.” It was both cute and a bit worrisome. They seem to have survived just fine, though. 

Why is it called “lipofuscin”?

I really like learning about the etymology of medical terms – it makes them so much easier to remember. Sometimes in class I’ll stop and tell you guys what a certain word root means, so that when you see it somewhere else, you’ll have some idea of what’s going on.

Here’s a post I wrote on lipofuscin. I wrote it in February (my least favorite month of the year), so there’s some excessive misery and complaining at the beginning. But if you can skip over that bit, you’ll see why the Latin fuscus is so perfect for this pigment we call lipofuscin!

Cell Injury lecture study guide and resources

Cell injury is a very dense topic, as you may have noticed. So I made a lecture summary to help you focus on what’s most important. I’ll be using this summary when I write quiz and exam questions – so if you know what is in the summary, you should be well-prepared.

Here are some more resources in case it helps to have things described in different ways:

A quick review of cell injury goes through cell injury in some detail (but still in an understandable way).

What’s going on inside a cell when it gets injured? is an even quicker review of cell injury (under 250 words! Yay!).

Top 15 things to know about cell injury is a little more in depth but still follows Dr. Dolan’s lecture outline.

If you feel more like doing a crossword puzzle, we’ve got you covered for that too! Note: for some reason, the crossword works best on browsers other than Chrome. I’m hoping to get that bug worked out, but for now, just try it on Safari or Firefox.

Welcome to General Pathology!

Hi everyone! I’m super excited to have another class with you! We start class on Monday May 16, and I want to give you a little information about the course so you have some idea of what to expect.

Pathology is usually described as the study of disease, and that’s a good working definition. But actually, the word “pathology” is derived from the Greek pathos, which is variously translated as suffering, emotion, calamity, or just anything that arouses sorrow or pity. That’s pretty appropriate, since diseases tend to bring about suffering and sorrow. In our course, we’ll stick to the first definition, and keep our focus on diseases. And I’ll do my best to make sure that the course itself doesn’t cause you any suffering or sorrow!

General Pathology (DDS 6253) and Systemic Pathology (DDS 6254) are technically two separate courses – but they are really quite similar in their structure and format, so that’s why they both share this website. General Pathology covers basic, introductory pathology topics like inflammation, cell injury, and neoplasia. You need to know about these topics so that you can make sense out of Systemic Pathology, which covers diseases by organ system (everything but the oral cavity) and Oral Pathology (which is self-explanatory).

This website will feel familiar to you because it’s pretty similar to our General Histology and Oral Histology websites. It’s divided into General Pathology and Systemic Pathology (each course has its own dropdown menu above), and the page structure will look familiar:

  • Home: course updates and random interesting stuff I think you might like
  • Lectures: course schedule and lecture recordings
  • About: course info (grading etc.) and syllabus
  • Crosswords: I’ll add new ones as we go along
  • Kahoots: to help you study

Okay – I think that about does it! Whew. If you have any questions, or just want to talk, please feel free to email me any time.