Hypothalamus–pituitary–gonadal axis in cryptorchid boys

Gilvydas Verkauskas

Institute of Clinical Medicine, Faculty of Medicine, Vilnius University, Vilnius, Lithuania

Corespondence; Prof. Dr med. Verkauskas, Head of the Centre of Children’s Surgery, Orthopaedics and Traumatology, Vilnius University Hospital Santaros Klinikos, Vilnius, Lithuania

Table of contents

Abstract
Paper
References
Author

Abstract

Cryptorchidism affects ~2–5% of male infants at birth and ~1% at 1 year, and is strongly associated with later subfertility and an increased risk of testicular cancer. Beyond mechanical maldescent, a growing body of data suggests that in a sizeable subset of boys, cryptorchidism reflects a disturbance of the hypothalamus–pituitary–gonadal (HPG) axis during fetal life and especially during mini-puberty—the postnatal surge of gonadotropins and testosterone that orchestrates Sertoli and Leydig cell maturation and the transformation of fetal gonocytes into adult dark (Ad) spermatogonia, the stem cell pool for adult spermatogenesis. This article synthesizes evidence on HPG function in cryptorchid boys, integrates prospective histology–endocrine correlations, and evaluates how timing and modality of therapy (orchiopexy alone versus combined with hormone/gonadotropin therapy) influence germ-cell outcomes and adult fertility. Drawing on published studies and the author’s clinical observations and cohort analyses, we argue that: (1) unilateral cryptorchidism often behaves as a bilateral disease at the tissue level; (2) routine serum hormones after mini-puberty have limited diagnostic power for individual risk stratification unless interpreted against histology; (3) the most consistent endocrine signal of high infertility risk is relative LH insufficiency during mini-puberty, not a primary FSH defect; (4) orchiopexy improves anatomic position but does not restore a previously abrogated mini-puberty; and (5) targeted endocrine rescue—particularly GnRH/gonadotropin-based induction of mini-puberty—can normalize Ad spermatogonia formation and improve long-term semen quality in selected patients. Practical implications include earlier evaluation focused on risk stratification (not merely scheduling surgery), judicious use of testicular biopsy in expert hands, and clinical trials of mini-puberty induction guided by robust biomarkers and safety endpoints.

Résumé

La cryptorchidie touche environ 2 à 5 % des nourrissons de sexe masculin à la naissance et environ 1 % à l’âge d’un an. Elle est fortement associée à une hypofertilité ultérieure et à un risque accru de cancer du testicule. Au-delà de la maldescente mécanique, de plus en plus de données suggèrent que chez un nombre important de garçons, la cryptorchidie reflète une perturbation de l’axe hypothalamo-hypophyso-gonadique (HHG) pendant la vie fœtale, et plus particulièrement pendant la mini-puberté : la poussée postnatale de gonadotrophines et de testostérone qui orchestre la maturation des cellules de Sertoli et de Leydig et la transformation des gonocytes fœtaux en spermatogonies foncées (Ad), constituant le réservoir de cellules souches pour la spermatogenèse adulte. Cet article synthétise les données sur la fonction de l’axe HHG chez les garçons cryptorchides, intègre les corrélations histologiques et endocriniennes prospectives et évalue l’influence du moment et des modalités du traitement (orchidopexie seule ou associée à une hormonothérapie/gonadotrophine) sur le devenir des cellules germinales et la fertilité à l’âge adulte. En nous appuyant sur des études publiées, nos observations cliniques et des analyses de cohortes, nous soutenons que : (1) la cryptorchidie unilatérale se comporte souvent comme une maladie bilatérale au niveau tissulaire ; (2) les dosages hormonaux sériques de routine après la mini-puberté ont une valeur diagnostique limitée pour la stratification individuelle du risque, à moins d’être interprétés en fonction de l’histologie ;  (3) le signal endocrinien le plus constant d’un risque élevé d’infertilité est une insuffisance relative de LH pendant la mini-puberté, et non un déficit primaire en FSH ; (4) l’orchidopexie améliore la position anatomique, mais ne rétablit pas une mini-puberté antérieurement interrompue ; et (5) une hormonothérapie ciblée – en particulier l’induction de la mini-puberté par la GnRH/gonadotrophines – peut normaliser la formation des spermatogonies Ad et améliorer la qualité du sperme à long terme chez certains patients. Les implications pratiques comprennent une évaluation plus précoce axée sur la stratification des risques (et non pas seulement sur la planification de l’intervention chirurgicale), une utilisation judicieuse de la biopsie testiculaire entre des mains expertes et des essais cliniques d’induction de mini-puberté guidés par des biomarqueurs robustes et des critères d’évaluation de la sécurité.
Open slides

Introduction

Cryptorchidism (undescended testis, UDT) is a common pediatric condition with heterogeneous etiologies and phenotypes. While surgical relocation (orchiopexy) before 12 months has become standard to reduce risks of impaired spermatogenesis and malignancy, the persistent observation of suboptimal adult semen parameters in many men treated in childhood, even after timely surgery, indicates that maldescent is frequently accompanied by primary testicular dysgenesis and/or disturbances of the HPG axis in critical developmental windows [18].

