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Piper Classification - Subgroups
Condylar marrow edema can occur from chronic loading or from trauma. In addition, medications such as steroids may result in development of edema of the condylar head. Edema can be diagnosed only through MR imaging. If a patient has no edema in their condylar head, they are subgrouped E0. If the edema involves the condylar head, they are classified E1, and if it involves the condylar neck region, they are classified E2. Edema of the condylar head may resolve spontaneously or alternatively, it may need to be decompressed through a corticotomy procedure.
Avascular necrosis of the mandibular condylar head can occur for several reasons. However, suffice it to say that alteration of blood flow to the condylar head can result initially in ischemia and subsequently in necrosis. There are multiple etiologies for the development of ischemia at the ends of bone structures. It is believed that the angulation and pattern of discal displacement in the temporomandibular joint may play a vital role in the development of AVN in these patients. The primary blood supply can also enter the condylar head at the lateral pole and at the posterior portion of the condyle. Hence, because of the variability of anatomy, patients may present variable risks for development of AVN. The greatest associated finding anatomically that we have been able to document is displacement of the disc from the medial pole. That is, this seems to be the greatest risk factor for a patient to develop AVN.
Once AVN develops there are several definable phases. The first would be the necrotic phase wherein there are no radiographic changes. This would be subgrouped N. In this situation, the hypoxia is sufficient to result in cellular death. Typically, hematopoietic cells and bone cells are more sensitive to hypoxia than fat cells. Avascular necrosis in the acute phase can be diagnosed only through MR imaging or biopsy. In the MR imaging, the fat cell line has to have undergone necrosis in order to make this determination. Alternatively, biopsy may show necrosis at an earlier stage than one may pick up with MR. There is a hyperemic phase in the perimeter of the necrotic tissue. This is an attempt by the body to repair the area of necrotic debris. During the repair process, dead debris is removed by the body. This results in decreased trabecular bone support to the overlying cortex. As part of the healing, the patient also develops a fibrotic stage. Hence, we would categorize these patients as NH for hyperemia and NF for fibrosis. Following hyperemia and fibrosis, there is structural deformity of the condylar head with collapse of the surface. Eventually, this collapsed bone may become sclerotic, and hence these patients are subcategorized NS. It should be noted that within the same condylar head one or all of these various phases of necrosis may be present. Generally, it is more probable to find all phases of necrosis in a large bone structure such as the femoral head. In the mandibular condylar head, it is more probable that only a single phase may be picked up with biopsy.
The third hard tissue subgroup in the Piper Classification is regressive remodeling. This refers to the degree of condylar deformity which occurs secondary to blood supply alteration of the condylar head. If there has been no change in the shape and form of the condylar head, then these patients are subgrouped R0. In this situation, there is no deformity structurally in the condyle. Alternatively, if there is subarticular collapse involving the upper-most portion of the condylar head, then these patients are subgrouped R1. If there is gross structural deformity of the lower condylar head, then these patients are subgrouped R2.
Regressive remodeling results in a decreased vertical dimension of the condylar ramus area. This in turn can lead to structural alteration of the facial skeleton. In general, we describe these patients as either adaptive or non-adaptive.
For completeness of this classification system, please realize that all of these various phases, that is, soft tissue stages, hard tissue subgroups and skeletal malformations are all interdepentent and co-exist.
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