# 骺板发育不良（Physeal Dysplasia）

- 器官 / 系统：骨 / 骨骼肌肉系统（bone / musculoskeletal-system）
- NTP 数据编号：ntp-0583
- 规范 URL：https://www.labsmart.cn/ntp/bone-physeal-dysplasia.html
- 中文图谱总页锚点：https://www.labsmart.cn/ntp-atlas.html#bone-physeal-dysplasia
- 原始出处：https://ntp.niehs.nih.gov/atlas/nnl/musculoskeletal-system/bone/PhysealDysplasia
- 授权：美国联邦政府作品，公有领域；引用请标注 NTP Nonneoplastic Lesion Atlas
- 适用说明：仅供科研使用，不用于临床诊断

## 一句话结论
骨骺软骨发育不良（dysplasia）（Figure 1、Figure 2）由矿化缺陷和软骨吸收减少所致。

## 病变描述（中文）
骨骺软骨发育不良（dysplasia）（Figure 1、Figure 2）由矿化缺陷和软骨吸收减少所致。抑制血管长入骨骺的药物可导致骨骺增厚和发育不良（Figure 1）；这是软骨吸收减少的一个示例。这导致增大的软骨细胞持续存在（Figure 2）以及肥厚带扩大，从而使生长板中央显著增宽、外周边缘逐渐变细。在大鼠的晚期病变中，骨骺变得不规则，未矿化软骨的增大延伸部深入干骺端内。病变最常见于生长最快的骨骼，包括桡骨、胫骨、跖骨和掌骨。当存在全身性矿化缺陷时，未矿化类骨质增多（hyperosteoidosis）可能是晚期病变的组成部分。在大鼠中，可沿肋骨外侧缘形成“佝偻病串珠（rachitic rosary）”，即显著增大的肋软骨交界。骨骺发育不良可作为营养缺乏、代谢性疾病或化学暴露继发矿化障碍的结果而发生。当这些病变由矿化过程中的营养障碍（维生素 D、钙或磷缺乏）所致，尤其是在生长板处时，被称为佝偻病（rickets）。通常，“骨软化（osteomalacia）”一词曾被用于描述骨骺软骨的矿化缺陷；然而，这并不是首选的命名，因为“骨软化”（见 Bone - Increased Osteoid）用于描述未矿化骨基质（类骨质）增多，导致骨小梁普遍增厚和骨密度总体降低，而不是像骨骺发育不良中所见的那样，表现为骨骺或骺软骨矿化延迟或受损。此外，“骨软化”一词表示大体形态学改变，应被认为不适用于组织学特征描述。干扰钙、磷或维生素 D 代谢的化合物可导致矿化障碍。软骨发育不良也可由化学暴露或代谢障碍诱导的矿化缺陷所致。

## 诊断与分级建议（NTP 共识，中文）
骨骺发育不良应予以记录并给出严重程度分级。可在描述中尝试将这些病变与营养性（佝偻病）、代谢性或化合物相关病因联系起来。相关链接：Bone - Increased Osteoid

## 英文原文 · Comment
Dysplasia of physeal cartilage ( Figure 1 and Figure 2 ) results from defective mineralization and decreased cartilage resorption. Pharmaceutical agents that inhibit vascular penetration of the physis can lead to physeal thickening and dysplasia ( Figure 1 ); this is an example of decreased cartilage resorption. This leads to a persistence of enlarged chondrocytes ( Figure 2 ) and an enlarged zone of hypertrophy, resulting in a growth plate that is markedly widened centrally and tapered at the peripheral margins. In advanced lesions in the rat, the physes become irregular, with enlarged extensions of unmineralized cartilage extending deep within the metaphysis. Lesions are most prevalent in the fastest-growing bones, including the radius, tibia, metatarsals, and metacarpals. Increased amounts of unmineralized osteoid (hyperosteoidosis) may be a component of advanced lesions when a systemic defect in mineralization is present. In rats, the formation of a "rachitic rosary," or markedly enlarged costochondral junctions, may occur along the lateral margins of the ribs. Physeal dysplasia may occur as a result of disturbances in mineralization secondary to nutritional deficiencies, metabolic disease, or chemical exposure. When these lesions occur as a result of a nutritional disturbance (deficiency in vitamin D, calcium, or phosphorus) in mineralization, particularly at the growth plate, they are referred to as rickets. Often, the term "osteomalacia" has been used to describe defective mineralization of epiphyseal cartilage; however, this is not the preferred nomenclature, since "osteomalacia" (see Bone - Increased Osteoid ) is used to describe increased amounts of unmineralized bone matrix (osteoid) causing generalized thickening of bony trabeculae, and an overall decrease in bone density, rather than delayed or impaired mineralization of physeal or epiphyseal cartilage, as seen in physeal dysplasia. Furthermore, the term "osteomalacia" denotes a gross morphologic change and should be considered inappropriate for histologic characterization. Compounds interfering with calcium, phosphorus, or vitamin D metabolism may result in disturbances in mineralization. Dysplasia of cartilage may also result from defective mineralization induced by chemical exposure or metabolic disturbances.

## 英文原文 · Recommendation
Physeal dysplasia should be recorded and given a severity grade. An attempt to associate these lesions with nutritional (rickets), metabolic, or compound-related etiologies can be made in the narrative. Related Links: Bone - Increased Osteoid

## 配图
- https://www.labsmart.cn/ntp-atlas-images/ntp_0531.jpg
- https://www.labsmart.cn/ntp-atlas-images/ntp_0533.jpg

整理：北京天融慧通科技有限责任公司（LabSmart）｜ https://www.labsmart.cn