A central theme of contemporary andrology is mini-puberty: a transient activation of the HPG axis from ~2–4 weeks to ~3–6 months postnatally, when pulsatile GnRH drives pituitary LH and FSH secretion, raising testosterone in boys and stimulating Sertoli cell products (AMH, inhibin B). Mini-puberty calibrates reproductive “set-points” and promotes transformation of fetal gonocytes into Ad spermatogonia—the stem cells essential for future spermatogenesis [2, 5, 13, 14]. Mini-puberty metrics—most notably serum testosterone near 3 months—predict adult total sperm count in population cohorts, underscoring causality between early HPG activity and later fertility [1, 18].

For cryptorchid boys, two (nonexclusive) mechanistic frames have been debated for decades: (i) predominantly testicular dysgenesis (primary germ cell/Sertoli cell defects), and (ii) a neuroendocrine endophenotype featuring relative gonadotropin (especially LH) insufficiency during mini-puberty. Clinical series, endocrine studies, and biopsy-linked cohorts now suggest both patterns exist; crucially, the endocrine signature and tissue phenotype co-segregate and guide treatment response [13,18].

This paper reviews the biology of the HPG axis relevant to cryptorchidism, examines evidence for endocrine abnormalities in cryptorchid boys (with and without biopsy stratification), and discusses therapeutic implications, integrating data from randomized and longitudinal studies of GnRH/gonadotropin therapy and orchiopexy. Observations, figures, and interpretations are aligned with remarks delivered at the 5th International Andrology Symposium, Cryptorchidism: Molecular Biology Meets Endocrinology and Surgery, Valletta, Malta, 26–27 September 2025 (transcript excerpts cited where relevant) and with the author’s published cohort work [12].

Developmental physiology: the HPG axis and mini-puberty

Fetal and early postnatal windows

Testicular descent involves a hormonally orchestrated transabdominal and inguinoscrotal phases driven by INSL3, gonadotropins and androgens with key roles for the gubernaculum and epididymis, which guides and precedes the testis into the scrotum [6, 11]. In parallel, intra-testicular events include migration and maturation of gonocytes toward the basement membrane and their transformation into Ad spermatogonia, a step tightly coupled to androgen and FSH/inhibin B signaling during mini-puberty [3, 13,14].

Mini-puberty in boys is characterized by elevated LH (stimulating testosterone production) and FSH (driving Sertoli cell proliferation and inhibin B). Large normative and disorder-specific datasets, including systematic reviews, confirm the existence and clinical utility of this window; its disruption in congenital hypogonadotropic hypogonadism (CHH) underscores causality, and recent consensus statements endorse early gonadotropin therapy for CHH to induce mini-puberty [3, 10].

Mini-puberty and later fertility

A landmark Nordic birth cohort showed that higher serum testosterone at ~3 months predicts higher total sperm count in adulthood, even after adjustment for confounders [1]. This finding substantiates mini-puberty as a programmable set-point with lifelong impact. Reviews from 2020 to 2024 and 2025 updates reiterate that biomarkers in infancy correlate with pubertal/adult reproductive parameters [2, 5, 9, 13].

Cryptorchidism as an HPG disorder: what do hormones really show?

Population studies vs biopsy-linked cohorts

In unselected cryptorchid cohorts during mini-puberty, several studies reported higher FSH (± higher LH) with lower inhibin B compared with controls, signaling Sertoli cell dysfunction; others found subtler or no differences—discrepancies that reflect phenotypic heterogeneity, small sample sizes, and absence of histological stratification [2, 14, 22].

When endocrine data are paired with biopsy, a clearer pattern emerges: testes with severe germ cell depletion and Sertoli-cell–only (SCO) histology often coincide with relative LH insufficiency [12, 23]. In our prospective study of cryptorchid boys, the high-risk (adverse histology) group exhibited lower basal LH despite similar ages, supporting a central (HPG) insufficiency endotype [12]. The same signal has been observed in independent Danish cohorts when boys are separated by biopsy-defined good vs bad histology [24]. (Fig.1) These data help reconcile why non-biopsy cohorts can look “normal” or only subtly abnormal: risk is concentrated in a subset with specific histology and LH dynamics.

Is unilateral cryptorchidism a “bilateral disease”?

