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The function of the periodontium is to support the teeth. The periodontium is a connective tissue organ that is protected by epithelium. It provides for attachment of teeth to the bone in the jaws, affording an apparatus that adapts continually to support the teeth during function. There are four connective tissues located in the periodontium: lamina propria of the gingiva, periodontal ligament, cementum and alveolar bone.5
The entire alveolar process is comprised of alveolar bone and supporting bone. Melcher5 described alveolar bone as “the thimble of bone lining the socket of the tooth”. Supporting bone surrounds the alveolar bone.
The keratinized stratified squamous epithelium protects the lamina propria of the gingiva on its masticatory surfaces. The nonkeratinized epithelium protects the lamina propria on its crevicular and junctional surfaces. The alveolar part of the periodontium is comprised of the periodontal ligament, alveolar bone and cementum; and it is important to review it as a unit.5
Some areas of importance to investigators are the biological processes that control how the periodontal tissues respond to wounding, and how cells from the different tissues of the periodontium interact when more than one periodontal tissue is affected in the wound.5
This course will review different aspects of the potential for the gingival epithelium and connective tissue to heal after wounding, and as well as the potential for healing in the alveolar bone, periodontal ligament and cementum.5
Gingival connective tissue and epithelium are well recognized for their remarkable ability to regenerate. There is evidence to support the finding that crevicular and junctional epithelium have the capacity to quickly regenerate. In addition the junctional epithelium can reattach to enamel, cementum, dentin, and under certain conditions they may even attach to calculus. It has also been reported that cells originating from the germinative layers of keratinized masticatory epithelium can give rise to cells that differentiate as regenerating crevicular and junctional epithelium. Lamina propria has the ability to regenerate very quickly after wounding, and differentiation of gingival fibers occurs at the same time.5
Scientists are intrigued by the fact that gingiva has the ability to regenerate after wounding and to frequently restore the architecture of its fibers, while most other connective tissues such as skin demonstrate the tendency to scar after wounding with newly-formed fibers that are disoriented. Some researchers have proposed that forces transmitted from the teeth to the regenerating connective tissue control the differentiation and orientation of gingival fibers. Another possible explanation is that the gingival connective tissue attachment to bone or cementum prevents contraction and distortion of the newly formed fibers during the healing process.5
The difference between regeneration and repair is an important distinction. Regeneration implies that the architecture and function in a healing wound have been restored to pre-wounding status. Repair implies that the wound has been healed by a tissue that is unable to completely restore architecture or function.5
Regeneration of bone is of paramount importance in treating periodontal disease. Regeneration of bone after wounding is accomplished by four types of bone cells that occupy different physiological compartments: osteocytes, bone cells residing in bone marrow, cells located in the endosteum, and osteogenic cells in the periosteum.5
In the vicinity of a wound, osteocytes may be active, but it is questionable whether they contribute significantly to the restoration of bone in a defect. While bone marrow is believed to contain a population of highly potent osteoprogenitor cells that may remain separate from hemopoietic and endosteal cell populations, information about whether they contribute to the healing of bone is ambiguous. These osteoprogenitor cells are thought to be responsible for the osteogenic response that occurs when bone marrow is transplanted.5
All internal surfaces of bone are covered by endosteal cells. There is some evidence that these cells may be metabolically active with a significant role in wound repair at various sites including mandibular bone. Cartilage is hardly ever laid down by these cells, and is seen only infrequently in endosteal callus. However, the deposition of cartilage by the cells in periosteal callus is common.5
Cells in the periosteum contribute significantly to healing process in bone wounding, especially in fractures of long bones. There are two important characteristics of the periosteum that support its role in the healing process: The periosteum is comprised of two layers. The outer layer does not seem to have any osteogenic potential, but the cambium, or inner layer, is osteogenic. Since the outer layers of cells next to the fibrous periosteum are frequently populated with dividing cells, they contribute an uninterrupted source of new osteoblasts.5
The cells on the surface of the bone display characteristics of active osteoblasts. Whereas, the cells approaching the bone surface progressively display morphological characteristics associated with active synthesis. In this condition of activity, the periosteal osteogenic layer may exist in a state of equilibrium, i.e., the production of new cells that can differentiate into osteoblasts will equal the loss of cells that are under the influence of osteocytes. If there is an increase in the production of new cells only, or if the transformation of osteoblasts to osteocytes decreases, the osteogenic layer will increase in thickness. If the reverse occurs, the osteogenic layer will thin out.5
As any part of the bone comes close to the termination of its growth, the progenitor cells in the periosteal osteogenic layer cease to divide, while cellular differentiation continues and osteogenesis proceeds until all of the cells have become osteocytes, except for the progenitor cells. The morphological structure of the periosteum assumes that of mature bone. It is made of a fibrous layer that covers a single layer of progenitor cells in the osteogenic layer that is now attenuated or tapering off in activity.5
The progenitor cells appear to remain uncommitted, thereby retaining their ability to divide upon reactivation by trauma or stimulation to initiate bone remodeling. Interestingly, the progenitor cells are capable of differentiating into either chondroblasts or osteoblasts after injury. When a wound is undergoing active repair in an adult animal, the periosteum in that area may closely approximate that found in a young animal that is still growing.5
In the life cycle of the periosteum, it is these two stages that have clinical significance. Soon after a young animal suffers a long bone fracture, some periosteal cells begin dividing and others undertake the synthesis of extracellular protein at the same time. In older animals, the sequence is different. Progenitor cell division begins first, and later the differentiating progeny synthesize extracellular protein.5
