Osteocytes: Structure, Function & Diseases

Osteocytes are mature bone cells enclosed by osteoblasts of the bone matrix. When bone is defective, osteocytes die because of inadequate nutrient supply, prompting the bone-degrading osteoclasts. Pathologic osteocytes may be relevant to diseases such as osteoporosis.

What are osteocytes?

Human bone is alive. Immature osteoblasts form what is called the bone matrix. This network of immature bone cells includes the mature bone cells. Also known as osteocytes, they make up the majority of bone cells in terms of numbers. Osteoblasts are their precursor stage. The maturation of osteoblasts occurs during osteogenesis. This term refers to the formation of new bone tissue. The body is constantly forming new bone tissue and remodeling or adapting the bone structure to stresses. Constant demineralization and remineralization takes place in bone. Osteoclasts break down old bone substance and are thus responsible for demineralization. Osteoblasts take over the mineralization. They are trapped during osteogenesis and become mature osteocytes in this cavity system. So-called gap junctions connect the osteocytes to each other. These are cell-to-cell channels that serve to exchange nutrients. The function of osteocytes has not yet been conclusively clarified. However, they are presumably involved in bone resorption.

Anatomy and structure

Osteoblasts form what is known as the bone matrix. This is the basic organic substance of bone that is still unmineralized. Major components of the bone matrix are type I collagen fibers and mucopolysaccharides. They make the bone compressively elastic. The embryonic connective tissue is also called mesenchyme. Osteoblasts form from it in the immediate vicinity of the blood capillaries. These immature bone cells form soft osteoid. This is bone substance that has not yet calcified. Over time, the osteoblasts enrich the osteoid with the calcium phosphate hydroxyapatite. This storage hardens and stabilizes the bone. Some osteoblasts are surrounded on all sides by bone matrix. These osteoblasts are the osteocytes. They are mononuclear cells in a cavity system with mineralized bone substance. The lacuna system of osteocytes lies between the individual lamellae of bone. A cell body is located in each lacuna. The cell spurs are located in the fine canicular tubules. The cell spurs connect the osteocytes through gap junctions.

Function and tasks

Bone formation and bone resorption take place permanently in human bones. Every seven years, humans receive a new skeleton, so to speak. The skeleton adapts to new conditions through remodeling. Bones that are subjected to stress, for example, become thicker and more resilient over the course of time. Bones that are not moved or subjected to little stress become thinner and weaker. Osteoclasts and osteoblasts play a key role in bone metabolism. Osteoblasts build up bone. Osteoclasts break down bone and prevent endless growth of bone substance. Degradation by osteoclasts is required, for example, in microfractures or fractures. The cells degrade defective bone substance in these phenomena. They dissolve the bone by two mechanisms. First, the mineral salts of the bone are dissolved out so that the substance becomes softer. This occurs through a lowered pH in the cavity between the bone substance and an osteoclast. The low pH is maintained by an active transport of protons. After dissolving out the mineral salts, the osteoclasts release proteolytic enzymes. These enzymes dissolve the collagenous bone matrix and subsequently phagocytose the collagen fragments thus released. The two degradation mechanisms of osteoclasts give rise to howship lacunae, also called the feeding track of osteoclasts. Each osteoclast can theoretically degrade the same amount of bone that requires nearly 100 osteoblasts to build. Osteoclast activity is hormonally controlled and activated by parathyroid hormone. Inactivation occurs through calcitonin. A regulatory function is now also attributed to osteocytes. In defective bone, no or hardly any nutrient supply takes place via the gap junction. As a consequence, the osteocytes in defective bone matrix die. Only with this death of the osteocytes are the osteoclasts called into action.

Diseases

Bone can be affected by various dysregulations. For example, decreased osteoclast activity has as much disease value as increased osteoclast activity or decreased osteoblast activity. Pathologic osteocytes may play a role in dysregulation of osteoclast activity. However, since the exact function of osteocytes is not yet known, this is a rather speculative relationship. When osteoclast activity is reduced, bone proliferates. Bone cancer can develop in this way. However, decreased osteoclast activity is also associated with diseases such as genetic osteoporosis. Increased osteoclast activity breaks down more bone than osteoblasts can form. This phenomenon plays a role in genetic osteoporosis. In addition, diseases such as hyperparathyroidism, osteodystrophia deformans, aseptic bone necrosis and rheumatoid arthritis are characterized by this phenomenon. The same is true for periodontitis and osteogenesis imperfecta. What role osteocytes play in the above diseases remains the subject of research. Since dead osteocytes are the first to call osteoclasts into action, a causal relationship between the structure of osteocytes and some of the diseases mentioned cannot be ruled out.

Typical and common bone diseases

  • Osteoporosis
  • Bone pain
  • Bone fracture
  • Paget’s disease