Multiple clinical and histological series report pathology in the contralateral scrotal testis of boys with unilateral UDT, from reduced germ cells per tubule to impaired Ad spermatogonia counts, implying systemic or central influences rather than purely local maldescent [8,18]. Experimental models and human histology underscore that ostensibly “normal” contralateral testes often harbor maturational defects [Huff]. Early classic pathology and more recent analyses concordantly indicate bilateral impact, indicating suboptimal minipuberty [8].

Why routine hormones after 12–18 months disappoint

By ~12–18 months, LH has largely returned to quiescence; group differences narrow and clinical assays may lack sensitivity at low concentrations. Thus, single time-point hormones beyond mini-puberty are poor individual classifiers unless paired with histology or dynamic tests. This explains why ROC curves based on routine LH/FSH/inhibin B around 15 months are weak in unselected cohorts [8].

Histology as the ground truth: Ad spermatogonia and germcell counts

The number of Ad spermatogonia per tubule (AdS/T) and the germ cells/tubule (G/T) are powerful predictors of adult semen quality. Pioneering and subsequent work showed that failure of Ad transformation during mini-puberty is tightly associated with oligozoospermia/azoospermia in adulthood—even when orchiopexy was timely and technically successful [1,3, 13, 18]. A 2019 series specifically assessed unilateral UDT and developed histological risk criteria for azoospermia; again, tissue readouts outperformed routine hormones for risk stratification [8, 18].

Surgery helps—but cannot “rewind” a missed mini-puberty

Orchiopexy outcomes

Earlier orchiopexy (ideally before 12 months) improves testicular growth and some surrogate fertility markers, but does not fully normalize germ-cell development if mini-puberty was defective beforehand. Post-orchiopexy histology months to years later often shows no histological rescue if the Ad pool was not established, aligning with the concept that surgery corrects position but not prior endocrine programming [9,13,18].

Epididymal anomalies and obstruction: an overlooked axis

Epididymal and vaso-epididymal anomalies, present in ~20% of UDTs, are frequently associated with sperm outflow obstruction and can limit fertility despite otherwise favorable testicular histology [25,26,27]. The epididymis and gubernaculum play leading roles in descent; embryologic and comparative studies (mouse–opossum) and focused reviews emphasize that the epididymis often “leads” and the testis follows—an anatomic nuance with practical implications for surgery and counseling [11,20].

Endocrine rescue of mini-puberty: evidence for GnRH/gonadotropins

Reports that “there is no difference” in mini-puberty hormones in cryptorchid infants typically suffer from: (1) absence of biopsy stratification; (2) inclusion of mixed phenotypes (congenital, acquired/ascending); (3) cross-sectional timing outside peak mini-puberty; (4) assay sensitivity limits at very low LH after 6–9 months; and (5) small sample sizes. When these biases are addressed, a consistent picture emerges:

  • During classic mini-puberty (≈2–4 months): cryptorchid infants as a group often have higher FSH and lower inhibin B; LH/testosterone defects are subtler and cohort-dependent [17, 2, 5search].
  • In histology-defined high-risk cases after mini-puberty: lower LH (relative gonadotropin insufficiency) is the discriminant signal; FSH is frequently non-discriminatory at the individual level [15; conference transcript].
  • After mini-puberty (~>9–12 months): routine hormones poorly separate risk strata; consider biopsy and/or dynamic testing.

Reconciling apparently conflicting endocrine studies

Reports that “there is no difference” in mini-puberty hormones in cryptorchid infants typically suffer from: (1) absence of biopsy stratification; (2) inclusion of mixed phenotypes (congenital, acquired/ascending); (3) cross-sectional timing outside peak mini-puberty; (4) assay sensitivity limits at very low LH after 6–9 months; and (5) small sample sizes. When these biases are addressed, a consistent picture emerges:

  • During classic mini-puberty (≈2–4 months): cryptorchid infants as a group often have higher FSH and lower inhibin B; LH/testosterone defects are subtler and cohort-dependent [17, 2, 5search].
  • In histology-defined high-risk cases after mini-puberty: lower LH (relative gonadotropin insufficiency) is the discriminant signal; FSH is frequently non-discriminatory at the individual level [15; conference transcript].
  • After mini-puberty (~>9–12 months): routine hormones poorly separate risk strata; consider biopsy and/or dynamic testing.

