Unfortunately, as of now there is no clear direction on how to manipulate the circadian clock to alter longitudinal bone growth.

Prolonged bioluminescence monitoring in mouse ex vivo bone culture revealed persistent circadian rhythms in articular cartilages and growth plates.

“we revealed a robust and extremely long-lasting circadian rhythm in ex vivo culture maintained for over six months from the femoral bone of a PERIOD2(Luciferase) mouse{How do we manipulate or re-initiate this circadian cycle for height growth?}. Furthermore, we also identified robust circadian clocks in flat bones. High- or low-magnification real-time bioluminescence microscopic imaging revealed that the robust circadian rhythms emanated from the articular cartilage and the epiphyseal cartilage within the growth plate of juvenile animals. Stimulation by forskolin or dexamethasone treatment caused type 0 phase resetting, indicating canonical entraining properties of the bone clock. Together, our findings from long-term ex vivo culture revealed that “tissue-autonomous” circadian rhythm in the articular cartilage and the growth plate of femoral bone functions for several months even in an organ culture condition, and provided a useful in vitro assay system investigating the role of the biological clock in bone formation or development.”

“the plasma PTH rhythm persisted under “constant routine” conditions where subjects were deprived of any exogenous time information, indicating that the rhythm is driven by the intrinsic circadian clock”

“At the molecular level, the circadian clock is composed of a set of clock genes forming cell-autonomous transcription/translation feedback loops; the molecular oscillators in turn drive the expression of output genes governing a variety of clock-controlled physiological processes. Specifically, two transcription factors, BMAL1 and CLOCK, heterodimerize and transactivate core clock genes such as Period genes (Per1 and Per2), Cryptochome1 (Cry1), and Rev-Erb genes (Rev-Erbα and Rev-Erbβ). Expressions of these genes (Bmal1, Per1, Per2, Cry1, Cry2, RevErbα and RevErbβ) show clear circadian rhythms with distinct peak times”

“circadian bioluminescence rhythms from long bones (proximal femoral ends and radiuses) and flat bones (calvariae and scapulae) showed similar period lengths”<-so the circadian rhythm may not be something that distinguishes between long and flat bones.

“both epiphyseal cartilage and articular cartilage in femoral trochlea  showed clear circadian rhythms for 4 days”

“expression of certain clock genes has been shown in growth plates”

” local circadian clocks in the epiphyseal cartilage may affect bone growth in juvenile animals.”

“Exogenous time cues (e.g. light) can reset internal clocks.”

“[The] phase of the bone clock [that] was strongly altered by forskolin, functions to increase intracellular cAMP levels through adenylate cyclase activation. Therefore, it is possible that in vivo circadian phase can be reset by endogenous substance(s) via the cAMP pathway in the bone. The hormone PTH increases intracellular cAMP levels via the PTH/PTHrP receptor, consequently inducing Per1 and Per2 expression through the cAMP–PKA–CREB pathway. In addition, sympathetic signaling stimulated by leptin has been shown to regulate bone remodeling in part through a β-adrenergic receptor (β-AR). The β-AR agonist isoproterenol also enhances intracellular cAMP levels and up-regulates Per1/2 and Bmal1 expression in primary mouse osteoblasts. In accordance, isoproterenol has been reported to stimulate the circadian rhythmic expression of Per1/2/3 and Bmal1 in human SaM-1 osteoblastic cells”

“DEX, synthetic glucocorticoids (GCs), was found to reset the bone circadian rhythm. GCs are secreted from the adrenal gland in a circadian manner. Although the SCN is not reset by GCs due to a lack of glucocorticoid receptor (GR) expression, circadian clocks in peripheral organs such as the liver, kidney, and heart are highly responsive to GCs. GCs are considered as internal time-cues which relay timing information within the body and synchronize the peripheral clocks, including bones, as shown here. At the molecular level, GCs bind to GR and regulate target gene expression via glucocorticoid response elements. Previous studies have identified Per1, Per2, and E4bp4 as direct targets of GRs in mice”

Forskolin alters Ca2+ and cAMP levels, I haven’t seen any studies regarding the effects of Forskolin on longitudinal bone growth.  Dexamethasone is widely known to inhibit longitudinal bone growth.  However, Dexamethasone is also known to help induce chondrogenic differentiation.

The transcription factors SOX9 and SOX5/SOX6 cooperate genome-wide through super-enhancers to drive chondrogenesis.

