Appositional Ossification: Function, Tasks, Role & Diseases

Appositional ossification is the growth in thickness of bone. Appositional growth occurs at circumference and originates at the stratum osteogenicum of the periosteum. If a bone grows aimlessly in width but no longer in length, restrictions of motion set in.

What is appositional ossification?

Appositional ossification is the growth in thickness of bone. The medical term ossification or osteogenesis names bone formation. Bone growth occurs either in length or in width. Growth in width is also called thickness growth or appositional ossification. Length growth does not take place permanently. Thickness growth, on the other hand, is a permanent body process. New layers of tissue attach to the bone from the outside during appositional ossification. This makes the growth process a process of perichondral ossification. This refers to indirect bone formation from the outside, which occurs via the intermediate step of cartilage. Appositional ossification affects both plate and short bones, as well as long tubular bones, and is an important part of bone remodeling. Through thickness growth, bones adapt to certain loads or specific stresses, for example. Osteoblasts, osteoclasts and osteocytes are involved in the ossification process. The basic substance for all bone formation processes is the embryonic connective tissue mesenchyme.

Function and task

In appositional ossification, new bone tissue is attached externally to existing bone tissue. Thickness growth always occurs at the cuff of the bone shaft and originates from the stratum osteogenicum. Towards the middle of the diaphysis, the new bone material attaches to the existing bone from the outside. Periosteal cells form this new material during differentiation. The periosteum is a thin layer of tissue on the outer surface of all bones. The inner layer consists of osteoblastic stem cells for bone regeneration. The outer layer contains cell-poor connective tissue full of collagen fibers. The osteoblasts perform appositional growth. As embryonic mesenchymal cells, these cells are capable of synthesizing a collagenous bone matrix and produce osteoid for this purpose. As bone formation progresses, the osteoblasts distance themselves from each other and wall each other into the bone substance. Thus, a fine system of individual canals is formed. During perichondral ossification, osteoblasts separate from the cartilaginous membrane and deposit themselves in the form of a ring around the cartilage model. In this way, they give rise to a bone cuff. Perichondral ossification always occurs at the midshaft of long tubular bones. At the shaft part close to the epiphysis, the thickness growth of the bones takes place from within and is accomplished by the accumulation of cells of the endost. Like length growth, thickness growth of bones also takes place under the influence of hormones. As soon as the growth plate of bones has closed, they are no longer capable of length growth. Hormones then no longer activate length growth processes, but only the processes of appositional ossification. The hormones intended for this purpose are hormones of the anterior pituitary, some thyroid hormones and sex hormones. In addition to the growth hormone STH (somatotropic hormone), the sex hormones testosterone and estrogen play a major role in the hormonal regulation of ossification. Bone thickness growth ensures that bone substance can withstand weight changes and new loading positions. Length growth is stimulated by the same hormones as thickness growth for good reason. As bones grow in length, the weight they must withstand increases. Length growth must therefore always be accompanied by appositional ossification so that the bone does not break in the new loading situation. Length and thickness growth are consequently ideally matched in the body.

Diseases and complaints

Bone growth can be affected by various diseases. One of the best-known diseases with devastating effects on indirect ossification and thus appositional osteogenesis is osteogenesis imperfecta. This mutation-related disease is also known as brittle bone disease. The causative mutation affects the COL1A1 and COL1A2 genes. These genes determine the assembly of type I collagens.The genetic defect causes an abnormal messenger substance to reach the body’s cells. Thus, they produce incomplete or otherwise abnormal collagen fibers. Patients with brittle bone disease suffer from deformed collagen rods that provide little stability to the bones. Some types of brittle bone disease are also characterized by collagen rods that are normal but too limited in number. In all cases, patients suffer from fragile bones that are prone to fracture. Brittle bone disease is a structural bone disease. In contrast, achondroplasia is an actual bone growth disorder. In this disease, the epiphyseal joints close too early. Length growth is no longer possible after joint closure. However, appositional growth of the bones continues. The same is true for desmal ossification. As a result, the harmony between length and thickness growth no longer exists. The imbalance of the growth processes shifts the body proportions of the patients. On the trunk and head, normal growth is present in most cases. However, the growth in length of the limbs stagnates prematurely. The excessive growth in thickness can cause considerable discomfort. This is especially true for larger bones. Mechanical motion can be restricted by excessive appositional ossification, for example. For example, in many cases the range of motion of the joints is reduced by the steadily increasing thickness. Excessive ossification processes occur particularly often after bone fractures. Hormonal disorders can also cause ossification disorders that affect both length and thickness growth. If both forms of growth are affected to the same extent, the symptoms are usually less severe. If length growth is already complete, excessive growth hormone causes only thickness growth and thus, as in achondroplasia, limits the affected person’s ability to move.