Answering this question requires you understand the mechanism of osteoclast stimulation by parathyroid hormone (FA 2020 p332).

Parathyroid hormone stimulates osteoclases indirectly by stimulating the release of RANKL bu osteoblasts which will bind to RANK receptor on osteoclasts and stimulate the resorption of bone. This is a paracrine process because paracrine signaling refers to stimulation by neighboring cells (short distances).

This patient has osteoporosis from hyperparathyroidism.

Hyperparathyroidism osteoporosis leads to hypercalcemia from CORTICAL SUBPERIOSTEAL EROSIONS

whereas osteoporosis from age/menopause affects trabecular bone. The latter has normal bone mineralization and normal lab values (normal Ca and PO43-)

I wrongly chose IL-2. IL-1 is a potent cytokine that can induce bone erosion in inflammatory sites such as rheumatoid joint regions via activation of osteoclasts. (via a receptor activator of NF-κB ligand (RANKL)/RANK-independent mechanism. IL-1 has a synergistic effect on RANKL-induced osteoclast formation.) https://www.jimmunol.org/content/183/3/1862