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Where Periosteal Apposition Occurs
Long Bones
During growth, the outer diameter of long bones (e.g. femur, tibia, humerus etc.) increase by periosteal bone deposition. This helps form the shape of the skeleton and helps maintain bone strength when we get older.
Clavicles And Other Flat Bones
Bones like the clavicles, ribs and pelvis will also remodel. During development the shape and size of these bones will change, however this may vary depending on the bone/area being looked at.
Craniofacial Bones
Regional bone deposition and resorption will happen in bones like the mandible, maxilla and zygomatic bones. This helps the shape of the face and development of the skeleton.
Periosteal Apposition Introduction
Periosteal apposition is the deposition of new bone tissue onto the outside of a bone. This is one of the mechanisms that can cause changes in bone size and shape throughout life. Unlike longitudinal growth, which increases the length of long bones using growth plates, periosteal apposition can increase the diameter of the bone. This can occur in many areas of the skeleton including the femur, tibia, clavicles, ribs, pelvis and craniofacial bones.
How Periosteal Apposition Occurs[color=#A690FD[/color]
The periosteum surrounds the majority of bones. It contains cells involved in bone formation as well as blood vessels, nerves and connective tissue.
Overall, the process will occur as follows:
Bone forming cells (e.g. osteoblasts) will create and mineralize new bone matrix.
If this occurs on the outer part of the bone, the bone can increase in external dimensions.
If at the same time there are changes occurring on the internal surface of the bone (known as endosteal remodeling), this can lead to changes in cortical bone thickness. Over time this will cause changes to the overall shape of the bone due to changes in bone formation and resorption. Periosteal apposition is part of the bone modeling and remodeling process.
Findings From Research[color=#5046FE[/color][color=#A18CFD[/color]
✤Study 1: Continuance of Periosteal Apposition (I) (1990)
A literature review looking at 42 studies into age related changes in skeletal dimensions was conducted. There was evidence to suggest that some cranial and post-cranial bones in adults continue to enlarge due to small amounts of new bone being deposited. Several factors were discussed as a reason for this, including biomechanical adaptation and compensatory changes. However it should be noted that these are not well investigated hypotheses and the changes were often minor.
Overall: Periosteal apposition is not limited to growing children and facial bones. Some bones continue to increase in outer dimensions during adulthood. The amount of change can vary.
✤Study 2: Cortical Bone Development and Maintenance and Porosity (2024)
The interplay between different osteoblasts and osteoclasts and different signaling pathways determines cortical thickness, size and strength. This review describes research in both human and animals that has identified changes in these processes during growth and aging.
Overall: There are multiple processes that affect bone size. Although periosteal apposition plays a key role, there are not enough processes to fully account for changes in bone width and density.
✤Study 3: Cell replication in craniofacial periosteum (2011)
Nine young pigs were used to obtain samples of periosteum from the mandible, hard palate and zygoma.
It was found that areas of bone apposition had increased cellular proliferation in the inner layers of the periosteum compared to areas of bone resorption. This study showed that both formation and resorption can occur at the same time on a bone depending on what surface they are on and what role they play in bone development.
Factors That Influence Periosteal Apposition[color=#A48FFD[/color]
Factor | What the research suggests |
|---|---|
Age and development | Apposition is generally more active during skeletal growth. |
Mechanical loading | Bone geometry can adapt to mechanical demands, although the response depends on the site and loading conditions. |
Hormonal and cellular signaling | Biological signals regulate the activity of bone-forming and bone-resorbing cells. |
Anatomical location | Different surfaces of the same bone can undergo different patterns of formation and resorption. |
Aging | Periosteal responses can decline, although bone formation and repair remain possible. |
Clavicles, Shoulder Width and Frame
The clavicle plays a role in determining the width of the shoulder bideltoid , as it connects to the sternum and scapulae. How long the clavicle is, its angle and its relationship with the rest of the skeleton will affect how the upper frame looks. As with any bone, periosteal apposition is important to consider as they will have bone modelling throughout development. However, the length of the clavicle and therefore the width of the shoulders is dependent on many factors including: longitudinal growth, clavicle end growth, scapula placement, ribcage size and muscle growth.
It can be separated into 3 parts:
✤The length of the bone increasing: may alter the overall dimensions of the shoulder bidelt
✤The external diameter of the bone increasing: alters external length
✤The increase of musculature of the deltoids and upper back: could increase the apparent width of the shoulders. Research into periosteal apposition can support this.
Mandible
The mandible is interesting as it has a final shape due to many coordinated processes, the body, ramus, angle, mentum and condyle are all relevant parts of the jaw. As there is varying areas of bone deposition and resorption, the mandible shape can change. For example, the ramus and body contribute to the overall shape of the jaw. The mentum helps to create the shape of the lower face. The prominence of these parts will depend on genetic factors, timing of development, occlusion and the angle of the mandible. A study was carried out in 2025 looking into periosteal bone modelling in various areas of the face including the mandible. It found that the mandible had patterns of bone modelling that corresponded with the shape of the face.
Zygomatic [color=#9F8AFD[/color]
The zygomatic bones make up much of the skeletal framework of the cheek. They contribute to forming the zygomatic arches on either side of the skull. The appearance of these bones depends on many factors. The protrusion of the cheekbones, the shape of the maxilla, positioning of the eye sockets and amount of soft tissue overlying will all affect the appearance of prominent cheekbones. Bone modelling via the periosteum will play a role in creating the cheekbones. However, some areas will have resorption occurring whilst others have deposition. This creates the final shape.