Clinical decision-making: a practical algorithm

  1. Early referral focused on evaluation, not automatic surgery. Aim to assess by 2–4 months to exploit the mini-puberty window for endocrine phenotyping (LH, FSH, testosterone, inhibin B), with attention to assay sensitivity and age-appropriate reference intervals [2,3,5,13].
  2. Plan orchiopexy by 6–12 months but acknowledge limits. Early surgery improves many parameters yet does not rescue missed mini-puberty; technique must be tailored, with particular attention to epididymal/vas anomalies that may predict obstructive components of future infertility [4,19,25,26,27]. Consider targeted testicular biopsy by expert surgeons to quantify Ad S/T and G/T. Histology is the strongest predictor of infertility risk and therapy responsiveness [1,7,10].
  3. Consider endocrine induction of mini-puberty in selected cases. For infants with evidence of mini-puberty failure (low LH/testosterone at 2–4 months, severe histology, bilateral UDT, micropenis, CHH suspicion), discuss GnRH/gonadotropin therapy using protocols supported by trials and systematic reviews; ideally within clinical trials or registries to ensure standardized dosing, monitoring, and long-term follow-up [11,16,21].
  4. Long-term follow-up into adolescence and adulthood. Track testicular volume, semen parameters (when appropriate), and endocrine status. Even unilateral cases warrant counseling on bilateral disease risk at the tissue level [1,12].

Special topics

Acquired/ascending testes vs. congenital UDT

Phenotypes differ: acquired cryptorchidism may have later onset and distinct endocrine features. Many negative endocrine studies included patients with ascending testes, diluting signals of genuine mini-puberty failure present in congenital cases (author’s caution; conference transcript).

The epididymis and the “guidance” hypothesis

Surgical observations and embryology argue that the epididymis often anchors the descent path: the gubernaculum attaches to the caudal epididymis and expands the inguinal canal; the testis “follows” down this tract [8, 11]. Recognizing and documenting epididymal disjunction or atresia during orchiopexy is crucial for prognostication of obstructive infertility.

Safety of early surgery

Operating at 6 months requires experienced teams; some series suggest higher complication rates in very small infants, though contemporary pediatric centers report excellent outcomes. The benefit–risk calculus should integrate endocrine status, testis position, anesthesia safety, and institutional expertise [17].

Synthesis and working model

Model A (HPG-intact dysgenesis): Primary testicular dysgenesis with intact HPG axis yields elevated FSH (due to low inhibin B), normal/near-normal LH/testosterone during mini-puberty, poor histology (SCO/fibrosis), and limited response to endocrine rescue. Surgery repositions but cannot create Ad spermatogonia de novo.

Model B (HPG-axis insufficiency during mini-puberty): Relative LH deficiency blunts Leydig activation, reduces intratesticular testosterone, and blocks the gonocyte→Ad transformation. Histology shows low AdS/T with otherwise salvageable architecture. Here, GnRH/gonadotropin therapy during the window can normalize AdS/T and later semen counts, while surgery alone improves position but not the stem cell pool [4,16,18,19].

Reality: Many boys sit along a spectrum; unilateral UDT often conceals bilateral tissue vulnerability. This heterogeneity explains disparate results in unstratified studies and highlights the need for individualized, biology-informed care.

Implications for the next decade

1. Standardize mini-puberty testing. Age-specific references, ultrasensitive LH assays, and harmonized sampling at ~10–14 weeks will sharpen phenotyping [5, 14].

2. Biopsy-guided trials. Randomized studies of mini-puberty induction should require baseline histology (AdS/T, G/T) and report tissue and molecular endpoints alongside clinical descent and semen outcomes [16, 19, 21].

3. Endpoints that matter. Adult total sperm count is the meaningful endpoint, as validated by population cohorts linking infant T to adult semen quality [1,13,18].

4. Epididymal/vas mapping. Routine intraoperative documentation (photography, standardized anomaly scoring) will inform obstruction-related infertility risk and direct adolescent/adult management [26,27].

5. Translational biology. Single-cell and spatial transcriptomics of infant testes pre- and post-GnRHa could decode the gene programs governing Ad formation and identify novel druggable targets [21].

Conclusions

Cryptorchidism is not merely a problem of malposition. For many boys it reflects a developmental endocrinopathy in which mini-puberty is blunted—most conspicuously through relative LH insufficiency—resulting in failure to establish the Ad spermatogonial pool. Orchiopexy is necessary but not sufficient to fix an early endocrine miss. Biopsy-informed care and timely endocrine induction of mini-puberty can rescue germ-cell development and improve adult semen outcomes in selected cases. The field’s task is to move from one-size-fits-all surgery to biology-tailored therapy that begins with early evaluation and ends with proven fertility gains.

Declaration Section

a) Ethics Approval and Consent to Participate Investigations were carried out in accordance with the Declaration of Helsinki of 1975, revised in 2008.
b) Consent for publication; Not applicable
c) Availability of data and supporting material; Not applicable
d) Competing interests Author/s declare that they have no competing interests
e) Funding: The author acknowledges support from Vilnius University and European
Social Funds (conference disclosure) and collaborations with European reference networks (eUROGEN).

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Gilvydas Verkauskas

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