“SOX9 is a transcriptional activator required for chondrogenesis, and SOX5 and SOX6 are closely related DNA-binding proteins that critically enhance its function. We use here genome-wide approaches to gain novel insights into the full spectrum of the target genes and modes of action of this chondrogenic trio. Using the RCS cell line as a faithful model for proliferating/early prehypertrophic growth plate chondrocytes, we uncover that SOX6 and SOX9 bind thousands of genomic sites, frequently and most efficiently near each other. SOX9 recognizes pairs of inverted SOX motifs, whereas SOX6 favors pairs of tandem SOX motifs. The SOX proteins primarily target enhancers. While binding to a small fraction of typical enhancers, they bind multiple sites on almost all super-enhancers (SEs) present in RCS cells. These SEs are predominantly linked to cartilage-specific genes. The SOX proteins effectively work together to activate these SEs and are required for in vivo expression of their associated genes. These genes encode key regulatory factors, including the SOX trio proteins, and all essential cartilage extracellular matrix components. Chst11, Fgfr3, Runx2 and Runx3 are among many other newly identified SOX trio targets. SOX9 and SOX5/SOX6 thus cooperate genome-wide, primarily through SEs, to implement the growth plate chondrocyte differentiation program.”

“Once settled in skeletogenic sites, progenitor cells coalesce into precartilaginous condensations and activate the chondrocyte differentiation program. Early-stage chondrocytes proliferate and build an abundant, cartilage-specific extracellular matrix. They express such genes as Col2a1 (encoding collagen type II) and Acan (proteoglycan aggrecan). Elongation of cartilage anlagen occurs in growth plates, structures in which chondrocytes proceed through terminal maturation steps in a precise spatial and temporal manner. They proliferate and produce cartilage matrix while aligning into longitudinal columns. They then cease proliferation, become prehypertrophic and express novel markers, such as Ihh (Indian hedgehog). As they become hypertrophic, they turn off most early markers and activate unique ones, including Col10a1 (collagen type X). They eventually die or switch to the osteoblast fate to participate in endochondral ossification. Chondrocytes forming permanent cartilage never proceed through these growth plate maturation steps. They keep expressing pancartilaginous early-chondrocyte markers and also express tissue-specific markers. For instance, superficial articular chondrocytes distinctively express Prg4 (lubricin).”

“Expression of the three SOX genes culminates in growth plate proliferating and prehypertrophic chondrocytes, and is abruptly turned off when chondrocytes undergo hypertrophy. SOX9 is required for chondrogenesis.”

“SOX9 is required to turn on and maintain chondrocyte-specific genes and that SOX5/6 strikingly augment SOX9’s transcriptional activity by securing SOX9 binding to DNA”

“The phenotype of RCS[rat chondrosarcoma] cells thus faithfully matches that of growth plate chondrocytes at the proliferating/early prehypertrophic stage. “<-For more on this read the study.

“RCS cells are bona fide growth plate proliferating/prehypertrophic chondrocytes “<-Since chondrosarcoma can occur in older individuals this is a very promising statement for the creation of neo-growth plates.

Subperiosteal Transmission Of Intra-Articular Pressure Between Articulated And Stationary Joints

“Hydrostatic pressures can be transmitted between synovial capsules. In each of ten rabbits, we simultaneously measured pressure in two joints, one of which was passively ranged, and the other of which was kept stationary. The intra-articular pressure inside the stationary joint changed every time its companion joint was ranged. But the pressure in the stationary joint did not change when the periosteum was transected above the ranged joint. This phenomenon was observed in all four animals that served as their own controls. The study suggests that the intra-articular pressure was transmitted through the space between the periosteum and the bone surface. Alternative explanations, like measurements of venous blood pressure, did not show correlation with hydrostatic pressure changes in the joints. The Floating Skeleton concept suggests a biomechanical rationale for this newly observed phenomenon: that there exists a subperiosteal hydrostatic connection of synovial joints, and that this “net” distributes excess pressures among joints through the periosteal sheath to sustain the integrity of the joint contacting surfaces over a lifetime.”

“correlation between synovial fluid pressure and the pressure in the blood capillary in the synovium”

“intra-articular pressure was transmitted hydrostatically through the subperiosteal space.”

“The subperiosteal fluid can be found in the cambial layer of the periosteum”

So essentially hydrostatic periosteum between the inner bone, the articular cartilage, and the periosteum are connected.