Buprenorphine itself is a partial agonist (meaning that it has agonist effects at receptor cites just like oxycodone, heroin or other full agonist. The difference is, buprenorphine only activates those receptors to a degree. The common way to visualize it is using a door as an analogy. With oxycodone, a dose of 5mg will open the door slightly, increase the dose, and it will keep opening the door more and more causing more agonist effects, ie.-euphoria, resperitory depression etc.. With a partial-agonist, like buprenorphine, the door will only open so much, so that increasing the dosage past a certain point will cause no more agonist effects.) Likewise, buprenorphine has antagonistic properties (like naloxone, which is an antagonist). It has a super high binding affinity, which will lock tightly into opiate receptors, kicking off full agonists and at certain dosages, it will block other full agonists like oxycodone, because the bupe is occupying the receptors, therefore the oxy has no where to go, than swim around in your blood stream until it is excreted.
However, buprenorphine has a higher binding affinity than naloxone, so the naloxone in suboxone is inactive. It's used as a scare tactic to make addicts think that crushing up and sniffing/shooting suboxone will throw them into withdrawals, and this is not true. Buprenorphine itself, is what causes precipitated withdrawal, when used on top of a full agonist, not naloxone