The multilayered osteogenic component of the periosteum of a young animal is part of an ongoing process evidenced by the division and differentiation of progenitor cells that are actively involved in osteogenesis. In a situation such as this, the progenerative activity will not only continue after the trauma, but may occur at a faster rate. Rather than dividing first, if the small number of cells in the periosteal cambium instead differentiated into osteoblasts, secreting and surrounding themselves with extracellular bone substance, there would be no remaining cells to divide and produce daughter cells. Thus, the periosteal cambium layer would soon disappear permanently.5
For this reason, division of the periosteal progenitor cells must be the first cellular activity to occur after trauma. Later, some daughter cells can differentiate into osteoblasts, supported by the remaining population of progenitor daughter cells which will ultimately divide again. This assures that there is a continual supply of cells available to differentiate into osteoblasts that will finally be entombed as osteocytes during bone deposition. For this reason, osteogenesis can begin shortly after a young animal is wounded but must be delayed in an adult.5
The periosteum responds to surgical treatment in a similar manner. When a periosteal flap is elevated from adult bone and replaced, the cells from the flap do not produce new bone. Instead, cells from the undisturbed periosteum around the flap take up the task of depositing new bone in the surgical site. However, cells from an elevated osteoperiosteal flap will deposit new bone.5
According to Melcher5 the surgical manipulations associated with the elevation of a periosteal flap are thought to damage most of the cells in the osteogenic layer of the adult periosteum, thus preventing the replaced periosteum from producing new bone. Whereas, the surgical manipulations associated with the elevation of an osteoperiosteal flap do not damage the cells, allowing them to proliferate, differentiate, mature and produce new bone after replacement of the flap.5
However, after a gingival flap is elevated and replaced, necrosis and resorption of bone may occur prior to osteogenesis. The repair process is impaired if the mucoperiosteum is excised. There is increased osteogenic activity and decreased resorption of the alveolar process. Although some of the alveolar process is lost after surgery, there is more complete restoration under a split-thickness flap and less under a full-thickness flap.5
Alveolar bone cells respond vigorously to trauma, as is observed in the significant osteogenesis occurring after the extraction of teeth. Not all cells respond to trauma as extensively. For example, the cells in the flat skull bones do not produce a strong osteogenic response to wounding. Orthodontic movement of teeth would be difficult to impossible without the vigorous osteogenic response of the endosteal and periosteal cells in the alveolar process and the cells residing on the periodontal surface of alveolar bone.5
Cells from both the mucoperiosteum and endosteum of the alveolar process make an important contribution to healing. Healing of alveolar bone may be discussed separately from that of the periodontal ligament, because it is cells from the periodontal ligament that regulate the deposition and resorption of bone from the periodontal surface of alveolar bone.5
The periodontal surface of the alveolar bone is considered to be an internal surface of bone because it is covered by endosteum and not by periosteum. Cells from the periodontal ligament regulate important functions: 1. Osteogenesis and osteoclasis, which is the deposition and breakdown of bone; 2. Fibrogenesis and fibroclasis in the periodontal ligament itself, which is synthesis and resorption of periodontal ligament fibers; and 3. Cementogenesis and cementoclasis, which is the production and resorption of cementum on the root surface.5
Periodontal ligament cells play a vital role in the healing process in alveolar bone in a wound involving both the alveolar process and periodontal ligament. Most wounds associated with periodontal therapy affect both of these tissues. Regeneration of alveolar bone seems to be more aggressive than that of periodontal ligament tissues.5
Periodontal ligament regeneration takes place in wounds associated with the periodontal space but it is not always straight forward. If it is a large wound, bone cells may colonize it, leading to ankylosis and obliteration in that part of the periodontal space. It seems somewhat perplexing that in normal function a connective tissue can demonstrate a high rate of extracellular protein turnover, and contain cells with a high enough rate of deoxyribonucleic acid synthesis and mitosis to respond to a stimulus, and yet not heal more readily compared to bone.5
In a wound involving the periodontal ligament and alveolar bone, periodontal ligament regeneration is associated with regeneration of alveolar bone and reestablishment of the periodontal space. Cells that are believed to originate from the periodontal ligament are responsible for regeneration of cementum in the alveolar part of the periodontium. The development of cementum occurs quickly after orthodontic tooth movement and wounding, and cementum may also be resorbed after wounding.5
During a flap procedure, when gingival fibers are detached and cementum is removed from the root surface, it is epithelium and not cementum that covers the root during healing. Some experiments revealed that while cementogenesis occurred predictably, its most advanced development was in the most apical part of the wound next to the periodontal ligament. In response to gingival surgery, cells located in the coronal aspect of the periodontal ligament increased their DNA synthesis and migrated coronally.5
One of the goals of periodontal therapy is regeneration of the alveolar process. Research has indicated that cells from the alveolar process have the ability to induce regeneration after wounding, and the use of bone marrow grafts can facilitate the production of new bone.5
However, regeneration of the alveolar process after it is destroyed by periodontal disease is not predictable. This may be due in part to the isolated and hostile environment of the periodontium. While restoration of lost bone is often the focus of periodontal surgery, periodontal disease also destroys the lamina propria of the gingiva, cementum and periodontal ligament.5
A more comprehensive approach to the reconstruction of the peridontium would include regeneration of the entire periodontal complex, the periodontium that supports the tooth. Regeneration of the periodontal ligament is vital because it contains the cells (epithelium, connective tissue, and bone) that produce and maintain the periodontium. The periodontal ligament also provides the connection between the cementum and alveolar bone.5