Maxilla and Midface Projection
The maxilla makes up much of the upper jaw and holds the upper teeth. It also contributes to the orbital floor, lateral walls of the nasal opening and mid facial skeleton. This is a complicated area as there are many factors affecting mid face appearance. The position of the maxilla, protrusion of the alveolar area, shape of the nasal base, cheekbones and relationship between the upper and lower jaws all play a part. The maxilla was found to have more resorption than the other areas of the face in the study. There was also a change in development during adolescence to create more of a forward facing area. This indicates coordinated development. This means that mid face projection isn’t just adding extra bone to the front of maxilla.
View attachment 45853
Cortical Thickness vs Bone Width
This is an important factor to take into consideration.
✤Cortical thickness is the thickness of the dense outer layer of bone. Whereas external bone width is how wide the bone is on the outside.
✤These can vary independently. For example, the bone can widen on the outside but lose bone on the inside.
✤This is why periosteal apposition is looked at in terms of bone strength. The external diameter can increase to give greater resistance to bending. However, increases in cortical thickness, density and external diameter shouldn’t be seen as the same outcome.
Periosteal Inhibitors
Glucocorticoid receptor signaling
Glucocorticoids can bind to the glucocorticoid receptor leading to disruption of many pathways important for osteoblast proliferation, differentiation and cell survival. This can include inhibition of the Wnt/β-catenin or BMP pathways. Down regulation of osteogenic factors (RUNX2) and apoptosis of osteoblasts. This can lead to reduced bone matrix formation. There is experimental evidence to support that cortisol can reduce proliferation of periosteal cells in the skull. Further evidence to support reduced periosteal bone formation in animals treated with glucocorticoids. Glucocorticoids can have effects on many processes in bone. This includes osteoclasts, calcium regulation, muscles and other tissues. This can depend on the bone, amount of drug, duration and age.
Wnt/β-catenin signalling pathway
Wnt signalling occurs via the canonical pathway promoting osteoblast differentiation. Wnt ligands bind to Frizzled and LRP5/6 receptors leading to stabilisation of β-catenin and regulation of gene transcription. Inhibition of this pathway can occur with Sclerostin and DKK1. This will cause reduced osteogenesis via inhibition of signal transduction. This pathway is important in regulating the differentiation of progenitor cells in the periosteum. Experimental inhibition of the pathway using DKK1 can reduce bone healing via the periosteum. Neutralisation of DKK1 can help to improve regeneration. These are all natural regulators meaning drugs cannot replace them. For example Romosozumab can be used to inhibit sclerostin and increase bone formation. There is strong evidence to support that this pathway regulates osteoblast function. Depending on the circumstances this can be manipulated to inhibit normal periosteum formation.
Bone Morphogenetic Proteins
Bone morphogenetic proteins (BMP) are part of the TGF-β superfamily. They regulate bone development and can promote osteoblast differentiation. Once the receptors are activated signalling is passed through Smads inside the cell. This will effect transcription factors such as Runx2 and Osterix which are key during osteoblast development. This pathway is important for progenitor cells in the periosteum. Experimental inhibition of the BMP receptors can effect periosteum growth. This can depend on cortical, cancellous or periosteum. Deletion of BMP2 in the periosteum can cause significant issues with bone callus formation. Depending on ligands, receptors and development stage this pathway can have different effects. Inhibition of BMP can cause issues with normal bone development.
COX-2 Signalling
COX-2 is involved in the production of prostaglandins such as PGE2. This can play a role in inflammation and mechanotransduction. Activation of this pathway via mechanical loading can help to regulate progenitor cells and osteoblast function. Inhibition of this pathway has caused reduced formation in experimental models. Genetic deletion has caused issues with progenitor cell proliferation in the periosteum. This can depend on where in the bone and how much inhibition is occurring. Just because this pathway is inhibited in one region of the bone doesn’t mean it will be in another.
CXCL12/CXCR4 Signalling
CXCL12 binds to CXCR4 to help regulate migration, localisation and function of cells in tissue maintenance and repair. In bone this helps with recruitment of progenitor cells. Experimental inhibition of CXCR4 has caused reduced formation in the ulna via loading. This shows this pathway is involved with adaptive bone formation. However this shows that inhibition won’t necessarily cause reduced normal periosteum apposition. This pathway is also important in regulating migration of blood cells and mobilisation of haematopoietic stem cells meaning it will have a much larger effect on the body.
Transforming Growth Factor-β Signalling
Transforming growth factor beta (TGF-β) regulates cell proliferation, extracellular matrix production, progenitor cell function and intercellular communication. This helps bone respond to injury in the periosteum. This pathway can have complex effects. In the earlier stages TGF-β can encourage progenitor cell proliferation. Effects can depend on signalling environment. This pathway can interact with other pathways such as Wnt and BMP.
FGF and IGF Signalling
Fibroblast growth factors (FGF) and Insulin like growth factors (IGF) regulate cell proliferation, differentiation, matrix production and bone development. These are important pathways for maintaining healthy bone forming cells. The effects of FGF can vary depending on ligand/receptor. Some can encourage osteoblast proliferation whilst others can inhibit differentiation or bone development. IGF’s generally have a positive effect on osteoblast function and bone formation. This can depend on development stage.
This will mark the end of my last guide for around 2 weeks to a month. I'm gonna be moving, and my setup will be in storage until further notice.
This is the last day I'll have my setup for a while so i wanted to make a guide before i left.
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