Thread: How are alveolar walls destroyed when someone has emphysema?

I have searched the internet for many hours trying to find an answer and I can only find vague explanations.

So phagocytes release elastase which destroys elastin in the alveolar and bronchioles, this causes the alveolar to become enlarged making it harder to breathe out as they no longer go back down to their usual size which would push air out. Also, the bronchioles lose the elastin which supports them and keeps them open, making them more likely to collapse when coupled with the loss of positive pressure that is usually applied on them when the alveolar forces air out.

and then somehow the alveolar walls become destroyed which results in loss of surface area in the alveolar. I can find no explanation as for how they are destroyed. I can find some vague references to trapped air and coughing, and others to enlargement of alveolar walls somehow equals destruction. The star trek enterprise doesn't just beam the alveolar walls into space, how are they destroyed exactly once they have become enlarged? More enzymes from phagocytes break the walls down entirely? coughing? How do we go from loss of elasticity to destruction?

In emphysema there is mild chronic inflammation. Lots of macrophages/T-cells/neutrophils. Inflammatory meditors (e.g. leukotriene B4, IL-8, TNF, etc). Exact pathogenesis unclear. Ideas include protease-antiprotease mechanism and imbalance of oxidants/antioxidants.

If you have a chronic inflammatory process occurring in the tissues, you will have ongoing proteolytic activity (e.g. neutrophil granule release containing elastase, proteinase 3, and cathepsin G; also matrix metalloproteinases from macrophages/neutrophils).

Antioxidants (e.g. superoxide dismutase and glutathione) depleted by reactive oxygen species/free radicals (from neutrophils; also from smoking). Antioxidants prevent oxidative damage to tissue so their depletion leads to damage. Oxidative injury has many effects such inactivation of antiproteases.

Note there are many (freely accessible) papers that go into lots of details such as:
Pathogenesis of chronic obstructive pulmonary disease