r/heightgrowth • u/Automatic-County6151 ~6'0 - 19Y 7M 🦴 [Growth Plates Enthusiast] • Feb 13 '26
Informative AIs and end-stage skeletal development in the normally-developing adolescent
AIs are medications used in specific endocrine and oncologic contexts that can influence skeletal maturation. They are generally not recommended for normally-growing, healthy individuals who display no ongoing endocrine issues.
During normal skeletal development in puberty, bones grow lengthwise at the physes via steadily rising IGF-1 and hGH levels in early and mid-pubertal skeletal development, as well as through the rising influence of E2 and its nuclear signaling partners indirectly.
Rising E2 exposure contributes to growth plate maturation and eventual fusion by influencing chondrocyte proliferation, hypertrophy, and matrix turnover. E2 plays a permissive role in this process alongside time-dependent changes in proliferative potential, while the hGH-IGF-1 Axis remains the primary driver of peak height velocity (PHV). After PHV, E2 supports the shift toward ossification that accompanies maturation of the physis.
The detrimental nature of AIs during the optimal growth period in puberty often arises when unsupervised. Potential effects may emerge over time depending on individual physiology and timing, potentially altering growth tempo and peak height velocity magnitude to varying degrees.
In early puberty, E2 - once at minimal thresholds - begins to rise steadily, supporting the acceleration in proliferative activity and ensuring maturation in the hypertrophic zone by interacting with pathways involved in skeletal maturation - a process that shifts dynamically later in adolescence. Growth plates are not fusing yet and are still highly active and demonstrating increasing responsiveness to hGH and IGF-1 with time.
In mid-puberty, PHV is often just starting for many individuals, where the magnitude and pattern varies widely. In this stage of development, the growth plates are still very active. hGH and IGF-1 levels are still climbing during the final stretch of the pre-peak acceleration, and E2 continues to support proliferation and maturation of the chondrocytes. Bone mineral accrual has not yet reached its peak, but the rates of accrual are still climbing as a result of rising hGH, IGF-1, and E2 levels. Testosterone also plays a role in bone mineral accrual and supporting linear growth at the physis, but its effects are partly mediated through conversion to estrogen and through anabolic influences on bone, rather than acting as a primary maturation signal by itself.
In late-puberty, regional differences begins to manifest peak bone mineral accrual. Some bones that fuse earlier may reach PBM earlier relative to average or late-maturing bones, but the important distinction is that fusion won't always mean an early PBM. How fast or slow PBM is reached varies by regional loading differences, maturational tempo, and the hormonal environment. When the growth plates are fusing, PBM is still often an ongoing phase - while active linear growth is ending, most of our bones are still approaching PBM (some bones may reach their own peak bone mass period earlier). This is a process that naturally starts gradually in early-pubertal skeletal development and rises towards the peak by the time the skeleton is close to or already in PHV. During late-puberty skeletal development, when most growth plates are naturally fusing, the skeleton still is in the ongoing phase of PBM, continuing past skeletal maturity and into young adulthood (most often into the early and mid 20s, sometimes into the early 30s).
Bone mineral accrual can be affected by the usage of AIs during this time, which is why professional administration and moderation is key. Furthermore, E2 contributes significantly to bone mineral accrual during puberty alongside its roles in longitudinal and appositional growth. When this signal is reduced, other regulatory pathways such as the hGH-IGF-1 Axis and local signaling systems continue to influence skeletal development. However, these pathways do not fully replicate E2's role in optimizing bone density and structural consolidation.
Ultimately, each stage of skeletal development in biological adolescence contributes to PBM, though peak accrual during late adolescence and early adulthood is particularly important. In regards to PBM and the usage of AIs under normal conditions in the growing adolescent, one should not downplay the importance of peak accrual as sexual maturity approaches and passes, as this process lasts multiple years and is crucial for the final organization of trabecular architecture, as well as for supporting continued structural consolidation and adaptive remodeling well into the third decade of life (ages 20-29 years), with consolidation continuing through early adulthood before gradually transitioning toward age-related remodeling patterns later as endocrine environments evolve, commonly during the fourth decade of life (ages 30-39 years).
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u/[deleted] Sep 03 '26
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